Demyelinating Autoimmune Diseases, CNS
Demyelinating Diseases
Autoimmune Diseases
Polyradiculoneuropathy, Chronic Inflammatory Demyelinating
Multiple Sclerosis
Theilovirus
Encephalomyelitis, Autoimmune, Experimental
Myelin Sheath
Autoimmunity
Autoantibodies
Polyneuropathies
Central Nervous System
Myelin Proteins
Charcot-Marie-Tooth Disease
Neuromyelitis Optica
Oligodendroglia
Lupus Erythematosus, Systemic
Guillain-Barre Syndrome
Encephalomyelitis
Sural Nerve
Myelin Basic Protein
Autoantigens
Myelin-Oligodendrocyte Glycoprotein
Encephalomyelitis, Acute Disseminated
Myelin-Associated Glycoprotein
Spinal Cord
Maus Elberfeld virus
Autoimmune Diseases of the Nervous System
JC Virus
Mice, Inbred C57BL
Myelin P0 Protein
Myelin Proteolipid Protein
T-Lymphocytes
Central Nervous System Diseases
Targeted expression of baculovirus p35 caspase inhibitor in oligodendrocytes protects mice against autoimmune-mediated demyelination. (1/65)
The mechanisms underlying oligodendrocyte (OLG) loss and the precise roles played by OLG death in human demyelinating diseases such as multiple sclerosis (MS), and in the rodent model of MS, experimental autoimmune encephalomyelitis (EAE), remain to be elucidated. To clarify the involvement of OLG death in EAE, we have generated transgenic mice that express the baculovirus anti-apoptotic protein p35 in OLGs through the Cre-loxP system. OLGs from cre/p35 transgenic mice were resistant to tumor necrosis factor-alpha-, anti-Fas antibody- and interferon-gamma-induced cell death. cre/p35 transgenic mice were resistant to EAE induction by immunization with the myelin oligodendrocyte glycoprotein. The numbers of infiltrating T cells and macrophages/microglia in the EAE lesions were significantly reduced, as were the numbers of apoptotic OLGs expressing the activated form of caspase-3. Thus, inhibition of apoptosis in OLGs by p35 expression alleviated the severity of the neurological manifestations observed in autoimmune demyelinating diseases. (+info)Reliability and responsiveness of a graduated tuning fork in immune mediated polyneuropathies. The Inflammatory Neuropathy Cause and Treatment (INCAT) Group. (2/65)
The interobserver and intraobserver reliability of the Rydel-Seiffer (RS) graduated tuning fork was evaluated in 113 patients with a clinically stable immune mediated polyneuropathy (83 patients who had had Guillain-Barre syndrome (GBS) in the past, 22 with a chronic inflammatory demyelinating polyneuropathy (CIDP), and eight with a polyneuropathy associated with a gammopathy of undetermined significance). Additionally, the responsiveness of this instrument was serially investigated in 20 patients with recently diagnosed GBS or CIDP and changing clinical conditions. The measures were done in triplicate at eight different locations in the limbs and the values were compared with the recently published vibration threshold reference values. Good interobserver and intraobserver agreements (quadratic weighted kappa=0.67-0.98) and high responsiveness values (standardised response mean scores>0.8) were demonstrated for the RS tuning fork. These results provide, in addition to literature findings, further evidence for incorporation of this easily applicable instrument in routine neurological examination. (+info)CD28 costimulatory blockade exacerbates disease severity and accelerates epitope spreading in a virus-induced autoimmune disease. (3/65)
Theiler's murine encephalomyelitis virus (TMEV) is a natural mouse pathogen which causes a lifelong persistent infection of the central nervous system (CNS) accompanied by T-cell-mediated myelin destruction leading to chronic, progressive hind limb paralysis. TMEV-induced demyelinating disease (TMEV-IDD) is considered to be a highly relevant animal model for the human autoimmune disease multiple sclerosis (MS), which is thought to be initiated as a secondary consequence of a virus infection. Although TMEV-IDD is initiated by virus-specific CD4(+) T cells targeting CNS-persistent virus, CD4(+) T-cell responses against self myelin protein epitopes activated via epitope spreading contribute to chronic disease pathogenesis. We thus examined the ability of antibodies directed against B7 costimulatory molecules to regulate this chronic virus-induced immunopathologic process. Contrary to previous studies showing that blockade of B7-CD28 costimulatory interactions inhibit the initiation of experimental autoimmune encephalomyelitis, treatment of SJL mice at the time of TMEV infection with murine CTLA-4 immunoglobulin or a combination of anti-B7-1 and anti-B7-2 antibodies significantly enhanced clinical disease severity. Costimulatory blockade inhibited early TMEV-specific T-cell and antibody responses critical in clearing peripheral virus infection. The inhibition of virus-specific immune responses led to significantly increased CNS viral titers resulting in increased damage to myelin-producing oligodendrocytes. Following clearance of the costimulatory antagonists, epitope spreading to myelin epitopes was accelerated as a result of the increased availability of myelin epitopes leading to a more severe chronic disease course. Our results raise concern about the potential use of B7-CD28 costimulatory blockade to treat human autoimmune diseases potentially associated with acute or persistent virus infections. (+info)Attenuation of experimental autoimmune demyelination in complement-deficient mice. (4/65)
The exact mechanisms leading to CNS inflammation and myelin destruction in multiple sclerosis and in its animal model, experimental allergic encephalomyelitis (EAE) remain equivocal. In both multiple sclerosis and EAE, complement activation is thought to play a pivotal role by recruiting inflammatory cells, increasing myelin phagocytosis by macrophages, and exerting direct cytotoxic effects through the deposition of the membrane attack complex on oligodendrocytes. Despite this assumption, attempts to evaluate complement's contribution to autoimmune demyelination in vivo have been limited by the lack of nontoxic and/or nonimmunogenic complement inhibitors. In this report, we used mice deficient in either C3 or factor B to clarify the role of the complement system in an Ab-independent model of EAE. Both types of complement-deficient mice presented with a markedly reduced disease severity. Although induction of EAE led to inflammatory changes in the meninges and perivascular spaces of both wild-type and complement-deficient animals, in both C3(-/-) and factor B(-/-) mice there was little infiltration of the parenchyma by macrophages and T cells. In addition, compared with their wild-type littermates, the CNS of both C3(-/-) and factor B(-/-) mice induced for EAE are protected from demyelination. These results suggest that complement might be a target for the therapeutic treatment of inflammatory demyelinating diseases of the CNS. (+info)Demyelination but no cognitive, motor or behavioral deficits after adenovirus-mediated gene transfer into the brain. (5/65)
Adenovirus-mediated gene transfer of interferon gamma (AdIFN) elicits rejection of intracerebral Lewis lung carcinoma. In this system, gene transfer into brain parenchymal cells is both necessary and sufficient to generate the antitumor response. Despite persistent parenchymal inflammation and demyelination, wild-type mice injected intracerebrally with either AdIFN or beta-galactosidase adenovirus (AdBGAL) perform as well as non-injected animals in behavioral, memory, and motor tests. Both AdIFN and AdBGAL elicit demyelination whose incidence rises sharply when the lowest effective dose of AdIFN is exceeded. Therefore, transfer of interferon gamma into brain parenchyma does not seem to elicit detectable cognitive, behavioral or motor deficits. Furthermore, gene transfer into the brain, by adenoviral vectors currently in clinical trials, is associated with a narrow therapeutic window where the incidence of demyelination rises sharply soon after the effective dose is achieved. Gene Therapy (2000) 7, 2094-2098. (+info)Central nervous system disease in patients with macrophagic myofasciitis. (6/65)
Macrophagic myofasciitis (MMF), a condition newly recognized in France, is manifested by diffuse myalgias and characterized by highly specific myopathological alterations which have recently been shown to represent an unusually persistent local reaction to intramuscular injections of aluminium-containing vaccines. Among 92 MMF patients recognized so far, eight of them, which included the seven patients reported here, had a symptomatic demyelinating CNS disorder. CNS manifestations included hemisensory or sensorimotor symptoms (four out of seven), bilateral pyramidal signs (six out of seven), cerebellar signs (four out of seven), visual loss (two out of seven), cognitive and behavioural disorders (one out of seven) and bladder dysfunction (one out of seven). Brain T(2)-weighted MRI showed single (two out of seven) or multiple (four out of seven) supratentorial white matter hyperintense signals and corpus callosum atrophy (one out of seven). Evoked potentials were abnormal in four out of six patients and CSF in four out of seven. According to Poser's criteria for multiple sclerosis, the diagnosis was clinically definite (five out of seven) or clinically probable multiple sclerosis (two out of seven). Six out of seven patients had diffuse myalgias. Deltoid muscle biopsy showed stereotypical accumulations of PAS (periodic acid-Schiff)-positive macrophages, sparse CD8+ T cells and minimal myofibre damage. Aluminium-containing vaccines had been administered 3-78 months (median = 33 months) before muscle biopsy (hepatitis B virus: four out of seven, tetanus toxoid: one out of seven, both hepatitis B virus and tetanus toxoid: two out of seven). The association between MMF and multiple sclerosis-like disorders may give new insights into the controversial issues surrounding vaccinations and demyelinating CNS disorders. Deltoid muscle biopsy searching for myopathological alterations of MMF should be performed in multiple sclerosis patients with diffuse myalgias. (+info)MIP-1alpha, MCP-1, GM-CSF, and TNF-alpha control the immune cell response that mediates rapid phagocytosis of myelin from the adult mouse spinal cord. (7/65)
The slow immune response in the adult mammalian CNS results in slow myelin phagocytosis along degenerating white matter after injury. This has important consequences for axon regeneration because of the presence of axon growth inhibitors in myelin. In addition, abnormal immune cell responses in the CNS lead to demyelinating disease. Lysophosphatidylcholine (LPC) can induce an inflammatory response in the CNS, producing rapid demyelination without much damage to adjacent cells. In this study, we searched for the molecular switches that turn on this immune cell response. Using reverse transcription PCR analysis, we show that mRNA expression of macrophage inflammatory protein-1alpha (MIP-1alpha), macrophage chemotactic protein-1 (MCP-1), granulocyte macrophage-colony stimulating factor (GM-CSF), and tumor necrosis factor-alpha (TNF-alpha) in the spinal cord is rapidly and transiently upregulated after intraspinal injection of LPC. Neutralizing these signaling molecules with function-blocking antibodies suppresses recruitment of T-cells, neutrophils, and monocytes into the spinal cord, as well as significantly reduces the number of phagocytic macrophages and the demyelination induced by LPC. These findings will have important implications for CNS regeneration and demyelinating disease. (+info)A virus-induced molecular mimicry model of multiple sclerosis. (8/65)
Molecular mimicry is the process by which virus infection activates T cells that are cross-reactive with self antigens. Infection of SJL/J mice with the neurotropic picornavirus Theiler's murine encephalomyelitis virus (TMEV) leads to a progressive CD4(+) T cell-mediated demyelinating disease similar to multiple sclerosis. To study the potential of virus-induced molecular mimicry to initiate autoimmune demyelination, a nonpathogenic TMEV variant was engineered to encode a 30-mer peptide encompassing the immunodominant encephalitogenic myelin proteolipid protein (PLP139-151) epitope. Infection with the PLP139-151-encoding TMEV led within 10-14 days to a rapid-onset paralytic demyelinating disease characterized by PLP139-151-specific CD4(+) Th1 responses; insertion of a non-self ovalbumin sequence led to restoration of the normal late-onset disease. Early-onset disease was also observed in mice infected with a TMEV encoding PLP139-151 with an amino acid substitution at the secondary T cell receptor (TCR) contact residue (H147A), but not in mice infected with TMEV encoding a PLP139-151 substitution at the primary TCR contact (W144A). Most significantly, mice infected with TMEV encoding a Haemophilus influenzae mimic peptide, sharing only 6 of 13 amino acids with PLP139-151, displayed rapid-onset disease and developed cross-reactive PLP139-151-specific CD4(+) Th1 responses. To our knowledge, this is the first study showing that a naturally infectious virus encoding a myelin epitope mimic can directly initiate organ-specific T cell-mediated autoimmunity. (+info)Demyelinating autoimmune diseases of the central nervous system (CNS) are a group of disorders characterized by inflammation and damage to the myelin sheath, which is the protective covering that surrounds nerve fibers in the brain and spinal cord. This damage can result in various neurological symptoms, including muscle weakness, sensory loss, vision problems, and cognitive impairment.
