Degeneration of distal aspects of a nerve axon following injury to the cell body or proximal portion of the axon. The process is characterized by fragmentation of the axon and its MYELIN SHEATH.
An enzyme that catalyzes reversibly the transfer of the adenylyl moiety of ATP to the phosphoryl group of NMN to form NAD+ and pyrophosphate. The enzyme is found predominantly in the nuclei and catalyzes the final reaction in the major pathway for the biosynthesis of NAD in mammals. EC 2.7.7.1.
A nerve which originates in the lumbar and sacral spinal cord (L4 to S3) and supplies motor and sensory innervation to the lower extremity. The sciatic nerve, which is the main continuation of the sacral plexus, is the largest nerve in the body. It has two major branches, the TIBIAL NERVE and the PERONEAL NERVE.
Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations following the destruction of their cells of origin or interruption of their continuity with these cells. The pathology is characteristic of neurodegenerative diseases. Often the process of nerve degeneration is studied in research on neuroanatomical localization and correlation of the neurophysiology of neural pathways.
Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body.
Transection or severing of an axon. This type of denervation is used often in experimental studies on neuronal physiology and neuronal death or survival, toward an understanding of nervous system disease.
The lipid-rich sheath surrounding AXONS in both the CENTRAL NERVOUS SYSTEMS and PERIPHERAL NERVOUS SYSTEM. The myelin sheath is an electrical insulator and allows faster and more energetically efficient conduction of impulses. The sheath is formed by the cell membranes of glial cells (SCHWANN CELLS in the peripheral and OLIGODENDROGLIA in the central nervous system). Deterioration of the sheath in DEMYELINATING DISEASES is a serious clinical problem.
Disease or damage involving the SCIATIC NERVE, which divides into the PERONEAL NERVE and TIBIAL NERVE (see also PERONEAL NEUROPATHIES and TIBIAL NEUROPATHY). Clinical manifestations may include SCIATICA or pain localized to the hip, PARESIS or PARALYSIS of posterior thigh muscles and muscles innervated by the peroneal and tibial nerves, and sensory loss involving the lateral and posterior thigh, posterior and lateral leg, and sole of the foot. The sciatic nerve may be affected by trauma; ISCHEMIA; COLLAGEN DISEASES; and other conditions. (From Adams et al., Principles of Neurology, 6th ed, p1363)
Neuroglial cells of the peripheral nervous system which form the insulating myelin sheaths of peripheral axons.
NECROSIS occurring in the ANTERIOR CEREBRAL ARTERY system, including branches such as Heubner's artery. These arteries supply blood to the medial and superior parts of the CEREBRAL HEMISPHERE, Infarction in the anterior cerebral artery usually results in sensory and motor impairment in the lower body.
Treatment of muscles and nerves under pressure as a result of crush injuries.
Renewal or physiological repair of damaged nerve tissue.
The nerves outside of the brain and spinal cord, including the autonomic, cranial, and spinal nerves. Peripheral nerves contain non-neuronal cells and connective tissue as well as axons. The connective tissue layers include, from the outside to the inside, the epineurium, the perineurium, and the endoneurium.
Fibers that arise from cells within the cerebral cortex, pass through the medullary pyramid, and descend in the spinal cord. Many authorities say the pyramidal tracts include both the corticospinal and corticobulbar tracts.
The 2nd cranial nerve which conveys visual information from the RETINA to the brain. The nerve carries the axons of the RETINAL GANGLION CELLS which sort at the OPTIC CHIASM and continue via the OPTIC TRACTS to the brain. The largest projection is to the lateral geniculate nuclei; other targets include the SUPERIOR COLLICULI and the SUPRACHIASMATIC NUCLEI. Though known as the second cranial nerve, it is considered part of the CENTRAL NERVOUS SYSTEM.
Injuries to the PERIPHERAL NERVES.
Traumatic injuries to the brain, cranial nerves, spinal cord, autonomic nervous system, or neuromuscular system, including iatrogenic injuries induced by surgical procedures.
The functions and activities of living organisms or their parts involved in generating and responding to electrical charges .
Mice which carry mutant genes for neurologic defects or abnormalities.
A retrogressive pathological change in the retina, focal or generalized, caused by genetic defects, inflammation, trauma, vascular disease, or aging. Degeneration affecting predominantly the macula lutea of the retina is MACULAR DEGENERATION. (Newell, Ophthalmology: Principles and Concepts, 7th ed, p304)
Type III intermediate filament proteins that assemble into neurofilaments, the major cytoskeletal element in nerve axons and dendrites. They consist of three distinct polypeptides, the neurofilament triplet. Types I, II, and IV intermediate filament proteins form other cytoskeletal elements such as keratins and lamins. It appears that the metabolism of neurofilaments is disturbed in Alzheimer's disease, as indicated by the presence of neurofilament epitopes in the neurofibrillary tangles, as well as by the severe reduction of the expression of the gene for the light neurofilament subunit of the neurofilament triplet in brains of Alzheimer's patients. (Can J Neurol Sci 1990 Aug;17(3):302)
Degenerative changes in the RETINA usually of older adults which results in a loss of vision in the center of the visual field (the MACULA LUTEA) because of damage to the retina. It occurs in dry and wet forms.
A class of nerve fibers as defined by their structure, specifically the nerve sheath arrangement. The AXONS of the myelinated nerve fibers are completely encased in a MYELIN SHEATH. They are fibers of relatively large and varied diameters. Their NEURAL CONDUCTION rates are faster than those of the unmyelinated nerve fibers (NERVE FIBERS, UNMYELINATED). Myelinated nerve fibers are present in somatic and autonomic nerves.
Paired bundles of NERVE FIBERS entering and leaving the SPINAL CORD at each segment. The dorsal and ventral nerve roots join to form the mixed segmental spinal nerves. The dorsal roots are generally afferent, formed by the central projections of the spinal (dorsal root) ganglia sensory cells, and the ventral roots are efferent, comprising the axons of spinal motor and PREGANGLIONIC AUTONOMIC FIBERS.
'Nerve tissue proteins' are specialized proteins found within the nervous system's biological tissue, including neurofilaments, neuronal cytoskeletal proteins, and neural cell adhesion molecules, which facilitate structural support, intracellular communication, and synaptic connectivity essential for proper neurological function.
A diagnostic technique that incorporates the measurement of molecular diffusion (such as water or metabolites) for tissue assessment by MRI. The degree of molecular movement can be measured by changes of apparent diffusion coefficient (ADC) with time, as reflected by tissue microstructure. Diffusion MRI has been used to study BRAIN ISCHEMIA and tumor response to treatment.
Sensory ganglia located on the dorsal spinal roots within the vertebral column. The spinal ganglion cells are pseudounipolar. The single primary branch bifurcates sending a peripheral process to carry sensory information from the periphery and a central branch which relays that information to the spinal cord or brain.
The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors.
Inbred C57BL mice are a strain of laboratory mice that have been produced by many generations of brother-sister matings, resulting in a high degree of genetic uniformity and homozygosity, making them widely used for biomedical research, including studies on genetics, immunology, cancer, and neuroscience.
Diseases characterized by loss or dysfunction of myelin in the central or peripheral nervous system.
Neurons which activate MUSCLE CELLS.
Penetrating and non-penetrating injuries to the spinal cord resulting from traumatic external forces (e.g., WOUNDS, GUNSHOT; WHIPLASH INJURIES; etc.).
Quinolines are heterocyclic aromatic organic compounds consisting of a two-nitrogened benzene ring fused to a pyridine ring, which have been synthesized and used as building blocks for various medicinal drugs, particularly antibiotics and antimalarials.
Compounds that inhibit HMG-CoA reductases. They have been shown to directly lower cholesterol synthesis.
The extent to which the active ingredient of a drug dosage form becomes available at the site of drug action or in a biological medium believed to reflect accessibility to a site of action.
The giving of drugs, chemicals, or other substances by mouth.
A statistical means of summarizing information from a series of measurements on one individual. It is frequently used in clinical pharmacology where the AUC from serum levels can be interpreted as the total uptake of whatever has been administered. As a plot of the concentration of a drug against time, after a single dose of medicine, producing a standard shape curve, it is a means of comparing the bioavailability of the same drug made by different companies. (From Winslade, Dictionary of Clinical Research, 1992)
Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados.
The time it takes for a substance (drug, radioactive nuclide, or other) to lose half of its pharmacologic, physiologic, or radiologic activity.

Axonal injury in the internal capsule correlates with motor impairment after stroke. (1/279)

Background and Purpose--Magnetic resonance spectroscopy (MRS) in ischemic stroke has shown a correlation between N-acetylaspartate (NAA) loss from the infarcted region and disability. We tested the hypothesis that NAA loss in the descending motor pathways, measured at the level of the posterior limb of the internal capsule, would determine motor deficit after a cortical, subcortical, or striatocapsular stroke. Methods--Eighteen patients with first ischemic stroke causing a motor deficit were examined between 1 month and 5 years after stroke. T2-weighted imaging of the brain and localized proton (voxel, 1.5x2x2 cm3) MRS from the posterior limb of each internal capsule were performed and correlated to a motor deficit score. Results--Mean internal capsule NAA was significantly lower in the patient group as a whole compared with the control group (P<0.001). Reductions in internal capsule NAA on the side of the lesion were seen in cases of cortical stroke in which there was no extension of the stroke into the voxel as well as in cases of striatocapsular stroke involving the voxel region. There was a strong relationship between reduction in capsule NAA and contralateral motor deficit (log curve, r2=0.9, P<0.001). Conclusions--Axonal injury in the descending motor pathways at the level of the internal capsule correlated with motor deficit in patients after stroke. This was the case for strokes directly involving the internal capsule and for strokes in the motor cortex and subcortex in which there was presumed anterograde axonal injury.  (+info)

Temperature modulation reveals three distinct stages of Wallerian degeneration. (2/279)

After peripheral nerve transection, axons distal to the cut site rapidly degenerate, a process termed Wallerian degeneration. In wild-type mice the compound action potential (CAP) disappears by 3 d. Previous studies have demonstrated that cold temperatures and lower extracellular calcium ion (Ca2+) concentrations can slow the rate of Wallerian degeneration. We have incubated isolated sciatic nerve segments from wild-type and C57BL/Wld mice (which carry a gene slowing Wallerian degeneration) in vitro at 25 and 37 degrees C. At 25 degrees C we found that the degeneration rate of wild-type axons was slowed dramatically, with the CAP preserved up to 7 d post-transection. In contrast, at 37 degrees C the CAPs were minimal at 2 d. When the temperature of wild-type nerves was raised to 37 degrees C after 24-72 hr at 25 degrees C, degeneration occurred within the subsequent 24 hr. Wld nerves, too, were preserved longer at 25 degrees C but, on return to 37 degrees C, degenerated promptly. Cooling the nerve within 12 hr after axotomy enhanced axonal preservation. Neither wild-type nor Wld nerves showed different degeneration rates when they were incubated with 250 microM or 5 or 10 mM extracellular Ca2+ for 1-2 d, suggesting that an abrupt increase in intracellular Ca2+ occurs at the time of axonal destruction. Wallerian degeneration, thus, appears to progress through three distinct stages. Initiation occurs at the time of injury with subsequent temperature-dependent and -independent phases. Nerves appear to remain intact and are able to exclude Ca2+ from entering until an as yet unknown process finally increases axolemmal permeability.  (+info)

Mice lacking complex gangliosides develop Wallerian degeneration and myelination defects. (3/279)

Gangliosides are a family of sialic acid-containing glycosphingolipids highly enriched in the mammalian nervous system. Although they are the major sialoglycoconjugates in the brain, their neurobiological functions remain poorly defined. By disrupting the gene for a key enzyme in complex ganglioside biosynthesis (GM2/GD2 synthase; EC 2.4.1.92) we generated mice that express only simple gangliosides (GM3/GD3) and examined their central and peripheral nervous systems. The complex ganglioside knockout mice display decreased central myelination, axonal degeneration in both the central and peripheral nervous systems, and demyelination in peripheral nerves. The pathological features of their nervous system closely resemble those reported in mice with a disrupted gene for myelin-associated glycoprotein (MAG), a myelin receptor that binds to complex brain gangliosides in vitro. Furthermore, GM2/GD2 synthase knockout mice have reduced MAG expression in the central nervous system. These results indicate that complex gangliosides function in central myelination and maintaining the integrity of axons and myelin. They also support the theory that complex gangliosides are endogenous ligands for MAG. The data extend and clarify prior observations on a similar mouse model, which reported only subtle conduction defects in their nervous system [Takamiya, K., Yamamoto, A., Furukawa, K., Yamashiro, S., Shin, M., Okada, M., Fukumoto, S., Haraguchi, M., Takeda, N., Fujimura, K., et al. (1996) Proc. Natl. Acad. Sci. USA 93, 10662-10667].  (+info)

Peripheral nerve lesions in a case of equine motor neuron disease. (4/279)

A male 14-year-old Arab horse was pathologically diagnosed as equine motor neuron disease (EMND), which was kept as a breeding horse on a farm in Tokachi district of Hokkaido in Japan. On examination of the peripheral nerves, the most characteristic feature was Wallerian-type degeneration revealed by myelinoclasis associated with myelin ovoids which were sometimes infiltrated by macrophages. The other abnormalities were axonal swellings which were surrounded by thin myelin sheaths. Ultrastructurally, the axonal swelling was due to an accumulation of neurofilaments, and was accompanied by a thin and degenerating myelin sheaths. In teased nerve fiber preparations, the most conspicuous change was myelinoclasis represented by segmentation into myelin ovoids or balls. Occasionally, segmental demyelination and axonal degeneration characterized by multifocal axonal swelling were observed.  (+info)

Evidence that Wallerian degeneration and localized axon degeneration induced by local neurotrophin deprivation do not involve caspases. (5/279)

The selective degeneration of an axon, without the death of the parent neuron, can occur in response to injury, in a variety of metabolic, toxic, and inflammatory disorders, and during normal development. Recent evidence suggests that some forms of axon degeneration involve an active and regulated program of self-destruction rather than a passive "wasting away" and in this respect and others resemble apoptosis. Here we investigate whether selective axon degeneration depends on some of the molecular machinery that mediates apoptosis, namely, the caspase family of cysteine proteases. We focus on two models of selective axon degeneration: Wallerian degeneration of transected axons and localized axon degeneration induced by local deprivation of neurotrophin. We show that caspase-3 is not activated in the axon during either form of degeneration, although it is activated in the dying cell body of the same neurons. Moreover, caspase inhibitors do not inhibit or retard either form of axon degeneration, although they inhibit apoptosis of the same neurons. Finally, we cannot detect cleaved substrates of caspase-3 and its close relatives immunocytochemically or caspase activity biochemically in axons undergoing Wallerian degeneration. Our results suggest that a neuron contains at least two molecularly distinct self-destruction programs, one for caspase-dependent apoptosis and another for selective axon degeneration.  (+info)

The macrophage in acute neural injury: changes in cell numbers over time and levels of cytokine production in mammalian central and peripheral nervous systems. (6/279)