The most common demyelinating autoimmune disease of the CNS is multiple sclerosis (MS), which affects approximately 2.3 million people worldwide. Other examples include neuromyelitis optica spectrum disorder (NMOSD), acute disseminated encephalomyelitis (ADEM), and transverse myelitis.
These conditions are thought to arise when the immune system mistakenly attacks the myelin sheath, leading to inflammation, damage, and scarring (sclerosis) in the CNS. The exact cause of this autoimmune response is not fully understood, but it is believed to involve a complex interplay between genetic, environmental, and immunological factors.
Treatment for demyelinating autoimmune diseases of the CNS typically involves a combination of medications to manage symptoms, reduce inflammation, and modify the course of the disease. These may include corticosteroids, immunosuppressive drugs, and disease-modifying therapies (DMTs) that target specific components of the immune system.
Demyelinating diseases are a group of disorders that are characterized by damage to the myelin sheath, which is the protective covering surrounding nerve fibers in the brain, optic nerves, and spinal cord. Myelin is essential for the rapid transmission of nerve impulses, and its damage results in disrupted communication between the brain and other parts of the body.
The most common demyelinating disease is multiple sclerosis (MS), where the immune system mistakenly attacks the myelin sheath. Other demyelinating diseases include:
1. Acute Disseminated Encephalomyelitis (ADEM): An autoimmune disorder that typically follows a viral infection or vaccination, causing widespread inflammation and demyelination in the brain and spinal cord.
2. Neuromyelitis Optica (NMO) or Devic's Disease: A rare autoimmune disorder that primarily affects the optic nerves and spinal cord, leading to severe vision loss and motor disability.
3. Transverse Myelitis: Inflammation of the spinal cord causing damage to both sides of one level (segment) of the spinal cord, resulting in various neurological symptoms such as muscle weakness, numbness, or pain, depending on which part of the spinal cord is affected.
4. Guillain-Barré Syndrome: An autoimmune disorder that causes rapid-onset muscle weakness, often beginning in the legs and spreading to the upper body, including the face and breathing muscles. It occurs when the immune system attacks the peripheral nerves' myelin sheath.
5. Central Pontine Myelinolysis (CPM): A rare neurological disorder caused by rapid shifts in sodium levels in the blood, leading to damage to the myelin sheath in a specific area of the brainstem called the pons.
These diseases can result in various symptoms, such as muscle weakness, numbness, vision loss, difficulty with balance and coordination, and cognitive impairment, depending on the location and extent of the demyelination. Treatment typically focuses on managing symptoms, modifying the immune system's response, and promoting nerve regeneration and remyelination when possible.
Autoimmune diseases are a group of disorders in which the immune system, which normally protects the body from foreign invaders like bacteria and viruses, mistakenly attacks the body's own cells and tissues. This results in inflammation and damage to various organs and tissues in the body.
In autoimmune diseases, the body produces autoantibodies that target its own proteins or cell receptors, leading to their destruction or malfunction. The exact cause of autoimmune diseases is not fully understood, but it is believed that a combination of genetic and environmental factors contribute to their development.
There are over 80 different types of autoimmune diseases, including rheumatoid arthritis, lupus, multiple sclerosis, type 1 diabetes, Hashimoto's thyroiditis, Graves' disease, psoriasis, and inflammatory bowel disease. Symptoms can vary widely depending on the specific autoimmune disease and the organs or tissues affected. Treatment typically involves managing symptoms and suppressing the immune system to prevent further damage.
Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP) is a rare neurological disorder characterized by progressive and persistent inflammation of the peripheral nerves' myelin sheaths, leading to significant damage and impaired nerve function. Myelin is the fatty insulation that surrounds and protects nerve fibers, enabling efficient electrical conduction and communication between the brain, spinal cord, and muscles.
In CIDP, the immune system mistakenly attacks the myelin sheath, causing its gradual deterioration (demyelination) and subsequent impairment of nerve function. This results in symptoms such as progressive muscle weakness, numbness, tingling, or sensory loss affecting both sides of the body. The onset of CIDP can be either acute or insidious, with symptoms developing slowly over several months.
CIDP is typically classified into two categories based on the distribution of nerve involvement:
1. Distal acquired demyelinating symmetric (DADS) neuropathy: This form of CIDP affects the longest nerves first, leading to symmetrical sensory and motor disturbances in the feet and hands.
2. Asymmetric or multifocal acquired demyelinating sensory and motor neuropathy: In this form, the damage is more localized and asymmetrical, affecting various parts of the peripheral nervous system.
The diagnosis of CIDP relies on a combination of clinical presentation, electrodiagnostic studies (nerve conduction studies and electromyography), and supportive findings from cerebrospinal fluid analysis and nerve biopsy. Treatment usually involves immunosuppressive therapies to control the immune response and promote nerve recovery, such as corticosteroids, intravenous immunoglobulins, or plasma exchange. Early diagnosis and treatment can significantly improve outcomes and prevent long-term disability in patients with CIDP.
Multiple Sclerosis (MS) is a chronic autoimmune disease that affects the central nervous system (CNS), which includes the brain, spinal cord, and optic nerves. In MS, the immune system mistakenly attacks the protective covering of nerve fibers, called myelin, leading to damage and scarring (sclerosis). This results in disrupted communication between the brain and the rest of the body, causing a variety of neurological symptoms that can vary widely from person to person.
The term "multiple" refers to the numerous areas of scarring that occur throughout the CNS in this condition. The progression, severity, and specific symptoms of MS are unpredictable and may include vision problems, muscle weakness, numbness or tingling, difficulty with balance and coordination, cognitive impairment, and mood changes. There is currently no cure for MS, but various treatments can help manage symptoms, modify the course of the disease, and improve quality of life for those affected.
Theilovirus is not typically considered a separate virus in modern virology. Instead, it is now classified as a genotype (genotype 3) of the human parechovirus (HPeV), which belongs to the family Picornaviridae. HPeVs are small, non-enveloped, single-stranded RNA viruses that can cause various clinical manifestations, ranging from mild respiratory or gastrointestinal symptoms to severe neurological diseases in infants and young children.
Historically, Theilovirus was first identified as a separate virus in 1958 by H. Theil and K. Maassab, isolated from the feces of healthy children. It was initially classified as a member of the Enterovirus genus but was later reclassified as a distinct genus, Theilovirus, in 1999. However, subsequent genetic analysis revealed that Theilovirus is closely related to HPeVs, and it is now considered a genotype within the HPeV species.
In summary, Theilovirus is not a separate medical term or virus but rather a historical name for what is now classified as human parechovirus genotype 3 (HPeV3).
Autoimmune encephalomyelitis (EAE) is a model of inflammatory demyelinating disease used in medical research to study the mechanisms of multiple sclerosis (MS) and develop new therapies. It is experimentally induced in laboratory animals, typically mice or rats, through immunization with myelin antigens or T-cell transfer. The resulting immune response leads to inflammation, demyelination, and neurological dysfunction in the central nervous system (CNS), mimicking certain aspects of MS.
EAE is a valuable tool for understanding the pathogenesis of MS and testing potential treatments. However, it is essential to recognize that EAE is an experimental model and may not fully recapitulate all features of human autoimmune encephalomyelitis.
The myelin sheath is a multilayered, fatty substance that surrounds and insulates many nerve fibers in the nervous system. It is essential for the rapid transmission of electrical signals, or nerve impulses, along these nerve fibers, allowing for efficient communication between different parts of the body. The myelin sheath is produced by specialized cells called oligodendrocytes in the central nervous system (CNS) and Schwann cells in the peripheral nervous system (PNS). Damage to the myelin sheath, as seen in conditions like multiple sclerosis, can significantly impair nerve function and result in various neurological symptoms.
Autoimmunity is a medical condition in which the body's immune system mistakenly attacks and destroys healthy tissues within the body. In normal function, the immune system recognizes and fights off foreign substances such as bacteria, viruses, and toxins. However, when autoimmunity occurs, the immune system identifies self-molecules or tissues as foreign and produces an immune response against them.
This misguided response can lead to chronic inflammation, tissue damage, and impaired organ function. Autoimmune diseases can affect various parts of the body, including the joints, skin, glands, muscles, and blood vessels. Some common examples of autoimmune diseases are rheumatoid arthritis, lupus, multiple sclerosis, type 1 diabetes, Hashimoto's thyroiditis, and Graves' disease.
The exact cause of autoimmunity is not fully understood, but it is believed to involve a combination of genetic, environmental, and lifestyle factors that trigger an abnormal immune response in susceptible individuals. Treatment for autoimmune diseases typically involves managing symptoms, reducing inflammation, and suppressing the immune system's overactive response using medications such as corticosteroids, immunosuppressants, and biologics.
Cardiovirus infections refer to diseases caused by viruses belonging to the Cardiovirus genus of the Picornaviridae family. These viruses are small, single-stranded, positive-sense RNA viruses that infect a wide range of hosts, including humans, animals, and birds.
In humans, the most common cardiovirus is the human enterovirus 71 (HEV71), which primarily causes hand, foot, and mouth disease (HFMD). HFMD is a mild, self-limiting illness characterized by fever, sore throat, and rash on the hands, feet, and mouth. However, in some cases, HEV71 infection can lead to severe neurological complications such as encephalitis, meningitis, and acute flaccid paralysis.