We evaluated the timing and density of ED-1-positive macrophage accumulation (ED 1 is the primary antibody for the macrophage) and measured cytokine production by macrophages in standardized compression injuries to the spinal cord and sciatic nerves of individual rats 3, 5, 10 and 21 days post-injury. The actual site of mechanical damage to the nervous tissue, and a more distant site where Wallerian degeneration had occurred, were evaluated in both the peripheral nervous system (PNS) and the central nervous system (CNS) at these time points. The initial accumulation of activated macrophages was similar at both the central and peripheral sites of damage. Subsequently, macrophage densities at all locations studied were statistically significantly higher in the spinal cord than in the sciatic nerve at every time point but one. The peak concentrations of three cytokines, tumor necrosis factor &agr; (TNF &agr; ), interleukin-1 (IL-1) and interleukin-6 (IL-6), appeared earlier and were statistically significantly higher in injured spinal cord than in injured sciatic nerve. We discuss the meaning of these data relative to the known differences in the reparative responses of the PNS and CNS to injury.  (+info)

Improved functional outcome in patients with hemorrhagic stroke in putamen and thalamus compared with those with stroke restricted to the putamen or thalamus. (7/279)

BACKGROUND AND PURPOSE: We analyzed the effect of late intensive inpatient rehabilitation on the functional outcome of patients with subcortical hemorrhagic stroke. METHODS: Patients who were nonambulatory with hemorrhagic stroke in the internal capsule and putamen (n=55), the thalamus (n=24), or all 3 regions (n=15) underwent intensive inpatient rehabilitation. Patients with surgical intervention or an episode of ventricular hemorrhage were excluded. Lesion location was evaluated by MRI 4 months after the ictus. RESULTS: Demographic data, initial disability, and impairment measures were comparable in the 3 groups. Functional outcome demonstrated significant differences in mobility subscores (P<0.05) of the Functional Independence Measure such that patients with injury in the 3 regions were more likely to ambulate independently than were patients in the other groups. Lesion location data demonstrated that the ventral anterior nucleus of the thalamus was always spared; the ventral posterior (lateral and medial) nucleus was always damaged, and the ventral lateral nucleus was frequently damaged. Putaminal damage always included the postcommissural area. In addition, the entire posterior half limb of the internal capsule was always damaged. CONCLUSIONS: Subcortical lesions to multiple structures in the basal ganglia-thalamocortical motor circuits permitted enhanced motor recovery. Lesion location predicted the level of independent ambulation and the rate of recovery in patients with stroke who were nonambulatory before neurorehabilitation therapy.  (+info)

A developmentally regulated switch directs regenerative growth of Schwann cells through cyclin D1. (8/279)

Sciatic nerve axons in cyclin D1 knockout mice develop normally, become properly ensheathed by Schwann cells, and appear to function normally. However, in the Wallerian degeneration model of nerve injury, the mitotic response of Schwann cells is completely inhibited. The mitotic block is Schwann cell autonomous and developmentally regulated. Rescue analysis (by "knockin" of cyclin E) indicates that D1 protein, rather than regulatory elements of the D1 gene, provides the essential Schwann cell function. Genetic inhibition of the Schwann cell cycle shows that neuronal responses to nerve injury are surprisingly independent of Schwann cell mitotic responses. Even axonal regrowth into the distal zone of a nerve crush injury is not markedly impaired in cyclin D1-/- mice.  (+info)

Wallerian degeneration is a process that occurs following damage to the axons of neurons (nerve cells). After an axon is severed or traumatically injured, it undergoes a series of changes including fragmentation and removal of the distal segment of the axon, which is the part that is separated from the cell body. This process is named after Augustus Waller, who first described it in 1850.

The degenerative changes in the distal axon are characterized by the breakdown of the axonal cytoskeleton, the loss of myelin sheath (the fatty insulating material that surrounds and protects the axon), and the infiltration of macrophages to clear away the debris. These events lead to the degeneration of the distal axon segment, which is necessary for successful regeneration of the injured nerve.

Wallerian degeneration is a crucial process in the nervous system's response to injury, as it enables the regrowth of axons and the reestablishment of connections between neurons. However, if the regenerative capacity of the neuron is insufficient or the environment is not conducive to growth, functional recovery may be impaired, leading to long-term neurological deficits.

Nicotinamide-nucleotide adenylyltransferase (NNAT) is an enzyme that plays a crucial role in the metabolism of nicotinamide adenine dinucleotide (NAD+), which is a coenzyme involved in various redox reactions in the body. NNAT catalyzes the interconversion between nicotinamide mononucleotide (NMN) and NAD+ through the transfer of an adenylyl group.

The reaction catalyzed by NNAT is as follows:

NMN + ATP → NAD+ + PP\_i

NNAT is found in various tissues, including the brain, where it has been implicated in neuronal development and survival. Mutations in the NNAT gene have been associated with neurological disorders such as epilepsy and intellectual disability. Additionally, NNAT has been identified as a potential target for the development of therapies aimed at treating neurodegenerative diseases and cancer.

The sciatic nerve is the largest and longest nerve in the human body, running from the lower back through the buttocks and down the legs to the feet. It is formed by the union of the ventral rami (branches) of the L4 to S3 spinal nerves. The sciatic nerve provides motor and sensory innervation to various muscles and skin areas in the lower limbs, including the hamstrings, calf muscles, and the sole of the foot. Sciatic nerve disorders or injuries can result in symptoms such as pain, numbness, tingling, or weakness in the lower back, hips, legs, and feet, known as sciatica.

Nerve degeneration, also known as neurodegeneration, is the progressive loss of structure and function of neurons, which can lead to cognitive decline, motor impairment, and various other symptoms. This process occurs due to a variety of factors, including genetics, environmental influences, and aging. It is a key feature in several neurological disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and multiple sclerosis. The degeneration can affect any part of the nervous system, leading to different symptoms depending on the location and extent of the damage.

An axon is a long, slender extension of a neuron (a type of nerve cell) that conducts electrical impulses (nerve impulses) away from the cell body to target cells, such as other neurons or muscle cells. Axons can vary in length from a few micrometers to over a meter long and are typically surrounded by a myelin sheath, which helps to insulate and protect the axon and allows for faster transmission of nerve impulses.

Axons play a critical role in the functioning of the nervous system, as they provide the means by which neurons communicate with one another and with other cells in the body. Damage to axons can result in serious neurological problems, such as those seen in spinal cord injuries or neurodegenerative diseases like multiple sclerosis.

Axotomy is a medical term that refers to the surgical cutting or severing of an axon, which is the long, slender projection of a neuron (nerve cell) that conducts electrical impulses away from the cell body and toward other cells. Axons are a critical component of the nervous system, allowing for communication between different parts of the body.

Axotomy is often used in research settings to study the effects of axonal injury on neuronal function and regeneration. This procedure can provide valuable insights into the mechanisms underlying neurodegenerative disorders and potential therapies for nerve injuries. However, it is important to note that axotomy can also have significant consequences for the affected neuron, including changes in gene expression, metabolism, and overall survival.

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.

Sciatic neuropathy is a condition that results from damage or injury to the sciatic nerve, which is the largest nerve in the human body. The sciatic nerve originates from the lower spine (lumbar and sacral regions) and travels down through the buttocks, hips, and legs to the feet.

Sciatic neuropathy can cause various symptoms, including pain, numbness, tingling, weakness, or difficulty moving the affected leg or foot. The pain associated with sciatic neuropathy is often described as sharp, shooting, or burning and may worsen with movement, coughing, or sneezing.

The causes of sciatic neuropathy include compression or irritation of the nerve due to conditions such as herniated discs, spinal stenosis, bone spurs, tumors, or piriformis syndrome. Trauma or injury to the lower back, hip, or buttocks can also cause sciatic neuropathy.

Diagnosing sciatic neuropathy typically involves a physical examination and medical history, as well as imaging tests such as X-rays, MRI, or CT scans to visualize the spine and surrounding structures. Treatment options may include pain management, physical therapy, steroid injections, or surgery, depending on the severity and underlying cause of the condition.

Schwann cells, also known as neurolemmocytes, are a type of glial cell that form the myelin sheath around peripheral nervous system (PNS) axons, allowing for the rapid and efficient transmission of nerve impulses. These cells play a crucial role in the maintenance and function of the PNS.

Schwann cells originate from the neural crest during embryonic development and migrate to the developing nerves. They wrap around the axons in a spiral fashion, forming multiple layers of myelin, which insulates the nerve fibers and increases the speed of electrical impulse transmission. Each Schwann cell is responsible for myelinating a single segment of an axon, with the gaps between these segments called nodes of Ranvier.

Schwann cells also provide structural support to the neurons and contribute to the regeneration of injured peripheral nerves by helping to guide the regrowth of axons to their targets. Additionally, Schwann cells can participate in immune responses within the PNS, such as releasing cytokines and chemokines to recruit immune cells during injury or infection.

Anterior cerebral artery infarction refers to the death of brain tissue (also known as an infarct) in the territory supplied by the anterior cerebral artery (ACA) due to insufficient blood flow. The ACA supplies oxygenated blood to the frontal lobes of the brain, which are responsible for higher cognitive functions such as reasoning, problem-solving, and decision-making, as well as motor control of the lower extremities.

An infarction in this territory can result from various causes, including atherosclerosis, embolism, thrombosis, or vasospasm. Symptoms of an ACA infarction may include weakness or paralysis on one side of the body (usually the lower extremities), difficulty with coordination and balance, urinary incontinence, changes in personality or behavior, and impaired cognitive function. The severity of symptoms depends on the extent and location of the infarct. Immediate medical attention is necessary to prevent further damage and improve the chances of recovery.

A nerve crush injury is a type of peripheral nerve injury that occurs when there is excessive pressure or compression applied to a nerve, causing it to become damaged or dysfunctional. This can happen due to various reasons such as trauma from accidents, surgical errors, or prolonged pressure on the nerve from tight casts, clothing, or positions.

The compression disrupts the normal functioning of the nerve, leading to symptoms such as numbness, tingling, weakness, or pain in the affected area. In severe cases, a nerve crush injury can cause permanent damage to the nerve, leading to long-term disability or loss of function. Treatment for nerve crush injuries typically involves relieving the pressure on the nerve, providing supportive care, and in some cases, surgical intervention may be necessary to repair the damaged nerve.

Nerve regeneration is the process of regrowth and restoration of functional nerve connections following damage or injury to the nervous system. This complex process involves various cellular and molecular events, such as the activation of support cells called glia, the sprouting of surviving nerve fibers (axons), and the reformation of neural circuits. The goal of nerve regeneration is to enable the restoration of normal sensory, motor, and autonomic functions impaired due to nerve damage or injury.

Peripheral nerves are nerve fibers that transmit signals between the central nervous system (CNS, consisting of the brain and spinal cord) and the rest of the body. These nerves convey motor, sensory, and autonomic information, enabling us to move, feel, and respond to changes in our environment. They form a complex network that extends from the CNS to muscles, glands, skin, and internal organs, allowing for coordinated responses and functions throughout the body. Damage or injury to peripheral nerves can result in various neurological symptoms, such as numbness, weakness, or pain, depending on the type and severity of the damage.

The pyramidal tracts, also known as the corticospinal tracts, are bundles of nerve fibers that run through the brainstem and spinal cord, originating from the cerebral cortex. These tracts are responsible for transmitting motor signals from the brain to the muscles, enabling voluntary movement and control of the body.

The pyramidal tracts originate from the primary motor cortex in the frontal lobe of the brain and decussate (cross over) in the lower medulla oblongata before continuing down the spinal cord. The left pyramidal tract controls muscles on the right side of the body, while the right pyramidal tract controls muscles on the left side of the body.

Damage to the pyramidal tracts can result in various motor impairments, such as weakness or paralysis, spasticity, and loss of fine motor control, depending on the location and extent of the damage.

The optic nerve, also known as the second cranial nerve, is the nerve that transmits visual information from the retina to the brain. It is composed of approximately one million nerve fibers that carry signals related to vision, such as light intensity and color, from the eye's photoreceptor cells (rods and cones) to the visual cortex in the brain. The optic nerve is responsible for carrying this visual information so that it can be processed and interpreted by the brain, allowing us to see and perceive our surroundings. Damage to the optic nerve can result in vision loss or impairment.

Peripheral nerve injuries refer to damage or trauma to the peripheral nerves, which are the nerves outside the brain and spinal cord. These nerves transmit information between the central nervous system (CNS) and the rest of the body, including sensory, motor, and autonomic functions. Peripheral nerve injuries can result in various symptoms, depending on the type and severity of the injury, such as numbness, tingling, weakness, or paralysis in the affected area.

Peripheral nerve injuries are classified into three main categories based on the degree of damage:

1. Neuropraxia: This is the mildest form of nerve injury, where the nerve remains intact but its function is disrupted due to a local conduction block. The nerve fiber is damaged, but the supporting structures remain intact. Recovery usually occurs within 6-12 weeks without any residual deficits.
2. Axonotmesis: In this type of injury, there is damage to both the axons and the supporting structures (endoneurium, perineurium). The nerve fibers are disrupted, but the connective tissue sheaths remain intact. Recovery can take several months or even up to a year, and it may be incomplete, with some residual deficits possible.
3. Neurotmesis: This is the most severe form of nerve injury, where there is complete disruption of the nerve fibers and supporting structures (endoneurium, perineurium, epineurium). Recovery is unlikely without surgical intervention, which may involve nerve grafting or repair.

Peripheral nerve injuries can be caused by various factors, including trauma, compression, stretching, lacerations, or chemical exposure. Treatment options depend on the type and severity of the injury and may include conservative management, such as physical therapy and pain management, or surgical intervention for more severe cases.

Nervous system trauma, also known as neurotrauma, refers to damage or injury to the nervous system, including the brain and spinal cord. This type of trauma can result from various causes, such as vehicular accidents, sports injuries, falls, violence, or penetrating traumas. Nervous system trauma can lead to temporary or permanent impairments in sensory, motor, or cognitive functions, depending on the severity and location of the injury.

Traumatic brain injury (TBI) is a common form of nervous system trauma that occurs when an external force causes brain dysfunction. TBIs can be classified as mild, moderate, or severe, based on factors such as loss of consciousness, memory loss, and neurological deficits. Mild TBIs, also known as concussions, may not cause long-term damage but still require medical attention to ensure proper healing and prevent further complications.

Spinal cord injuries (SCI) are another form of nervous system trauma that can have severe consequences. SCI occurs when the spinal cord is damaged due to a sudden, traumatic blow or cut, causing loss of motor function, sensation, or autonomic function below the level of injury. The severity and location of the injury determine the extent of impairment, which can range from partial to complete paralysis.

Immediate medical intervention is crucial in cases of nervous system trauma to minimize secondary damage, prevent complications, and optimize recovery outcomes. Treatment options may include surgery, medication, rehabilitation, or a combination of these approaches.

Electrophysiological processes refer to the electrical activities that occur within biological cells or organ systems, particularly in nerve and muscle tissues. These processes involve the generation, transmission, and reception of electrical signals that are essential for various physiological functions, such as nerve impulse transmission, muscle contraction, and hormonal regulation.

At the cellular level, electrophysiological processes are mediated by the flow of ions across the cell membrane through specialized protein channels. This ion movement generates a voltage difference across the membrane, leading to the development of action potentials, which are rapid changes in electrical potential that travel along the cell membrane and transmit signals between cells.