Another important cardiovirus is the Theiler's murine encephalomyelitis virus (TMEV), which primarily infects mice and causes a biphasic disease characterized by an initial phase of flaccid paralysis followed by a second phase of chronic demyelination. TMEV has been used as a model to study the mechanisms of viral-induced demyelination and has provided valuable insights into the pathogenesis of multiple sclerosis.
Cardiovirus infections are typically diagnosed through the detection of viral RNA or antigens in clinical specimens such as stool, throat swabs, or cerebrospinal fluid. Treatment is generally supportive and aimed at managing symptoms, as there are no specific antiviral therapies available for cardiovirus infections. Prevention measures include good hygiene practices, such as handwashing and avoiding close contact with infected individuals.
Autoantibodies are defined as antibodies that are produced by the immune system and target the body's own cells, tissues, or organs. These antibodies mistakenly identify certain proteins or molecules in the body as foreign invaders and attack them, leading to an autoimmune response. Autoantibodies can be found in various autoimmune diseases such as rheumatoid arthritis, lupus, and thyroiditis. The presence of autoantibodies can also be used as a diagnostic marker for certain conditions.
Polyneuropathy is a medical condition that refers to the damage or dysfunction of peripheral nerves (nerves outside the brain and spinal cord) in multiple areas of the body. These nerves are responsible for transmitting sensory, motor, and autonomic signals between the central nervous system and the rest of the body.
In polyneuropathies, this communication is disrupted, leading to various symptoms depending on the type and extent of nerve damage. Commonly reported symptoms include:
1. Numbness or tingling in the hands and feet
2. Muscle weakness and cramps
3. Loss of reflexes
4. Burning or stabbing pain
5. Balance and coordination issues
6. Increased sensitivity to touch
7. Autonomic dysfunction, such as bowel, bladder, or digestive problems, and changes in blood pressure
Polyneuropathies can be caused by various factors, including diabetes, alcohol abuse, nutritional deficiencies, autoimmune disorders, infections, toxins, inherited genetic conditions, or idiopathic (unknown) causes. The treatment for polyneuropathy depends on the underlying cause and may involve managing underlying medical conditions, physical therapy, pain management, and lifestyle modifications.
The Central Nervous System (CNS) is the part of the nervous system that consists of the brain and spinal cord. It is called the "central" system because it receives information from, and sends information to, the rest of the body through peripheral nerves, which make up the Peripheral Nervous System (PNS).
The CNS is responsible for processing sensory information, controlling motor functions, and regulating various autonomic processes like heart rate, respiration, and digestion. The brain, as the command center of the CNS, interprets sensory stimuli, formulates thoughts, and initiates actions. The spinal cord serves as a conduit for nerve impulses traveling to and from the brain and the rest of the body.
The CNS is protected by several structures, including the skull (which houses the brain) and the vertebral column (which surrounds and protects the spinal cord). Despite these protective measures, the CNS remains vulnerable to injury and disease, which can have severe consequences due to its crucial role in controlling essential bodily functions.
Myelin proteins are proteins that are found in the myelin sheath, which is a fatty (lipid-rich) substance that surrounds and insulates nerve fibers (axons) in the nervous system. The myelin sheath enables the rapid transmission of electrical signals (nerve impulses) along the axons, allowing for efficient communication between different parts of the nervous system.
There are several types of myelin proteins, including:
1. Proteolipid protein (PLP): This is the most abundant protein in the myelin sheath and plays a crucial role in maintaining the structure and function of the myelin sheath.
2. Myelin basic protein (MBP): This protein is also found in the myelin sheath and helps to stabilize the compact structure of the myelin sheath.
3. Myelin-associated glycoprotein (MAG): This protein is involved in the adhesion of the myelin sheath to the axon and helps to maintain the integrity of the myelin sheath.
4. 2'3'-cyclic nucleotide 3' phosphodiesterase (CNP): This protein is found in oligodendrocytes, which are the cells that produce the myelin sheath in the central nervous system. CNP plays a role in maintaining the structure and function of the oligodendrocytes.
Damage to myelin proteins can lead to demyelination, which is a characteristic feature of several neurological disorders, including multiple sclerosis (MS), Guillain-Barré syndrome, and Charcot-Marie-Tooth disease.
Charcot-Marie-Tooth disease (CMT) is a group of inherited disorders that cause nerve damage, primarily affecting the peripheral nerves. These are the nerves that transmit signals between the brain and spinal cord to the rest of the body. CMT affects both motor and sensory nerves, leading to muscle weakness and atrophy, as well as numbness or tingling in the hands and feet.
The disease is named after the three physicians who first described it: Jean-Martin Charcot, Pierre Marie, and Howard Henry Tooth. CMT is characterized by its progressive nature, meaning symptoms typically worsen over time, although the rate of progression can vary significantly among individuals.
There are several types of CMT, classified based on their genetic causes and patterns of inheritance. The two most common forms are CMT1 and CMT2:
1. CMT1: This form is caused by mutations in the genes responsible for the myelin sheath, which insulates peripheral nerves and allows for efficient signal transmission. As a result, demyelination occurs, slowing down nerve impulses and causing muscle weakness, particularly in the lower limbs. Symptoms usually begin in childhood or adolescence and include foot drop, high arches, and hammertoes.
2. CMT2: This form is caused by mutations in the genes responsible for the axons, the nerve fibers that transmit signals within peripheral nerves. As a result, axonal degeneration occurs, leading to muscle weakness and atrophy. Symptoms usually begin in early adulthood and progress more slowly than CMT1. They primarily affect the lower limbs but can also involve the hands and arms.
Diagnosis of CMT typically involves a combination of clinical evaluation, family history, nerve conduction studies, and genetic testing. While there is no cure for CMT, treatment focuses on managing symptoms and maintaining mobility and function through physical therapy, bracing, orthopedic surgery, and pain management.
Neuromyelitis optica (NMO), also known as Devic's disease, is an autoimmune disorder that affects the central nervous system (CNS). It primarily causes inflammation and damage to the optic nerves (which transmit visual signals from the eye to the brain) and the spinal cord. This results in optic neuritis (inflammation of the optic nerve, causing vision loss) and myelitis (inflammation of the spinal cord, leading to motor, sensory, and autonomic dysfunction).
A key feature of NMO is the presence of autoantibodies against aquaporin-4 (AQP4-IgG), a water channel protein found in astrocytes (a type of glial cell) in the CNS. These antibodies play a crucial role in the development of the disease, as they target and damage the AQP4 proteins, leading to inflammation, demyelination (loss of the protective myelin sheath around nerve fibers), and subsequent neurological dysfunction.
NMO is distinct from multiple sclerosis (MS), another autoimmune disorder affecting the CNS, as it has different clinical features, radiological findings, and treatment responses. However, NMO can sometimes be misdiagnosed as MS due to overlapping symptoms in some cases. Accurate diagnosis of NMO is essential for appropriate management and treatment, which often includes immunosuppressive therapies to control the autoimmune response and prevent further damage to the nervous system.
Oligodendroglia are a type of neuroglial cell found in the central nervous system (CNS) of vertebrates, including humans. These cells play a crucial role in providing support and insulation to nerve fibers (axons) in the CNS, which includes the brain and spinal cord.
More specifically, oligodendroglia produce a fatty substance called myelin that wraps around axons, forming myelin sheaths. This myelination process helps to increase the speed of electrical impulse transmission (nerve impulses) along the axons, allowing for efficient communication between different neurons.
In addition to their role in myelination, oligodendroglia also contribute to the overall health and maintenance of the CNS by providing essential nutrients and supporting factors to neurons. Dysfunction or damage to oligodendroglia has been implicated in various neurological disorders, such as multiple sclerosis (MS), where demyelination of axons leads to impaired nerve function and neurodegeneration.
Systemic Lupus Erythematosus (SLE) is a complex autoimmune disease that can affect almost any organ or system in the body. In SLE, the immune system produces an exaggerated response, leading to the production of autoantibodies that attack the body's own cells and tissues, causing inflammation and damage. The symptoms and severity of SLE can vary widely from person to person, but common features include fatigue, joint pain, skin rashes (particularly a "butterfly" rash across the nose and cheeks), fever, hair loss, and sensitivity to sunlight.
Systemic lupus erythematosus can also affect the kidneys, heart, lungs, brain, blood vessels, and other organs, leading to a wide range of symptoms such as kidney dysfunction, chest pain, shortness of breath, seizures, and anemia. The exact cause of SLE is not fully understood, but it is believed to involve a combination of genetic, environmental, and hormonal factors. Treatment typically involves medications to suppress the immune system and manage symptoms, and may require long-term management by a team of healthcare professionals.
Guillain-Barré syndrome (GBS) is a rare autoimmune disorder in which the body's immune system mistakenly attacks the peripheral nervous system, leading to muscle weakness, tingling sensations, and sometimes paralysis. The peripheral nervous system includes the nerves that control our movements and transmit signals from our skin, muscles, and joints to our brain.
The onset of GBS usually occurs after a viral or bacterial infection, such as respiratory or gastrointestinal infections, or following surgery, vaccinations, or other immune system triggers. The exact cause of the immune response that leads to GBS is not fully understood.
GBS typically progresses rapidly over days or weeks, with symptoms reaching their peak within 2-4 weeks after onset. Most people with GBS experience muscle weakness that starts in the lower limbs and spreads upward to the upper body, arms, and face. In severe cases, the diaphragm and chest muscles may become weakened, leading to difficulty breathing and requiring mechanical ventilation.
The diagnosis of GBS is based on clinical symptoms, nerve conduction studies, and sometimes cerebrospinal fluid analysis. Treatment typically involves supportive care, such as pain management, physical therapy, and respiratory support if necessary. In addition, plasma exchange (plasmapheresis) or intravenous immunoglobulin (IVIG) may be used to reduce the severity of symptoms and speed up recovery.
While most people with GBS recover completely or with minimal residual symptoms, some may experience long-term disability or require ongoing medical care. The prognosis for GBS varies depending on the severity of the illness and the individual's age and overall health.
Encephalomyelitis is a medical term that refers to inflammation of both the brain (encephalitis) and spinal cord (myelitis). This condition can be caused by various infectious agents, such as viruses, bacteria, fungi, or parasites, or it can be due to an autoimmune response where the body's own immune system attacks the nervous tissue.
The symptoms of encephalomyelitis can vary widely depending on the extent and location of the inflammation, but they may include fever, headache, stiff neck, seizures, muscle weakness, sensory changes, and difficulty with coordination or walking. In severe cases, encephalomyelitis can lead to permanent neurological damage or even death.
Treatment for encephalomyelitis typically involves addressing the underlying cause, such as administering antiviral medications for viral infections or immunosuppressive drugs for autoimmune reactions. Supportive care, such as pain management, physical therapy, and rehabilitation, may also be necessary to help manage symptoms and promote recovery.