In clinical medicine, electrophysiological studies (EPS) are often used to diagnose and manage various cardiac arrhythmias and neurological disorders. These studies involve the recording of electrical activity from the heart or brain using specialized equipment, such as an electrocardiogram (ECG) or an electroencephalogram (EEG). By analyzing these recordings, physicians can identify abnormalities in the electrical activity of these organs and develop appropriate treatment plans.

Neurologic mutant mice are genetically engineered or spontaneously mutated rodents that are used as models to study various neurological disorders and conditions. These mice have specific genetic modifications or mutations that affect their nervous system, leading to phenotypes that resemble human neurological diseases.

Some examples of neurologic mutant mice include:

1. Alzheimer's disease models: Mice that overexpress genes associated with Alzheimer's disease, such as the amyloid precursor protein (APP) or presenilin 1 (PS1), to study the pathogenesis and potential treatments of this disorder.
2. Parkinson's disease models: Mice that have genetic mutations in genes associated with Parkinson's disease, such as alpha-synuclein or parkin, to investigate the mechanisms underlying this condition and develop new therapies.
3. Huntington's disease models: Mice that carry an expanded CAG repeat in the huntingtin gene to replicate the genetic defect seen in humans with Huntington's disease and study disease progression and treatment strategies.
4. Epilepsy models: Mice with genetic mutations that cause spontaneous seizures or increased susceptibility to seizures, used to investigate the underlying mechanisms of epilepsy and develop new treatments.
5. Stroke models: Mice that have surgical induction of stroke or genetic modifications that increase the risk of stroke, used to study the pathophysiology of stroke and identify potential therapeutic targets.

Neurologic mutant mice are essential tools in biomedical research, allowing scientists to investigate the complex interactions between genes and the environment that contribute to neurological disorders. These models help researchers better understand disease mechanisms, develop new therapies, and test their safety and efficacy before moving on to clinical trials in humans.

Retinal degeneration is a broad term that refers to the progressive loss of photoreceptor cells (rods and cones) in the retina, which are responsible for converting light into electrical signals that are sent to the brain. This process can lead to vision loss or blindness. There are many different types of retinal degeneration, including age-related macular degeneration, retinitis pigmentosa, and Stargardt's disease, among others. These conditions can have varying causes, such as genetic mutations, environmental factors, or a combination of both. Treatment options vary depending on the specific type and progression of the condition.

Neurofilament proteins (NFs) are type IV intermediate filament proteins that are specific to neurons. They are the major structural components of the neuronal cytoskeleton and play crucial roles in maintaining the structural integrity, stability, and diameter of axons. Neurofilaments are composed of three subunits: light (NFL), medium (NFM), and heavy (NFH) neurofilament proteins, which differ in their molecular weights. These subunits assemble into heteropolymers to form the neurofilament core, while the C-terminal tails of NFH and NFM extend outward from the core, interacting with other cellular components and participating in various neuronal functions. Increased levels of neurofilament proteins, particularly NFL, in cerebrospinal fluid (CSF) and blood are considered biomarkers for axonal damage and neurodegeneration in several neurological disorders, such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS).

Macular degeneration, also known as age-related macular degeneration (AMD), is a medical condition that affects the central part of the retina, called the macula. The macula is responsible for sharp, detailed vision, which is necessary for activities such as reading, driving, and recognizing faces.

In AMD, there is a breakdown or deterioration of the macula, leading to gradual loss of central vision. There are two main types of AMD: dry (atrophic) and wet (exudative). Dry AMD is more common and progresses more slowly, while wet AMD is less common but can cause rapid and severe vision loss if left untreated.

The exact causes of AMD are not fully understood, but risk factors include age, smoking, family history, high blood pressure, obesity, and exposure to sunlight. While there is no cure for AMD, treatments such as vitamin supplements, laser therapy, and medication injections can help slow its progression and reduce the risk of vision loss.

Myelinated nerve fibers are neuronal processes that are surrounded by a myelin sheath, a fatty insulating substance that is produced by Schwann cells in the peripheral nervous system and oligodendrocytes in the central nervous system. This myelin sheath helps to increase the speed of electrical impulse transmission, also known as action potentials, along the nerve fiber. The myelin sheath has gaps called nodes of Ranvier where the electrical impulses can jump from one node to the next, which also contributes to the rapid conduction of signals. Myelinated nerve fibers are typically found in the peripheral nerves and the optic nerve, but not in the central nervous system (CNS) tracts that are located within the brain and spinal cord.

Spinal nerve roots are the initial parts of spinal nerves that emerge from the spinal cord through the intervertebral foramen, which are small openings between each vertebra in the spine. These nerve roots carry motor, sensory, and autonomic fibers to and from specific regions of the body. There are 31 pairs of spinal nerve roots in total, with 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal pair. Each root has a dorsal (posterior) and ventral (anterior) ramus that branch off to form the peripheral nervous system. Irritation or compression of these nerve roots can result in pain, numbness, weakness, or loss of reflexes in the affected area.

Nerve tissue proteins are specialized proteins found in the nervous system that provide structural and functional support to nerve cells, also known as neurons. These proteins include:

1. Neurofilaments: These are type IV intermediate filaments that provide structural support to neurons and help maintain their shape and size. They are composed of three subunits - NFL (light), NFM (medium), and NFH (heavy).

2. Neuronal Cytoskeletal Proteins: These include tubulins, actins, and spectrins that provide structural support to the neuronal cytoskeleton and help maintain its integrity.

3. Neurotransmitter Receptors: These are specialized proteins located on the postsynaptic membrane of neurons that bind neurotransmitters released by presynaptic neurons, triggering a response in the target cell.

4. Ion Channels: These are transmembrane proteins that regulate the flow of ions across the neuronal membrane and play a crucial role in generating and transmitting electrical signals in neurons.

5. Signaling Proteins: These include enzymes, receptors, and adaptor proteins that mediate intracellular signaling pathways involved in neuronal development, differentiation, survival, and death.

6. Adhesion Proteins: These are cell surface proteins that mediate cell-cell and cell-matrix interactions, playing a crucial role in the formation and maintenance of neural circuits.

7. Extracellular Matrix Proteins: These include proteoglycans, laminins, and collagens that provide structural support to nerve tissue and regulate neuronal migration, differentiation, and survival.

Diffusion Magnetic Resonance Imaging (MRI) is a non-invasive medical imaging technique that uses magnetic fields and radio waves to produce detailed images of the body's internal structures, particularly the brain and nervous system. In diffusion MRI, the movement of water molecules in biological tissues is measured and analyzed to generate contrast in the images based on the microstructural properties of the tissue.

Diffusion MRI is unique because it allows for the measurement of water diffusion in various directions, which can reveal important information about the organization and integrity of nerve fibers in the brain. This technique has been widely used in research and clinical settings to study a variety of neurological conditions, including stroke, traumatic brain injury, multiple sclerosis, and neurodegenerative diseases such as Alzheimer's disease.

In summary, diffusion MRI is a specialized type of MRI that measures the movement of water molecules in biological tissues to generate detailed images of the body's internal structures, particularly the brain and nervous system. It provides valuable information about the microstructural properties of tissues and has important applications in both research and clinical settings.

Spinal ganglia, also known as dorsal root ganglia, are clusters of nerve cell bodies located in the peripheral nervous system. They are situated along the length of the spinal cord and are responsible for transmitting sensory information from the body to the brain. Each spinal ganglion contains numerous neurons, or nerve cells, with long processes called axons that extend into the periphery and innervate various tissues and organs. The cell bodies within the spinal ganglia receive sensory input from these axons and transmit this information to the central nervous system via the dorsal roots of the spinal nerves. This allows the brain to interpret and respond to a wide range of sensory stimuli, including touch, temperature, pain, and proprioception (the sense of the position and movement of one's body).

The Peripheral Nervous System (PNS) is that part of the nervous system which lies outside of the brain and spinal cord. It includes all the nerves and ganglia ( clusters of neurons) outside of the central nervous system (CNS). The PNS is divided into two components: the somatic nervous system and the autonomic nervous system.

The somatic nervous system is responsible for transmitting sensory information from the skin, muscles, and joints to the CNS, and for controlling voluntary movements of the skeletal muscles.

The autonomic nervous system, on the other hand, controls involuntary actions, such as heart rate, digestion, respiratory rate, salivation, perspiration, pupillary dilation, and sexual arousal. It is further divided into the sympathetic and parasympathetic systems, which generally have opposing effects and maintain homeostasis in the body.

Damage to the peripheral nervous system can result in various medical conditions such as neuropathies, neuritis, plexopathies, and radiculopathies, leading to symptoms like numbness, tingling, pain, weakness, or loss of reflexes in the affected area.

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.

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.

Motor neurons are specialized nerve cells in the brain and spinal cord that play a crucial role in controlling voluntary muscle movements. They transmit electrical signals from the brain to the muscles, enabling us to perform actions such as walking, talking, and swallowing. There are two types of motor neurons: upper motor neurons, which originate in the brain's motor cortex and travel down to the brainstem and spinal cord; and lower motor neurons, which extend from the brainstem and spinal cord to the muscles. Damage or degeneration of these motor neurons can lead to various neurological disorders, such as amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA).

Spinal cord injuries (SCI) refer to damage to the spinal cord that results in a loss of function, such as mobility or feeling. This injury can be caused by direct trauma to the spine or by indirect damage resulting from disease or degeneration of surrounding bones, tissues, or blood vessels. The location and severity of the injury on the spinal cord will determine which parts of the body are affected and to what extent.

The effects of SCI can range from mild sensory changes to severe paralysis, including loss of motor function, autonomic dysfunction, and possible changes in sensation, strength, and reflexes below the level of injury. These injuries are typically classified as complete or incomplete, depending on whether there is any remaining function below the level of injury.

Immediate medical attention is crucial for spinal cord injuries to prevent further damage and improve the chances of recovery. Treatment usually involves immobilization of the spine, medications to reduce swelling and pressure, surgery to stabilize the spine, and rehabilitation to help regain lost function. Despite advances in treatment, SCI can have a significant impact on a person's quality of life and ability to perform daily activities.

Quinolines are a class of organic compounds that consist of a bicyclic structure made up of a benzene ring fused to a piperidine ring. They have a wide range of applications, but they are perhaps best known for their use in the synthesis of various medications, including antibiotics and antimalarial drugs.

Quinolone antibiotics, such as ciprofloxacin and levofloxacin, work by inhibiting the bacterial enzymes involved in DNA replication and repair. They are commonly used to treat a variety of bacterial infections, including urinary tract infections, pneumonia, and skin infections.

Quinoline-based antimalarial drugs, such as chloroquine and hydroxychloroquine, work by inhibiting the parasite's ability to digest hemoglobin in the red blood cells. They are commonly used to prevent and treat malaria.

It is important to note that quinolines have been associated with serious side effects, including tendinitis and tendon rupture, nerve damage, and abnormal heart rhythms. As with any medication, it is important to use quinolines only under the supervision of a healthcare provider, and to follow their instructions carefully.

Hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitors, also known as statins, are a class of cholesterol-lowering medications. They work by inhibiting the enzyme HMG-CoA reductase, which plays a central role in the production of cholesterol in the liver. By blocking this enzyme, the liver is stimulated to take up more low-density lipoprotein (LDL) cholesterol from the bloodstream, leading to a decrease in LDL cholesterol levels and a reduced risk of cardiovascular disease.

Examples of HMG-CoA reductase inhibitors include atorvastatin, simvastatin, pravastatin, rosuvastatin, and fluvastatin. These medications are commonly prescribed to individuals with high cholesterol levels, particularly those who are at risk for or have established cardiovascular disease.

It's important to note that while HMG-CoA reductase inhibitors can be effective in reducing LDL cholesterol levels and the risk of cardiovascular events, they should be used as part of a comprehensive approach to managing high cholesterol, which may also include lifestyle modifications such as dietary changes, exercise, and weight management.

Biological availability is a term used in pharmacology and toxicology that refers to the degree and rate at which a drug or other substance is absorbed into the bloodstream and becomes available at the site of action in the body. It is a measure of the amount of the substance that reaches the systemic circulation unchanged, after administration by any route (such as oral, intravenous, etc.).

The biological availability (F) of a drug can be calculated using the area under the curve (AUC) of the plasma concentration-time profile after extravascular and intravenous dosing, according to the following formula:

F = (AUCex/AUCiv) x (Doseiv/Doseex)

where AUCex is the AUC after extravascular dosing, AUCiv is the AUC after intravenous dosing, Doseiv is the intravenous dose, and Doseex is the extravascular dose.

Biological availability is an important consideration in drug development and therapy, as it can affect the drug's efficacy, safety, and dosage regimen. Drugs with low biological availability may require higher doses to achieve the desired therapeutic effect, while drugs with high biological availability may have a more rapid onset of action and require lower doses to avoid toxicity.

Oral administration is a route of giving medications or other substances by mouth. This can be in the form of tablets, capsules, liquids, pastes, or other forms that can be swallowed. Once ingested, the substance is absorbed through the gastrointestinal tract and enters the bloodstream to reach its intended target site in the body. Oral administration is a common and convenient route of medication delivery, but it may not be appropriate for all substances or in certain situations, such as when rapid onset of action is required or when the patient has difficulty swallowing.

The term "Area Under Curve" (AUC) is commonly used in the medical field, particularly in the analysis of diagnostic tests or pharmacokinetic studies. The AUC refers to the mathematical calculation of the area between a curve and the x-axis in a graph, typically representing a concentration-time profile.

In the context of diagnostic tests, the AUC is used to evaluate the performance of a test by measuring the entire two-dimensional area underneath the receiver operating characteristic (ROC) curve, which plots the true positive rate (sensitivity) against the false positive rate (1-specificity) at various threshold settings. The AUC ranges from 0 to 1, where a higher AUC indicates better test performance:

* An AUC of 0.5 suggests that the test is no better than chance.
* An AUC between 0.7 and 0.8 implies moderate accuracy.
* An AUC between 0.8 and 0.9 indicates high accuracy.
* An AUC greater than 0.9 signifies very high accuracy.

In pharmacokinetic studies, the AUC is used to assess drug exposure over time by calculating the area under a plasma concentration-time curve (AUC(0-t) or AUC(0-\∞)) following drug administration. This value can help determine dosing regimens and evaluate potential drug interactions:

* AUC(0-t): Represents the area under the plasma concentration-time curve from time zero to the last measurable concentration (t).
* AUC(0-\∞): Refers to the area under the plasma concentration-time curve from time zero to infinity, which estimates total drug exposure.

Dietary fats, also known as fatty acids, are a major nutrient that the body needs for energy and various functions. They are an essential component of cell membranes and hormones, and they help the body absorb certain vitamins. There are several types of dietary fats:

1. Saturated fats: These are typically solid at room temperature and are found in animal products such as meat, butter, and cheese, as well as tropical oils like coconut and palm oil. Consuming a high amount of saturated fats can raise levels of unhealthy LDL cholesterol and increase the risk of heart disease.
2. Unsaturated fats: These are typically liquid at room temperature and can be further divided into monounsaturated and polyunsaturated fats. Monounsaturated fats, found in foods such as olive oil, avocados, and nuts, can help lower levels of unhealthy LDL cholesterol while maintaining levels of healthy HDL cholesterol. Polyunsaturated fats, found in foods such as fatty fish, flaxseeds, and walnuts, have similar effects on cholesterol levels and also provide essential omega-3 and omega-6 fatty acids that the body cannot produce on its own.
3. Trans fats: These are unsaturated fats that have been chemically modified to be solid at room temperature. They are often found in processed foods such as baked goods, fried foods, and snack foods. Consuming trans fats can raise levels of unhealthy LDL cholesterol and lower levels of healthy HDL cholesterol, increasing the risk of heart disease.