The sural nerve is a purely sensory peripheral nerve in the lower leg and foot. It provides sensation to the outer ( lateral) aspect of the little toe and the adjacent side of the fourth toe, as well as a small portion of the skin on the back of the leg between the ankle and knee joints.
The sural nerve is formed by the union of branches from the tibial and common fibular nerves (branches of the sciatic nerve) in the lower leg. It runs down the calf, behind the lateral malleolus (the bony prominence on the outside of the ankle), and into the foot.
The sural nerve is often used as a donor nerve during nerve grafting procedures due to its consistent anatomy and relatively low risk for morbidity at the donor site.
Myelin Basic Protein (MBP) is a key structural protein found in the myelin sheath, which is a multilayered membrane that surrounds and insulates nerve fibers (axons) in the nervous system. The myelin sheath enables efficient and rapid transmission of electrical signals (nerve impulses) along the axons, allowing for proper communication between different neurons.
MBP is one of several proteins responsible for maintaining the structural integrity and organization of the myelin sheath. It is a basic protein, meaning it has a high isoelectric point due to its abundance of positively charged amino acids. MBP is primarily located in the intraperiod line of the compact myelin, which is a region where the extracellular leaflets of the apposing membranes come into close contact without fusing.
MBP plays crucial roles in the formation, maintenance, and repair of the myelin sheath:
1. During development, MBP helps mediate the compaction of the myelin sheath by interacting with other proteins and lipids in the membrane.
2. MBP contributes to the stability and resilience of the myelin sheath by forming strong ionic bonds with negatively charged phospholipids in the membrane.
3. In response to injury or disease, MBP can be cleaved into smaller peptides that act as chemoattractants for immune cells, initiating the process of remyelination and repair.
Dysregulation or damage to MBP has been implicated in several demyelinating diseases, such as multiple sclerosis (MS), where the immune system mistakenly attacks the myelin sheath, leading to its degradation and loss. The presence of autoantibodies against MBP is a common feature in MS patients, suggesting that an abnormal immune response to this protein may contribute to the pathogenesis of the disease.
Autoantigens are substances that are typically found in an individual's own body, but can stimulate an immune response because they are recognized as foreign by the body's own immune system. In autoimmune diseases, the immune system mistakenly attacks and damages healthy tissues and organs because it recognizes some of their components as autoantigens. These autoantigens can be proteins, DNA, or other molecules that are normally present in the body but have become altered or exposed due to various factors such as infection, genetics, or environmental triggers. The immune system then produces antibodies and activates immune cells to attack these autoantigens, leading to tissue damage and inflammation.
Myelin-Oligodendrocyte Glycoprotein (MOG) is a protein found exclusively on the outermost layer of myelin sheath in the central nervous system (CNS). The myelin sheath is a fatty substance that surrounds and insulates nerve fibers, allowing for efficient and rapid transmission of electrical signals. MOG plays a crucial role in maintaining the integrity and structure of the myelin sheath. It is involved in the adhesion of oligodendrocytes to the surface of neuronal axons and contributes to the stability of the compact myelin structure. Autoimmune reactions against MOG have been implicated in certain inflammatory demyelinating diseases, such as optic neuritis, transverse myelitis, and acute disseminated encephalomyelitis (ADEM).
Acute disseminated encephalomyelitis (ADEM) is a rare inflammatory demyelinating disease of the central nervous system, characterized by a sudden onset of widespread inflammation and damage to the brain and spinal cord. It typically follows a viral infection or, less commonly, vaccination and is more prevalent in children than adults.
The condition involves the rapid development of multiple inflammatory lesions throughout the white matter of the brain and spinal cord. These lesions lead to demyelination, which means the loss of the protective myelin sheath surrounding nerve fibers, disrupting communication between neurons. This results in various neurological symptoms such as:
1. Encephalopathy (changes in consciousness, behavior, or mental status)
2. Weakness or paralysis of limbs
3. Visual disturbances
4. Speech and language problems
5. Seizures
6. Ataxia (loss of coordination and balance)
7. Sensory changes
8. Autonomic nervous system dysfunction (e.g., temperature regulation, blood pressure, heart rate)
The diagnosis of ADEM is based on clinical presentation, radiological findings, and laboratory tests to exclude other possible causes. Magnetic resonance imaging (MRI) typically shows multiple, large, bilateral lesions in the white matter of the brain and spinal cord. Cerebrospinal fluid analysis may reveal an elevated white blood cell count and increased protein levels.
Treatment for ADEM generally includes high-dose corticosteroids to reduce inflammation and improve outcomes. Intravenous immunoglobulin (IVIG) or plasma exchange (plasmapheresis) may be used if there is no response to steroid therapy. Most patients with ADEM recover completely or have significant improvement within several months, although some may experience residual neurological deficits.
Myelin-Associated Glycoprotein (MAG) is a glycoprotein found on the surface of myelin sheaths, which are the protective insulating layers around nerve fibers in the nervous system. MAG plays a role in the adhesion and interaction between the myelin sheath and the axon it surrounds. It's particularly important during the development and maintenance of the nervous system. Additionally, MAG has been implicated in the regulation of neuronal growth and signal transmission. In certain autoimmune diseases like Guillain-Barré syndrome, the immune system may mistakenly attack MAG, leading to damage of the myelin sheath and associated neurological symptoms.
Cuprizone is not a medical condition or disease, but rather a chemical compound that is used in laboratory settings for research purposes. Cuprizone, also known as bis-cyclohexanone oxaldihydrazone, is a copper chelator, which means it can bind to and remove copper ions from various substances.
In research, cuprizone is often used to induce demyelination in animal models of multiple sclerosis (MS) and other neurological disorders. Demyelination refers to the loss or damage of the myelin sheath, which is a fatty substance that surrounds and protects nerve fibers in the brain and spinal cord. When cuprizone is added to the diet of laboratory animals such as mice, it can cause demyelination in specific areas of the brain, making it a useful tool for studying the mechanisms underlying MS and other demyelinating diseases.
It's important to note that while cuprizone is a valuable research tool, it is not used as a medical treatment or therapy for any human conditions.
The spinal cord is a major part of the nervous system, extending from the brainstem and continuing down to the lower back. It is a slender, tubular bundle of nerve fibers (axons) and support cells (glial cells) that carries signals between the brain and the rest of the body. The spinal cord primarily serves as a conduit for motor information, which travels from the brain to the muscles, and sensory information, which travels from the body to the brain. It also contains neurons that can independently process and respond to information within the spinal cord without direct input from the brain.
The spinal cord is protected by the bony vertebral column (spine) and is divided into 31 segments: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal. Each segment corresponds to a specific region of the body and gives rise to pairs of spinal nerves that exit through the intervertebral foramina at each level.
The spinal cord is responsible for several vital functions, including:
1. Reflexes: Simple reflex actions, such as the withdrawal reflex when touching a hot surface, are mediated by the spinal cord without involving the brain.
2. Muscle control: The spinal cord carries motor signals from the brain to the muscles, enabling voluntary movement and muscle tone regulation.
3. Sensory perception: The spinal cord transmits sensory information, such as touch, temperature, pain, and vibration, from the body to the brain for processing and awareness.
4. Autonomic functions: The sympathetic and parasympathetic divisions of the autonomic nervous system originate in the thoracolumbar and sacral regions of the spinal cord, respectively, controlling involuntary physiological responses like heart rate, blood pressure, digestion, and respiration.
Damage to the spinal cord can result in various degrees of paralysis or loss of sensation below the level of injury, depending on the severity and location of the damage.
I'm sorry for the confusion, but "Maus Elberfeld virus" doesn't seem to be a recognized term in current medical or scientific literature. It is possible that there may be some mistake or misunderstanding in the spelling or the name of the virus you are looking for.
Elberfeld is a city in Germany and "Maus" means mouse in German, so it might be referring to some virus affecting mice in Elberfeld. However, I cannot find any specific information about a virus with this exact name.
If you have more context or details, I'd be happy to help you try to find the information you need!
Autoimmune diseases of the nervous system are a group of conditions that occur when the body's immune system mistakenly attacks healthy tissue in the brain, spinal cord, or nerves. These diseases can cause inflammation, damage to nerve cells, and interference with the transmission of nerve impulses, leading to various neurological symptoms.
Examples of autoimmune diseases that affect the nervous system include:
1. Multiple sclerosis (MS): A chronic disease characterized by damage to the protective covering of nerve fibers in the brain and spinal cord, causing a variety of neurological symptoms such as muscle weakness, vision problems, and difficulty with coordination and balance.
2. Myasthenia gravis: A condition that causes muscle weakness and fatigue, particularly affecting the eyes, face, and neck muscles. It occurs when the immune system attacks the receptors that transmit signals between nerves and muscles.
3. Guillain-Barré syndrome: A rare disorder in which the body's immune system attacks the nerves, causing muscle weakness, tingling, and numbness that can spread throughout the body. In severe cases, it can lead to paralysis and respiratory failure.
4. Neuromyelitis optica (NMO): A rare autoimmune disease that affects the optic nerve and spinal cord, causing vision loss, muscle weakness, and other neurological symptoms.
5. Autoimmune encephalitis: A group of conditions characterized by inflammation of the brain, caused by an overactive immune response. Symptoms can include seizures, memory loss, confusion, and behavioral changes.
6. Chronic inflammatory demyelinating polyneuropathy (CIDP): A rare disorder that causes progressive weakness and numbness in the legs and arms due to damage to the nerves' protective covering.
Treatment for autoimmune diseases of the nervous system typically involves medications to suppress the immune system and reduce inflammation, as well as physical therapy and other supportive measures to manage symptoms and maintain function.
The JC (John Cunningham) virus, also known as human polyomavirus 2 (HPyV-2), is a type of double-stranded DNA virus that belongs to the Polyomaviridae family. It is named after the initials of the patient in whom it was first identified.
JC virus is a ubiquitous virus, meaning that it is commonly found in the general population worldwide. Most people get infected with JC virus during childhood and do not experience any symptoms. After the initial infection, the virus remains dormant in the kidneys and other organs of the body.
However, in individuals with weakened immune systems, such as those with HIV/AIDS or who have undergone organ transplantation, JC virus can reactivate and cause a serious brain infection called progressive multifocal leukoencephalopathy (PML). PML is a rare but often fatal disease that affects the white matter of the brain, causing cognitive decline, weakness, and paralysis.
There is currently no cure for PML, and treatment is focused on managing the underlying immune deficiency and controlling the symptoms of the disease.
C57BL/6 (C57 Black 6) is an inbred strain of laboratory mouse that is widely used in biomedical research. The term "inbred" refers to a strain of animals where matings have been carried out between siblings or other closely related individuals for many generations, resulting in a population that is highly homozygous at most genetic loci.