It is recommended to limit intake of saturated and trans fats and to consume more unsaturated fats as part of a healthy diet.

In the context of pharmacology, "half-life" refers to the time it takes for the concentration or amount of a drug in the body to be reduced by half during its elimination phase. This is typically influenced by factors such as metabolism and excretion rates of the drug. It's a key factor in determining dosage intervals and therapeutic effectiveness of medications, as well as potential side effects or toxicity risks.

... is an active process of degeneration that results when a nerve fiber is cut or crushed and the part of ... Myelin clearance is the next step in Wallerian degeneration following axonal degeneration. The cleaning up of myelin debris is ... A related process of dying back or retrograde degeneration known as 'Wallerian-like degeneration' occurs in many ... and axon degeneration revisited: Nmnat1 cannot substitute for Wld(S) to delay Wallerian degeneration". Cell Death and ...
Wallerian degeneration Scalea TM (2005). "Does it matter how head injured patients are resuscitated?". In Valadka AB, Andrews ...
There is no wallerian degeneration. Conduction is intact in the distal segment and proximal segment, but no conduction occurs ... Other characteristics: Wallerian degeneration occurs distal to the site of injury. There is connective tissue lesion that may ... Wallerian degeneration occurs distal to the site of injury. There are sensory and motor deficits distal to the site of lesion. ... Connective tissue in the peripheral nervous system Neuroregeneration Wallerian degeneration "Peripheral Nerve Injuries". " ...
... this is known as Wallerian-like degeneration. Studies suggest that the degeneration happens as a result of the axonal protein ... Trauma and Wallerian Degeneration Archived 2 May 2006 at the Wayback Machine, University of California, San Francisco Coleman ... This is known as Wallerian degeneration. Dying back of an axon can also take place in many neurodegenerative diseases, ... "Wallerian degeneration, wld(s), and nmnat". Annual Review of Neuroscience. 33 (1): 245-67. doi:10.1146/annurev-neuro-060909- ...
Loss of NMNAT2 initiates Wallerian degeneration. By contrast, NMNAT2 enhancement opposes the actions of SARM1 which would lead ... Activation of NMNAT2 by Sirtuin 3 (SIRT3) may be a means of inhibiting axon degeneration and dysfunction. The catechin ... to axon degeneration, but this effect is not due to preventing SARM1 depletion of NAD+. Mice lacking NMNAT2 die before birth, ...
Recovery takes place without wallerian degeneration. Axonotmesis: Involves axonal degeneration, with loss of the relative ... leading to wallerian degeneration of the sensory fibre. Thus, no action potential detected at the distal end of spinal nerve. ... thus there is no wallerian degeneration of the sensory fibre, thus sensory action potential can still be detected at the distal ...
Wallerian degeneration is a process that occurs before nerve regeneration and can be described as a cleaning or clearing ... Schwann cells are active in Wallerian degeneration. They not only have a role in phagocytosis of myelin, but they also have a ... During Wallerian degeneration Schwann cells and macrophages interact to remove debris, specifically myelin and the damaged axon ... Stoll G, Griffin JW, Li CY, Trapp BD (October 1989). "Wallerian degeneration in the peripheral nervous system: participation of ...
Wallerian degeneration outside the lesions has been reported. In general, during the acute phase, the plaques of lesions were ... Wallerian Degeneration in the Corticospinal Tract Following Tumefactive Demyelination: Conventional and Advanced Magnetic ...
Wallerian degeneration often occurs in the near the proximity of the injury site. Neurapraxia is least serious form of nerve ... Wallerian degeneration does not occur in neurapraxia. In order for the condition to be considered neurapraxia, according to the ...
Wallerian degeneration in lesion-related tracts (lesion type 3). Around active NMO lesions AQP4 may selectively be lost in the ... Recently other type of immune cells, B Cells, have been also implicated in the pathogenesis of MS and in the degeneration of ... Pattern IV The scar presents sharp borders and oligodendrocyte degeneration, with a rim of normal appearing white matter. There ... such as demyelination or axonal degeneration (lesion type 5). Finally, lesions with a variable degree of astrocyte ...
... and finally Wallerian degeneration. Animal models demonstrate that extraneural pressures as low as 20 to 30 mm Hg disrupt ... Axonal degeneration was correlated with degree of endoneurial edema. In a few case reports (surgical resection of nerve, ... Myelin thinning was also noted along with evidence of fiber degeneration and regeneration. Experimental studies suggest a dose ... distal axon degeneration, extensive fibrosis, new axon growth, remyelination, and thickening of the perineurium and endothelium ...
... an iron-dependent form of cell death and Wallerian degeneration. Necroptosis is a programmed form of necrosis, or inflammatory ... Paraptosis Parthanatos Pyroptosis RIP kinases Wallerian degeneration Srivastava, R. E. in Molecular Mechanisms (Humana Press, ... Mosinger, Ogilvie (1998). "Suppression of developmental retinal cell death but not of photoreceptor degeneration in Bax- ...
... an iron-dependent form of cell death and Wallerian degeneration. Plant cells undergo particular processes of PCD similar to ...
Neuropraxia: no wallerian degeneration and complete and rapid recovery of function. Axonotmesis: wallerian degeneration and ... Neurotmesis: this type of injury involves the endoneurium with wallerian degeneration. Recovery is difficult. There are several ... If it is more than 3.5mA then it suggests the axonal degeneration. If it is more than 20 mA then it suggests immediate ... There may also be demyelination (loss of the nerve's myelin sheath) and degeneration of the nerve in the affected area but it ...
... protein plays a central role in the Wallerian degeneration pathway. The role for this gene in the Wallerian degeneration ... Loreto A, Di Stefano M, Gering M, Conforti L (December 2015). "Wallerian Degeneration Is Executed by an NMN-SARM1-Dependent ... Specific mutations in the human NMNAT2 gene, encoding a key regulator of SARM1 activity, have linked the Wallerian degeneration ... August 1998). "An 85-kb tandem triplication in the slow Wallerian degeneration (Wlds) mouse". Proceedings of the National ...
"Very early activation of m-calpain in peripheral nerve during Wallerian degeneration". J. Neurol. Sci. 196 (1-2): 9-20. doi: ... as well as secondary degeneration resulting from acute cellular stress following myocardial ischemia, cerebral (neuronal) ...
Yamada, K; Kizu, O; Ito, H; Nakamura, H; Yuen, S; Yoshikawa, K; Shiga, K; Nishimura, T (2003). "Wallerian degeneration of the ...
He was the first to describe the degeneration of severed nerve fibers, now known as Wallerian degeneration. The son of William ... The Wallerian degeneration is described in the 'Comptes Rendus,' 1 Dec. 1851. The demonstration of the cilio-spinal centre was ... and he invented the degeneration method of studying the paths of nerve impulses. He practically rediscovered the power which ...
During Wallerian degeneration, Schwann cells grow in ordered columns along the endoneurial tube, creating a band of Büngner ... When an axon is damaged, the distal segment undergoes Wallerian degeneration, losing its myelin sheath. The proximal segment ... The distal segment, however, experiences Wallerian degeneration within hours of the injury; the axons and myelin degenerate, ... Slower degeneration of the distal segment than that which occurs in the peripheral nervous system also contributes to the ...
Nerve injury Turner JE, Glaze KA (March 1977). "The early stages of Wallerian degeneration in the severed optic nerve of the ... Digestion chambers are a histologic finding in nerves that are undergoing Wallerian degeneration. Digestion chambers consist of ...