The C57BL/6 strain was established in 1920 by crossing a female mouse from the dilute brown (DBA) strain with a male mouse from the black strain. The resulting offspring were then interbred for many generations to create the inbred C57BL/6 strain.
C57BL/6 mice are known for their robust health, longevity, and ease of handling, making them a popular choice for researchers. They have been used in a wide range of biomedical research areas, including studies of cancer, immunology, neuroscience, cardiovascular disease, and metabolism.
One of the most notable features of the C57BL/6 strain is its sensitivity to certain genetic modifications, such as the introduction of mutations that lead to obesity or impaired glucose tolerance. This has made it a valuable tool for studying the genetic basis of complex diseases and traits.
Overall, the C57BL/6 inbred mouse strain is an important model organism in biomedical research, providing a valuable resource for understanding the genetic and molecular mechanisms underlying human health and disease.
Myelin P0 protein, also known as P0 or MPZ (myelin protein zero), is a major structural component of the myelin sheath in the peripheral nervous system. The myelin sheath is a multilayered membrane that surrounds and insulates nerve fibers to increase the speed of electrical impulse transmission.
P0 protein is a transmembrane glycoprotein, which means it spans the lipid bilayer of the myelin membrane and has sugar molecules (glycans) attached to it. It plays a crucial role in maintaining the compact structure of the myelin sheath by forming homodimers that interact with each other through their extracellular domains, creating tight junctions between the apposing layers of the myelin membrane.
P0 protein also contributes to the stability and integrity of the myelin sheath by interacting with other myelin proteins, such as connexin 32 and peripheral myelin protein 22 (PMP22). Mutations in the MPZ gene can lead to various peripheral neuropathies, including Charcot-Marie-Tooth disease type 1B and Dejerine-Sottas syndrome.
Myelin Proteolipid Protein (PLP) is a major component of the myelin sheath, which is a fatty insulating substance that covers and protects nerve fibers in the central nervous system (CNS). PLP makes up about 50% of the proteins found in the myelin sheath. It plays a crucial role in the structure and function of the myelin sheath, including maintaining its compactness and stability. Defects or mutations in the gene that encodes for PLP can lead to various demyelinating diseases, such as X-linked adrenoleukodystrophy (X-ALD) and Pelizaeus-Merzbacher disease (PMD), which are characterized by the degeneration of the myelin sheath and subsequent neurological impairments.
T-lymphocytes, also known as T-cells, are a type of white blood cell that plays a key role in the adaptive immune system's response to infection. They are produced in the bone marrow and mature in the thymus gland. There are several different types of T-cells, including CD4+ helper T-cells, CD8+ cytotoxic T-cells, and regulatory T-cells (Tregs).
CD4+ helper T-cells assist in activating other immune cells, such as B-lymphocytes and macrophages. They also produce cytokines, which are signaling molecules that help coordinate the immune response. CD8+ cytotoxic T-cells directly kill infected cells by releasing toxic substances. Regulatory T-cells help maintain immune tolerance and prevent autoimmune diseases by suppressing the activity of other immune cells.
T-lymphocytes are important in the immune response to viral infections, cancer, and other diseases. Dysfunction or depletion of T-cells can lead to immunodeficiency and increased susceptibility to infections. On the other hand, an overactive T-cell response can contribute to autoimmune diseases and chronic inflammation.
Central nervous system (CNS) diseases refer to medical conditions that primarily affect the brain and spinal cord. The CNS is responsible for controlling various functions in the body, including movement, sensation, cognition, and behavior. Therefore, diseases of the CNS can have significant impacts on a person's quality of life and overall health.
There are many different types of CNS diseases, including:
1. Infectious diseases: These are caused by viruses, bacteria, fungi, or parasites that infect the brain or spinal cord. Examples include meningitis, encephalitis, and polio.
2. Neurodegenerative diseases: These are characterized by progressive loss of nerve cells in the brain or spinal cord. Examples include Alzheimer's disease, Parkinson's disease, and Huntington's disease.
3. Structural diseases: These involve damage to the physical structure of the brain or spinal cord, such as from trauma, tumors, or stroke.
4. Functional diseases: These affect the function of the nervous system without obvious structural damage, such as multiple sclerosis and epilepsy.
5. Genetic disorders: Some CNS diseases are caused by genetic mutations, such as spinal muscular atrophy and Friedreich's ataxia.
Symptoms of CNS diseases can vary widely depending on the specific condition and the area of the brain or spinal cord that is affected. They may include muscle weakness, paralysis, seizures, loss of sensation, difficulty with coordination and balance, confusion, memory loss, changes in behavior or mood, and pain. Treatment for CNS diseases depends on the specific condition and may involve medications, surgery, rehabilitation therapy, or a combination of these approaches.
Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.
The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.
Examples of animal disease models include:
1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.
Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.
CNS demyelinating autoimmune diseases
Lipopolysaccharide
Gamma delta T cell
Leukodystrophy
Myelinoid
List of MeSH codes (C20)
Diffuse myelinoclastic sclerosis
Balo concentric sclerosis
Neuromyelitis optica spectrum disorder
Experimental autoimmune encephalomyelitis
CLDN11
Inflammatory demyelinating diseases of the central nervous system
Hereditary CNS demyelinating disease
MOG antibody disease
Chronic inflammatory demyelinating polyneuropathy
Lesional demyelinations of the central nervous system
CCL1
Neuroinflammation
Paresthesia
Remyelination
Reticulon 4
Aquaporin-4
Acute disseminated encephalomyelitis
Anne Haney Cross
Demyelinating disease
Multiple sclerosis research
Pathology of multiple sclerosis
Myelin basic protein
Gliosis
TNF inhibitor
Myelitis
CNS demyelinating autoimmune diseases - Wikipedia
Gene Therapy Approaches in an Autoimmune Demyelinating Disease: Multiple Sclerosis | Bentham Science
An updated histological classification system for multiple sclerosis lesions
Frontiers | Vitamin D Actions on CD4+ T Cells in Autoimmune Disease
Twin study reveals non-heritable immune perturbations in multiple sclerosis | Nature
Tissues Use Resident Dendritic Cells and Macrophages to Maintain Homeostasis and to Regain Homeostasis upon Tissue Injury: The...
Demyelination in rheumatic diseases | Journal of Neurology, Neurosurgery & Psychiatry
IJMS | Free Full-Text | A Novel Zinc Chelator, 1H10, Ameliorates Experimental Autoimmune Encephalomyelitis by Modulating Zinc...
Epigenetic and Environmental Regulation of Myeloid Cells during Inflammatory Demyelinating Disease - List Labs
DeCS - Términos Nuevos
DeCS - Términos Nuevos
DeCS - Términos Nuevos
DeCS - New terms
DeCS - New terms
DeCS - Termos Novos
DeCS - Términos Nuevos
DeCS - New terms
DeCS - Termos Novos
DeCS - New terms
DeCS - New terms
DeCS - Termos Novos
Leukoencephalitis, Acute Hemorrhagic | Profiles RNS
Pesquisa | Biblioteca Virtual em Saúde
Trem2 Activation On Microglia Promotes Myelin Debris Clearance And Remyelination In A Model Of Multiple Sclerosis. | Quanterix
Myasthenia gravis - Homeopathy Treatment and Homeopathic Remedies - Doctor Bhatia
Electroconvulsive Therapy in Multiple Sclerosis: A Review of Current Evidence | Psychiatrist.com
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Yongjin Yoo's Profile | Stanford Profiles
Multiple Sclerosis | springermedicine.com
Tuftsin Combines With Remyelinating Therapy and Improves Outcomes in Models of CNS Demyelinating Disease.下载|翻译|阅读
Demyelination15
- CNS demyelination autoimmune disease causes the myelin sheath to deteriorate since the sense of recognition of self is lost. (wikipedia.org)
- Based on the presence/absence and distribution of macrophages/microglia (inflammatory activity) and the presence/absence of ongoing demyelination (demyelinating activity), we suggest differentiating between active, mixed active/inactive, and inactive lesions with or without ongoing demyelination. (nih.gov)
- Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) characterised by multifocal areas of demyelination in the white matter of the brain and spinal cord. (bmj.com)
- Treatment with a new TREM2 agonistic antibody promoted the clearance of myelin debris in the cuprizone model of CNS demyelination. (quanterix.com)
- Multiple sclerosis (MS) is an autoimmune disease associated with inflammatory demyelination in the central nervous system (CNS). (stanford.edu)
- This targeted anti-inflammatory agent improves physical deficits in experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Here, we sought to determine whether tuftsin is also effective in combination with benztropine, an FDA-approved drug that stimulates remyelination, in both EAE and in the cuprizone model of demyelination. (shengsci.com)
- In the demyelinating form, segmental demyelination of peripheral nerves is thought to be immune mediated and both humoral and cell-mediated immune mechanisms have been implicated. (medscape.com)
- Multiple sclerosis (MS) is a chronic autoimmune disease characterized by inflammation and central nervous system (CNS) demyelination. (arupconsult.com)
- Testing for these autoantibodies is recommended in patients who present with acute central nervous system (CNS) demyelination and clinical, imaging, or laboratory features that are atypical for MS. Research to identify MS-specific autoantibodies is ongoing. (arupconsult.com)
- It is an autoimmune disease characterised by chronic inflammation, demyelination, gliosis (plaques or scarring) and neuronal loss with relapsing or progressive course. (vjim.org)
- MOG (35-55) is able to induce autoantibody production and relapsing-remitting neurological disease causing extensive plaque-like demyelination. (synchrone.studio)
- The Karandikar lab focuses on understanding the complex immune regulatory mechanisms underlying the autoimmune demyelinating disease, multiple sclerosis (MS). This is a chronic neurological inflammatory disease of the central nervous system (CNS) characterized by multifocal areas of demyelination, axonal damage and immune cell infiltration mediated by CD4 + and CD8 + T-lymphocytes. (uiowa.edu)
- Activity of this promoter served as surrogate for dynamics of the cytoskeleton gene transcription through recording of in vivo bioluminescence following diphtheria toxin-induced oligodendrocyte death and autoimmune demyelination. (biomedcentral.com)
- Pathologically, cerebral ALD is characterized by cerebral white matter demyelination, perivascular infiltrates, and loss of tight junctions resulting from an autoimmune- or cytokine-mediated inflammatory process (10) . (ajnr.org)
- Acute demyelinating encephalomyelitis featured intense inflammation, and perivenular demyelination in 33% of cases. (ox.ac.uk)
Lesions14
- Although a number of histological classification systems for CNS lesions have been used by different groups in recent years, no uniform classification exists. (nih.gov)
- In this paper, we propose a simple and unifying classification of MS lesions incorporating many elements of earlier histological systems that aims to provide guidelines for neuropathologists and researchers studying MS lesions to allow for better comparison of different studies performed with MS tissue, and to aid in understanding the pathogenesis of the disease. (nih.gov)
- Active and mixed active/inactive lesions can be further subdivided into lesions with ongoing myelin destruction (demyelinating lesions) and lesions in which the destruction of myelin has ceased, but macrophages are still present (post-demyelinating lesions). (nih.gov)
- Active and demyelinating lesions may be further subdivided into the early and late demyelinating lesions. (nih.gov)
- Neurological dysfunction in MS is attributed to focal demyelinated lesions in the central nervous system (CNS). (frontiersin.org)
- Histopathological analyses of CNS tissue from individuals with MS and mice with the murine model experimental autoimmune encephalomyelitis (EAE) have revealed substantial myeloid cell infiltration within inflamed lesions. (listlabs.com)
- Herein we demonstrate that TREM2 was highly expressed on myelin-laden phagocytes in active demyelinating lesions in the CNS of subjects with MS. In gene expression studies, macrophages from subjects with TREM2 genetic deficiency displayed a defect in phagocytic pathways. (quanterix.com)
- Acute relapses of MS manifest with focal demyelinating lesions in the white and gray matter of the brain and spinal cord. (psychiatrist.com)
- HCT in EAE mice leads to an enhancement of this myeloid state, as well as clinical improvement, reduction of demyelinated lesions, suppression of cytotoxic T cells, and amelioration of reactive astrogliosis reflected in reduced expression of EAE-associated gene signatures in oligodendrocytes and astrocytes. (stanford.edu)
- However, the results drew one blank after another until, finally, after five years of diagnostic limbo, the MRI scanner was suddenly able to pick up that I had central nervous system (CNS) lesions consistent with a demyelinating, neuro-degenerative disease. (rollinginspiration.co.za)
- Symptoms of MS are varied and depend on the location and severity of lesions within the CNS. (vjim.org)
- A typical MS is a distinct disease condition, in which spinal cord and optic nerves are mainly affected, but only few brain lesions are detected by MRI scans. (go.jp)
- SELs are chronic, active, demyelinated multiple sclerosis (MS) lesions, which are thought to be an early indicator of disease progression in MS. These data were presented at the 37th Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) days after the completion of enrolment into the Phase III EVOLUTION RMS program, in which evobrutinib is being investigated, was announced. (emdserono.com)
- The advent of disease-modifying medications appears to have significantly altered the course of MS. The administration of disease-modifying medications in the clinically isolated syndrome has been repeatedly demonstrated to delay the progression to clinically definite MS. [ 2 , 3 ] Not only may this therapy decrease relapse rates and new MRI lesions, but it may also reduce the development of confirmed disability. (medscape.com)
Inflammation14
- Gene therapy-induced antigen-specific Tregs inhibit neuro-inflammation and reverse disease in a mouse model of multiple sclerosis. (benthamscience.com)
- Inflammation in EAE and MS is preferentially targeted to certain CNS regions for reasons which are unclear. (listlabs.com)
- [ 3 ] Inflammation of the spinal anterior roots may lead to disruption of the blood-CNS barrier. (medscape.com)
- Inflammation in the central nervous system (CNS) is commonly associated with various degrees of tissue damage, such as loss of myelin and neurons. (atlasantibodies.com)
- This is true not only for acute brain trauma and hypoxic-ischemic brain damage following a stroke but also for chronic infection and neurodegenerative diseases, such as Alzheimer's disease, amyotrophic lateral sclerosis (ALS), Lewy body dementia, and leukoencephalopathies like multiple sclerosis (MS). In addition, local peritumoral inflammation plays a role in the clinical progression and malignancy of glioblastomas, the most aggressive primary brain tumors. (atlasantibodies.com)
- previously reported the effects of oral antibiotics on CNS inflammation in an experiment using a mouse model of MS in 2008 (*1). (go.jp)
- This study was the beginning and urged many researchers to analyze the association between gut microbiome and CNS inflammation. (go.jp)
- Chronic inflammation significantly contributes to photoreceptor death in blinding retinal diseases such as age-related macular degeneration (AMD) and retinitis pigmentosa (RP). (stria.tech)
- Myelin destruction may be caused by autoimmune reactions (e.g., multiple sclerosis), inflammation (e.g., optic neuritis, transverse myelitis, disseminated encephalomyelitis), or infectious agents (e.g. (mhmedical.com)
- A condition defined by demyelinating inflammation of the optic nerve that often occurs in association with multiple sclerosis and Devic's disease (neuromyelitis optica). (mhmedical.com)
- Increase in bioluminescence upon autoimmune inflammation was parallel to an oligodendrocyte-specific increased transcription of β-tubulin. (biomedcentral.com)
- Microglia/macrophage and lymphocyte inflammation were frequently found both in the parenchymal and meningeal compartments in non-demyelinated regions. (ox.ac.uk)
- Our findings suggest that chronic inflammation is frequent and leads to neurodegeneration in multiple sclerosis and neuromyelitis optica, regardless of disease stage. (ox.ac.uk)
- The chronic inflammation and subsequent neurodegeneration occurring along the optic pathway broadens the plaque-centred view of these diseases and partly explains the progressive neuroretinal changes observed in optic coherence tomography studies. (ox.ac.uk)
Experimental13
- In last two decades, there have been some remarkable successes of gene therapy approaches on the experimental mice model of MS - experimental autoimmune encephalomyelitis (EAE) which suggests that it is not far that the gene therapy approaches would start in human subjects ensuring the highest levels of safety and efficacy. (benthamscience.com)
- Previous studies in our lab revealed that chemical zinc chelation or zinc transporter 3 ( ZnT3 ) gene deletion suppresses the clinical features and neuropathological changes associated with experimental autoimmune encephalomyelitis (EAE). (mdpi.com)
- Autologous hematopoietic cell transplantation (HCT) is under investigation as a promising therapy for treatment-refractory MS. Here we identify a reactive myeloid state in chronic experimental autoimmune encephalitis (EAE) mice and MS patients that is surprisingly associated with neuroprotection and immune suppression. (stanford.edu)
- Results are plotted as the mean daily clinical score by experimental group S.D. 2.4 HMGB1 ELISA C-EAE mice Sotrastaurin were sacrificed at onset or peak of disease and blood was collected by cardiac puncture into Microtainer serum separation tubes (BD, Franklin Lakes, NJ). (biobender.com)
- A well-established animal model of MS is Experimental Autoimmune Encephalomyelitis (EAE), an inflammatory demyelinating disease of the CNS mostly induced in mice and rats. (synchrone.studio)
- Autoantibody response to MOG (35-55) has been observed in MS patients and MOG (35-55)-induced experimental autoimmune encephalomyelitis (EAE) C57/BL6 mice and Lewis rats. (synchrone.studio)
- In this study we examined the capacity of αB-crystallin or peptides derived thereof to induce experimental autoimmune encephalomyelitis (EAE) in SJL. (tno.nl)
- The myelin-associated protein, αB-crystallin, is considered a candidate autoantigen in multiple sclerosis (MS). In the present study, we examined the potential of αB-crystallin to induce experimental autoimmune encephalomyelitis (EAE) in Lewis rats. (tno.nl)
- It is essential to investigate the interplay between CD4 + and CD8 + T-lymphocytes during different stages of MS and in its animal model such as an Experimental Autoimmune Encephalomyelitis (EAE). (uiowa.edu)
- We demonstrate the absolute requirement for a functioning class II-restricted Ag processing pathway in the CNS for the initiation of experimental autoimmune encephalomyelitis (EAE). (aai.org)
- Experimental autoimmune encephalomyelitis (EAE) 3 is a CD4 + T cell-mediated disease of the CNS. (aai.org)
- At the Center for Immunology and Immune-based Diseases 5th Annual Retreat, Ms. Itani received a travel award for her poster presentation and work pertaining to CD8 T cell regulation in experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis. (uiowa.edu)
- Experimental demyelinating setups augmented oligodendrocyte-specific in vivo bioluminescence. (biomedcentral.com)
Pathogenesis8
- Evidence for CD4 + T-cell involvement in autoimmune disease pathogenesis and for paracrine calcitriol signaling to CD4 + T lymphocytes is summarized to support the thesis that calcitriol is sunlight's main protective signal transducer in autoimmune disease risk. (frontiersin.org)
- Much controversy exists around the complex and multifaceted pathogenesis of this prevalent disease. (stanford.edu)
- In the pathogenesis of Alzheimer ́s disease, microglia participate in amyloid Aβ- plaques formation and the associated pathology. (atlasantibodies.com)
- Therefore, it is imperative to explore the underlying pathogenesis and identify novel therapeutic targets to more effectively prevent and treat autoimmune diseases [ 3 ]. (biomedcentral.com)
- Consequently, dyslipidemia may be implicated in the pathogenesis and progression of autoimmune diseases, but the effects of various lipid-lowering drugs on autoimmune diseases warrant further investigation. (biomedcentral.com)
- These findings suggest that PCSK9i may be involved in the pathogenesis of autoimmune diseases through pathways other than lipid-lowering. (biomedcentral.com)
- Taken together, we propose that autoimmune CCR2 + CCR5 + CCR6 - Th1 cells play a crucial role in the pathogenesis of MS. (elsevierpure.com)
- Expanding the horizon of research into the pathogenesis of the white matter diseases: Proceedings of the 2021 Annual Workshop of the Albert Research Institute for White Matter and Cognition. (ouhsc.edu)
Encephalomyelitis1
- This report describes two cases of encephalomyelitis in patients with monkeypox disease that occurred during the current U.S. outbreak. (cdc.gov)
Pathophysiology1
- Hence, investigating how genetic predisposition and environmental triggers shape the interactions of individual immune cells is vital to understand the pathophysiology of autoimmune diseases including MS. (nature.com)
Optic9
- MS and other demyelinating processes, such as transverse myelitis and optic neuritis (which may be clinically isolated cases or be part of the clinical spectrum of MS), are sometimes difficult to differentiate from CNS involvement in systemic autoimmune diseases like systemic lupus erythematosus (SLE), antiphospholipid syndrome (APS), Sjoegren's syndrome (SS), and Adamantiades-Behcet disease (BD). (bmj.com)
- An overview of the clinical manifestations and treatment of demyelinating and autoimmune optic neuritis, which is the most common cause of subacute optic neuropathy in young adults. (springermedicine.com)
- However, that began to change gradually after I was diagnosed with a disease that damages the spinal cord, optic nerves and brain. (rollinginspiration.co.za)
- It manifests itself much like a similar disease called neuromyelitis optica, in the sense that it attacks my spinal cord and optic nerves but leaves my brain (and cognitive faculties) relatively unaffected. (rollinginspiration.co.za)
- Anterior optic pathway pathology in CNS demyelinating diseases. (ox.ac.uk)
- The anterior optic pathway is one of the preferential sites of involvement in CNS inflammatory demyelinating diseases, such as multiple sclerosis and neuromyelitis optica, with optic neuritis being a common presenting symptom. (ox.ac.uk)
- What is more, optic nerve involvement in these diseases is often subclinical, with optical coherence tomography demonstrating progressive neuroretinal thinning in absence of optic neuritis. (ox.ac.uk)
- Study on the association between IL-2R and IL-7R gene polymorphism and idiopathic demyelinating optic neuritis]. (cdc.gov)
- Autoimmune and immunogenetic profile of patients with optic neuritis in a population-based cohort. (cdc.gov)
Acute4
- Guillain-Barré syndrome (GBS), or acute inflammatory demyelinating polyradiculoneuropathy (AIDP), describes a heterogeneous condition with a number of redundant variants. (medscape.com)
- This interaction then causes the acute demyelinating polyradiculoneuropathy or, particularly in cases involving C jejuni infection, an acute axonal degeneration. (medscape.com)
- Patients with AE differ in the stage of their skin disease (acute, subacute, chronic). (tno.nl)
- Acute axonal injury affected 41.4% of cases and correlated with extent of inflammatory activity in each compartment even in cases that died at advanced age with over 20 years of disease duration. (ox.ac.uk)
Patients with autoimmune1
- AXL + SIGLEC6 + dendritic cells in cerebrospinal fluid and brain tissues of patients with autoimmune inflammatory demyelinating disease of CNS. (bvsalud.org)
NERVOUS SYSTEM17
- CNS demyelinating autoimmune diseases are autoimmune diseases which primarily affect the central nervous system. (wikipedia.org)
- Multiple Sclerosis (MS) is the most common autoimmune demyelinating disease of the Central Nervous System (CNS). (benthamscience.com)
- Multiple sclerosis (MS) is an incurable inflammatory demyelinating disorder of the central nervous system (CNS). (listlabs.com)
- Multiple sclerosis (MS) is an inflammatory, demyelinating, and neurodegenerative disease of the central nervous system (CNS) triggered by autoimmune mechanisms. (quanterix.com)
- 2 In other words the disease attacks the myelin sheath of the central nervous system (CNS). (brienrochelaw.com)
- Multiple sclerosis (MS) is a demyelinating disorder with central nervous system (CNS) involvement, leading to varied presentations. (vjim.org)
- Glial cells, comprising astrocytes, oligodendrocytes, and microglia, are the non-neuronal cell population of the central nervous system (CNS). (atlasantibodies.com)
- Multiple sclerosis (MS) is an autoimmune demyelinating disease of the central nervous system (CNS), which is the major neurological disease with onset in young adulthood. (go.jp)
- Multiple Sclerosis (MS) is an autoimmune demyelinating disease of the central nervous system (CNS) and the leading non-traumatic cause of neurological disability in young adults. (clinsurgeryjournal.com)
- A rare central nervous system demyelinating condition affecting children and young adults. (sdsu.edu)
- It is expressed exclusively in the central nervous system (CNS), specifically on the surface of myelinating oligodendrocytes and external lamellae of myelin sheath. (synchrone.studio)
- Classification of demyelinating diseases is made on the basis of whether the nerves affected are of the central nervous system or of the peripheral nervous system ( Table 114-1 ). (mhmedical.com)
- Furthermore, clinical markers (neurologic and cognitive scores) are relatively insensitive to early nervous system involvement and minor disease progression (9) . (ajnr.org)
- Any of various diseases affecting the white matter of the central nervous system. (ouhsc.edu)
- Neuromyelitis Optica Spectrum Disorder (NMOSD) Neuromyelitis optica spectrum disorder is a demyelinating disorder that predominantly affects the eyes and spinal cord but can affect other structures in the central nervous system (CNS) that. (msdmanuals.com)
- Preliminary study on the association of AQP4 promoter polymorphism with anti-aquaporin-4 antibody positivity in southern Han Chinese patients with idiopathic demyelinating disorders of central nervous system. (cdc.gov)
- Association Between the Single Nucleotide Polymorphism and the Level of Aquaporin-4 Protein Expression in Han and Minority Chinese with Inflammatory Demyelinating Diseases of the Central Nervous System. (cdc.gov)
Incurable4
- My neurologist handed me a diagnosis of multiple sclerosis (MS) and said that, although the disease is not fatal, it is indeed incurable. (rollinginspiration.co.za)
- Su then founded LIFNano Therapeutics, with first aim to treat Multiple Sclerosis (MS), an incurable autoimmune demyelinating disease that attacks the CNS. (healthtech-award.eu)
- It was, early on, thought that if a patient's wickedness exceeded his or her natural virtue, then the disease could be incurable. (medscape.com)
- By explaining these incurable causes, physicians were invoking the idea that the "French disease," or "mal francese," was sent as a punishment from God. (medscape.com)
Results from an autoimmune2
- It results from an autoimmune attack on the axon-myelin unit ( 8 ). (frontiersin.org)
- TM usually occurs as a postinfectious complication, and presumably results from an autoimmune process. (mhmedical.com)
Pathogenic3
- Multiple sclerosis (MS) is an autoimmune, demyelinating disease and therefore, the gold regular of treatment is to selectively suppress the pathogenic autoimmune response without compromising the complete arm from the adaptive immune system response. (biobender.com)
- Guillain-Barré syndrome (GBS) is an autoimmune-mediated disease with environmental triggers (eg, pathogenic or stressful exposures). (medscape.com)
- She showed that LIF is critical to prevent both autoimmune diseases and also pathogenic inflammatory diseases - and - remarkably - that these roles combine with LIF's natural healing power for the brain across all ages. (healthtech-award.eu)
Risk of autoimmune2
- We collected single nucleotide polymorphisms (SNPs) of PCSK9 from published genome-wide association studies statistics and conducted drug target MR analysis to detect the causal relationship between PCSK9 inhibitor and the risk of autoimmune diseases. (biomedcentral.com)
- It is thought that vaccine-induced protection from infection by far outweighs the risk of autoimmune exacerbation. (springer.com)
Axonal forms1
- Demyelinating and axonal forms of Guillain-Barré syndrome (GBS) have both been described. (medscape.com)
Pathology1
- After polyclonal stimulation, the CCR2 + CCR5 + T cells exhibited a distinct ability to produce matrix metalloproteinase-9 and osteopontin, which are involved in the CNS pathology of MS. Furthermore, after TCR stimulation, the CCR2 + CCR5 + T cells showed a higher invasive potential across an in vitro blood-brain barrier model compared with other T cells. (elsevierpure.com)
Progression14
- i) to ease specific symptoms or ii) to reduce disease progression. (benthamscience.com)
- Therefore, researchers have been working for the last four decades to discover better solutions by introducing gene therapy approaches in treating MS generally by following three strategies, i) prevention of specific symptoms, ii) halt or reverse disease progression and iii) heal CNS damage by promoting remyelination and axonal repair. (benthamscience.com)
- Diagnosis of MS relies primarily on clinical evaluation and imaging studies such as magnetic resonance imaging (MRI), particularly in patients who present with typical disease progression. (arupconsult.com)
- 13 Socioeconomic factors have been associated with poorer outcomes and higher disease activity, 14 although it remains unclear whether it plays a role in disease susceptibility or subsequent progression. (lww.com)
- The presented analysis is the first to show a BTK inhibitor significantly reducing SEL volume in patients with relapsing MS, providing further evidence to support the mechanism of action of evobrutinib in the treatment of RMS and underscoring the molecule's potential impact on neurodegeneration and disease progression," said Dr. Xavier Montalban, Chairman & Director Neurology-Neuroimmunology Department & Neurorehabilitation Unit, Multiple Sclerosis Centre of Catalonia (Cemcat), Vall d'Hebron University Hospital, Barcelona, Spain. (emdserono.com)
- Early assignment of disease progression among patients with X-linked adrenoleukodystrophy (ALD) is critical for the appropriate selection of effective therapy. (ajnr.org)
- We evaluated the association between contrast enhancement on T1-weighted spin-echo MR images and disease progression. (ajnr.org)
- 18 (86%) of the 21 patients had disease progression revealed by the follow-up evaluations based on MR imaging (Loes) and neurologic scores. (ajnr.org)
- for 18 (82%) of the 22 patients, no evidence of disease progression was revealed by the follow-up evaluations. (ajnr.org)
- Nevertheless, plasma assays have been found to be unreliable markers for disease progression, irrespective of subtype. (ajnr.org)
- The severity of the inflammatory process has been correlated with the rapidity of disease progression (11) . (ajnr.org)
- In this study, we evaluated the association between contrast enhancement on the T1-weighted spin-echo MR images of patients with X-linked ALD and disease progression based on clinical evaluation and MR imaging scores. (ajnr.org)
- Our null hypothesis was that there is no association between contrast enhancement and disease progression in X-linked ALD. (ajnr.org)
- Repeated studies have convincingly demonstrated that early treatment is critical in decreasing the rate of disease progression and, therefore, establishing the diagnosis in a timely fashion and initiating treatment is imperative. (medscape.com)
Microglia6
- Our data further support tuftsin's beneficial immunomodulatory activity in the context of EAE, and show that when studying remyelination in the absence of an autoimmune insult, tuftsin still activated microglia toward an anti-inflammatory fate, but benztropine was necessary for significant repair of the damaged myelin. (shengsci.com)
- Naïve resting microglia cells are essentially immobile and continuously scan the CNS microenvironment for "danger signals" with their highly motile pseudopodial extensions. (atlasantibodies.com)
- Different cues produced within the CNS tissue microenvironment choreograph the microglia specification to enable the dramatic changes of the activation state of these cells. (atlasantibodies.com)
- Single-cell molecular RNA-profiling of microglia isolated from the brains of patients with MS and Alzheimer ́s disease has enabled the discovery of novel microglia subtypes with unusual properties. (atlasantibodies.com)
- In fact, as antigen-presenting cells (APC), microglia are endowed with the ability to release pro-inflammatory cytokines and chemokines into the CNS tissue microenvironment. (atlasantibodies.com)
- Activated microglia are the primary regulators of the pro-and anti-inflammatory microenvironment of the CNS. (atlasantibodies.com)
Myelin sheath1
- A demyelinating disease is any disease in which the myelin sheath of the neuron is damaged. (mhmedical.com)
Macrophages3
- Resemblance of the triggering pathogens to antigens on peripheral nerves (ie, molecular mimicry) leads to an overzealous autoimmune response mounted by T-lymphocytes and macrophages. (medscape.com)
- They are the first-line defense innate immune cells, commonly regarded as "brain resident macrophages" and the sole resident immune cell type in the CNS 4 . (atlasantibodies.com)
- In both cases, T cells specific for CNS myelin infiltrate the CNS, causing the influx of macrophages and activation of CNS resident cells ( 4 ). (aai.org)
Chronic autoimmune2
- Systemic lupus erythematosus (SLE) is a chronic autoimmune connective tissue disorder, with a heterogeneous presentation. (lww.com)
- Multiple sclerosis (MS) is a chronic autoimmune condition affecting the CNS. (medscape.com)
Focal1
- Prominent MS mimickers, many with features of focal neurological disease separated in both time and space, are discussed in this article. (medscape.com)
Mice2
- Mice had been supervised for scientific symptoms of EAE after disease starting point daily, and paralyzed animals were provided easier usage of food and water. (biobender.com)
- CNS-specific bioluminescence in oLucR mice was quantitatively measured in vivo after injection of luciferin. (biomedcentral.com)
Multiple16
- as a novel combined immune gene therapy for Multiple Sclerosis disease. (benthamscience.com)
- Evidence linking sunlight, vitamin D, and the risk of multiple sclerosis and type 1 diabetes is summarized to develop the thesis that vitamin D is the environmental factor that most strongly influences autoimmune disease development. (frontiersin.org)
- The global burden has risen with the near tripling in the last half-century of multiple sclerosis (MS) ( 2 , 3 ), type 1 diabetes (T1D) ( 4 ), and other autoimmune diseases. (frontiersin.org)
- Multiple sclerosis and T1D have distinct target organs, genetic risk factors, onset ages, and female to male ratios, but target organ-specific T cells as initiators unite these diseases. (frontiersin.org)
- 12 In a 1964 study of seven patients, Dr. Henry Miller concluded, "these patients were probably already suffering from pathological multiple sclerosis without clinical signs, and that trauma converted a silent into an overt disease. (brienrochelaw.com)
- Follow-up integration of daSNV gene editing with clinical cohort analyses suggested that magnesium transport dysfunction may increase neuropsychiatric disease risk and indicated that common genetic pathomechanisms may mediate specific symptoms that are shared across multiple neuropsychiatric diseases. (stanford.edu)
- The advent of increasingly efficacious disease-modifying treatments (DMTs) for multiple sclerosis (MS) has undoubtedly altered its natural history. (springermedicine.com)
- Many biological markers have been explored in multiple sclerosis (MS) to better quantify disease burden and better evaluate response to treatments, beyond clinical and MRI data. (springermedicine.com)
- Autoantibody testing is important to differentiate between multiple sclerosis (MS) and other similar diseases. (arupconsult.com)
- Which diseases should be considered in the differential diagnosis when evaluating patients with possible multiple sclerosis? (arupconsult.com)
- Although MOG protein constitutes only 0.01-0.05% of the CNS myelin proteins, it is a major antigen candidate for inducing the autoimmune disease multiple sclerosis (MS). Myelin Basic Protein (MBP) and PLP (Myelin Proteolipid Protein) may play similar functions. (synchrone.studio)
- With the risk of coronary heart disease as a positive control, primary outcomes included the risk of systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), myasthenia gravis (MG), multiple sclerosis (MS), asthma, Crohn's disease (CD), ulcerative colitis (UC), and type 1 diabetes (T1D). (biomedcentral.com)
- Multiple sclerosis (MS) is a demyelinating disease of the CNS that is presumably mediated by CD4 + autoimmune T cells. (elsevierpure.com)
- Devic disease), once considered a variant of multiple sclerosis but now considered a distinct disorder. (msdmanuals.com)
- Association of multiple sclerosis susceptibility variants and early attack location in the CNS. (cdc.gov)
- Combinations of susceptibility genes are associated with higher risk for multiple sclerosis and imply disease course specificity. (cdc.gov)
Neurological disease1
- ROLLING INSPIRATION reader Anne Moon shares her experience of learning to drive with a neurological disease. (rollinginspiration.co.za)
AQP41
- For example, aquaporin-4 (AQP4) immunoglobulin G (IgG) serum autoantibody and myelin oligodendrocyte glycoprotein IgG (MOG IgG) autoantibody are specific for neuromyelitis optica spectrum disorders (NMOSDs) and MOG-associated disease (MOGAD), respectively. (arupconsult.com)
Multifactorial2
- It is a multifactorial disease which develops in an immune-mediated way under the influences of both genetic and environmental factors. (benthamscience.com)
- The causes of demyelinating diseases are multifactorial. (mhmedical.com)
Systemic2
- Here we conducted an in-depth pairwise analysis of the systemic immune compartment of 61 monozygotic twin pairs discordant for MS, in which both siblings carry the same genetic and early-life environmental risk for the disease, yet only one is affected by MS. This approach thus eliminated the majority of bias attributed to variable genetic and early environmental influences in a heterogenous population 17 , 18 . (nature.com)
- The disorder was recognized as early as the Middle Ages, with the 12th-century physician Rogerius being the first to apply the term lupus to the classic malar rash, and in 1872, Moric Kaposi first recognized the systemic nature of the disease. (lww.com)
Classification1
- A classification that sufficiently covers their phenotypic heterogeneity and plasticity during homeostasis and disease does not yet exist because cell culture-based phenotypes often do not match those found in vivo . (hindawi.com)
Disorders1
- Diagnosis of MS can be challenging because of variable disease presentation and significant clinical overlap with diseases such as neuromyelitis optica spectrum disorders (NMOSDs) and myelin oligodendrocyte glycoprotein-associated disease (MOGAD). (arupconsult.com)
Antigen1
- Her research focus involves using infection with Listeria monocytogenes to present CNS antigen endogenously to class I-restricted CD8 T cells, and gauging the subsequent response of those cells in inflammatory demyelinating disease. (uiowa.edu)
Leukodystrophies1
- these diseases are termed leukodystrophies. (mhmedical.com)
Remyelination3
- Importantly, tuftsin is required to transform the inflammatory CNS environment normally present in EAE/MS into one of an anti-inflammatory nature, and benztropine is required in the cuprizone model to improve remyelination. (shengsci.com)
- As the disease course evolves, there is less evidence of ongoing remyelination, further axonal loss, and more extensive gliosis. (docksci.com)
- The emergence of therapeutic agents that access the CNS, raise the possibility of enhancing the remyelination process both by acting directly upon myelinating cells and/ or indirectly via the immune-glial networks. (docksci.com)
Affects2
Molecular5
- This review summarizes and integrates research on vitamin D and CD4 + T-lymphocyte biology to develop new mechanistic insights into the molecular etiology of autoimmune disease. (frontiersin.org)
- A deep understanding of molecular mechanisms relevant to gene-environment interactions is needed to deliver etiology-based autoimmune disease prevention and treatment strategies. (frontiersin.org)
- Indeed, "functional and mechanistic work on the molecular etiology of disease remains one of the major challenges in modern biology" ( 5 ). (frontiersin.org)
- Finally, unanswered questions relating to vitamin D mechanisms in CD4 + T cells are highlighted to promote further research that may lead to a deeper understanding of autoimmune disease molecular etiology. (frontiersin.org)
- 8 Therefore "It is obvious that any mechanism which physically destroys the components of the BBB will render the CNS open to the cellular and molecular constituents of the blood. (brienrochelaw.com)
Disorder3
- It is an autoimmune disorder, in which weakness is caused by circulating antibodies that block acetylcholine receptors at the post-synaptic neuromuscular junction, [1] inhibiting the stimulative effect of the neurotransmitter acetylcholine. (doctorbhatia.com)
- In this case report, we will be discussing one such rare presentation of a rapidly progressive demyelinating disorder. (vjim.org)
- Neuromyelitis optica spectrum disorder (NMOSD) was previously regarded as a subtype of MS, but is now considered an independent disease, since the majority of the cases are characterized by the presence of anti-aquaporin 4 autoantibody. (go.jp)
Mechanisms4
- A deep understanding of disease mechanisms will be needed to deliver etiology-based strategies to reverse this vexing trend. (frontiersin.org)
- Gene-environment interactions, sunlight and vitamin D, and T lymphocytes as autoimmune disease initiators and vitamin D targets are discussed to explain the rationale for reviewing vitamin D mechanisms in T cells. (frontiersin.org)
- We drew mainly on MS and T1D research because intensive investigation has generated detailed insights into vitamin D mechanisms in these diseases and provided valuable guidance for research on other autoimmune diseases. (frontiersin.org)
- A recent chapter ( 6 ) and a review ( 7 ) have summarized vitamin D mechanisms in autoimmune diseases more generally. (frontiersin.org)
Heterogeneous1
- Alpers' Syndrome refers to a heterogeneous group of diseases that feature progressive cerebral deterioration and liver disease. (sdsu.edu)
Phagocytes1
- The plasticity of mononuclear phagocytes becomes obvious during dynamic or complex disease processes. (hindawi.com)
Centers for Diseas1
- Centers for Disease Control and Prevention. (cdc.gov)
Gene1
- Expression-gene mapping, network analyses and chromatin looping nominated candidate disease-relevant target genes modulated by these daSNVs. (stanford.edu)
Etiology1
- Finally, unanswered questions and potentially informative future research directions are highlighted to speed delivery of etiology-based strategies to reduce autoimmune disease. (frontiersin.org)
Tissues2
- Autoimmune diseases represent a failure of self-identification leading to an immune-mediated assault on host tissues. (frontiersin.org)
- A more tissue-centric view of these processes, claiming that the tissues define phenotype and function of resident and infiltrating immune cells to meet tissues needs during homeostasis and disease, seems provocative [ 4 , 5 ]. (hindawi.com)
Infectious Diseases1
- a number on par with the 'big three' infectious diseases -- HIV/AIDS, malaria and tuberculosis -- and air pollution, but clearly lower than the burden of dietary risk factors or unimproved water and sanitation. (50webs.com)
Plaques2
Subclinical1
- Here we report on a vaccinated patient who experienced the initial clinical manifestation of MS on a background of previously unknown, but likely pre-existing subclinical inflammatory CNS disease. (springer.com)
Symptoms2
- 1 In most cases (85%-90%), the disease initially presents with episodic neurologic symptoms, which are described as a clinically isolated syndrome. (psychiatrist.com)
- Preliminary disease symptoms were observed between 10 and 15 times post-immunization usually. (biobender.com)
AIDP1
- The CSF findings, in combination with certain clinical features, allowed AIDP to be distinguished from anterior horn cell diseases such as poliomyelitis, spinal muscular atrophy and from other neuropathies. (medscape.com)
Neuroinflammation1
- Neuroinflammation broadly defines the collective reactive immune response in the brain and spinal cord in response to injury and disease. (atlasantibodies.com)
Neurologic diseases1
- Treatment of MS differs from that of other diseases, and using MS medications to treat other immune-mediated neurologic diseases can exacerbate them. (arupconsult.com)
Attacks1
- The cell death in retinal degenerative diseases, such as age-related macular degeneration (AMD) or retinitis pigmentosa (RP), is often caused by the body's own immune system, which attacks retinal cells. (stria.tech)
Immune cells1
- Role of Regulatory Immune Cells and Molecules in Autoimmune Bullous Dermatoses. (shengsci.com)
Unclear1
- In this context, the role of surviving mature ODCs within and surrounding damaged CNS areas is still unclear. (biomedcentral.com)