Diffuse axonal injury Neurectomy Neurosurgery Wallerian degeneration "Online Medical Dictionary" Rubinsztein DC et al. (2005) ... Autophagy could either clear the way for neuronal degeneration or it could be a medium for cell destruction. Upon injury of a ... that the demyelination in multiple sclerosis lesions leads to axonal transection and ultimately axonal degeneration. This axon ...
Another possible effect of Bell's palsy is Wallerian degeneration (WD), which may take days to become evident. Because of the ... Electromyography Electromyoneurography Bell's palsy Microneurography Wallerian degeneration Neuropraxia Neurotmesis Axonotmesis ... Bendet, E., Vajtai, I., Maranta C., Fisch, U.: Rate and extent of early axonal degeneration of the human facial nerve. Ann Otol ... This is because the degeneration has not yet reached completion, and some fibers are still intact. Therefore, it is standard ...
When the axon is torn, Wallerian degeneration, in which the part of the axon distal to the break degrades, takes place within ... "Comparison of matrix metalloproteinase expression during wallerian degeneration in the central and peripheral nervous systems ... the axon is torn at the site of stretch and the part distal to the tear degrades by a process known as Wallerian degeneration. ... Special Issue: Axonal degeneration. 246: 35-43. doi:10.1016/j.expneurol.2012.01.013. PMC 3979341. PMID 22285252. Tang-Schomer ...
Nerve injury Neuroregeneration Wallerian degeneration Sasser, Karen L. "Medical Student Curriculum in Neurosurgery." Medical ... there is still profound muscle paralysis and degeneration in these areas, then it is likely to have been a neurotmesis injury. ...
... behavior and proliferation to become involved in Wallerian degeneration and Bungner bands. In Wallerian degeneration, Schwann ... Schwann cells are responsible for taking part in both Wallerian degeneration and bands of Bungner. When a peripheral nerve is ...
2002). "Human homologue of a gene mutated in the slow Wallerian degeneration (C57BL/Wld(s)) mouse". Gene. 284 (1-2): 23-9. doi: ... NMNAT1 enhancement opposes the actions of SARM1 which would lead to axon degeneration, but this effect is not due to preventing ... Mutations in this gene have been shown associated to the LCA9 form of the retinal degeneration pathology Leber's congenital ... "Mutations in NMNAT1 cause Leber congenital amaurosis and identify a new disease pathway for retinal degeneration". Nat. Genet. ...
When axonal transport is severely disrupted a degenerative pathway known as Wallerian-like degeneration is often triggered. ... Coleman MP & Freeman MF 'Wallerian degeneration, WldS and Nmnat' Annual Review of Neuroscience 2010, 33: 245-67 Engelberg-Kulka ... Because there is no known way to reverse the progressive degeneration of neurons, these diseases are considered to be incurable ... The first brain region to be substantially affected is the striatum, followed by degeneration of the frontal and temporal ...
If the compression continues and is severe enough, axons may be injured and Wallerian degeneration will occur. At this point ...
The basis of this hypothesis is as follows: after a lesion, axonal degeneration (via Wallerian degeneration) occurs. The post- ... to diffuse axon demyelination and degeneration of the seventh cranial nerve, results in a hemifacial paralysis due to non- ...
Degeneration appears distally in the paralysed facial nerve but this takes time, this process is called Wallerian degeneration ...
Wallerian degeneration is an active process of degeneration that results when a nerve fiber is cut or crushed and the part of ... Myelin clearance is the next step in Wallerian degeneration following axonal degeneration. The cleaning up of myelin debris is ... A related process of dying back or retrograde degeneration known as Wallerian-like degeneration occurs in many ... and axon degeneration revisited: Nmnat1 cannot substitute for Wld(S) to delay Wallerian degeneration". Cell Death and ...
Forty-three patients with wallerian degeneration seen on MR images after cerebral infarction were studied. When possible, ... imaging in active and chronic wallerian degeneration in the corticospinal tract were evaluated. ... Wallerian degeneration after cerebral infarction: evaluation with sequential MR imaging Radiology. 1989 Jul;172(1):179-82. doi ... The dynamic signal intensity changes at magnetic resonance (MR) imaging in active and chronic wallerian degeneration in the ...
I. An analysis in tissue culture of proliferation during development, Wallerian degeneration, and direct injury.. J Cell Biol ( ...
A condition caused by degeneration, atrophy, and destruction of the distal part of a nerve fibers axon and myelin, when ... Wallerian degeneration of the pyramidal tract. SNOMED CT: Wallerian degeneration (36161006); Secondary degeneration (36161006) ... Wallerian Degeneration Beyond the Corticospinal Tracts: Conventional and Advanced MRI Findings.. Chen YJ, Nabavizadeh SA, ... Clinical and Radiological Features of Wallerian Degeneration of the Middle Cerebellar Peduncles Secondary to Pontine Infarction ...
... motor nerve terminals following hypoxia-reperfusion injury occurs via mechanisms distinct from classic Wallerian degeneration. ... Morphological characteristics of motor neurons do not determine their relative susceptibility to degeneration in a mouse model ...
Enhanced oligodendrocyte survival after spinal cord injury in bax-deficient mice and mice with delayed Wallerian degeneration. ... Enhanced oligodendrocyte survival after spinal cord injury in bax-deficient mice and mice with delayed Wallerian degeneration ...
Elimination of motor nerve terminals in neonatal mice expressing a gene for slow wallerian degeneration (C57Bl/Wlds). European ... Elimination of motor nerve terminals in neonatal mice expressing a gene for slow wallerian degeneration (C57Bl/Wlds). / Parson ... Elimination of motor nerve terminals in neonatal mice expressing a gene for slow wallerian degeneration (C57Bl/Wlds). ... title = "Elimination of motor nerve terminals in neonatal mice expressing a gene for slow wallerian degeneration (C57Bl/Wlds)", ...
In spinal cord injury, the degeneration of the severed axons through anterograde or Wallerian degeneration (WD) is followed by ... Microglia also phagocytose axonal and myelin debris resulting from Wallerian degeneration of severed axons (D). (A) Surface- ... 2004). Gradual loss of myelin and formation of an astrocytic scar during Wallerian degeneration in the human spinal cord. Brain ... Gaudet, A. D., Popovich, P. G., and Ramer, M. S. (2011). Wallerian degeneration: gaining perspective on inflammatory events ...
Repair is a process of degeneration followed by regeneration. Wallerian degeneration occurs in peripheral nerves. It is a ... it is dysfunction and/or paralysis without loss of nerve sheath continuity and peripheral wallerian degeneration. [3, 14] Nerve ... has sparked much interest among researchers because of its ability to stimulate the wallerian degeneration and regeneration of ... 30] The mechanism of delayed degeneration is uncertain. The blood-nerve barrier has been demonstrated to become damaged, and ...
Wallerian degeneration. Control: peripheral nerve Bodian Method. Reagents: Protargol, Reducing Solution (Hydroquinone, ...
Wallerian degeneration is ongoing (Vargas and Barres, 2007). This may then mean that, where slow axonal degeneration occurs, ... 2007) Why is Wallerian degeneration in the CNS so slow? Annu Rev Neurosci 30:153-179, doi:10.1146/annurev.neuro.30.051606. ... We found abundant T-lymphocytes and MHCII expression in the lesion and in an area of Wallerian degeneration 7 weeks following ... Staining is evident both in the lesion and locations where there is axonal degeneration. Images are representative of 10 mice. ...
Wallerian degeneration is delayed when sufficient levels of proteins with NMNAT activity are maintained within axons after ... This has been proposed to form the basis of slow Wallerian degeneration (Wld (S)), a neuroprotective phenotype conferred by ... MEK Inhibitor U0126 Reverses Protection of Axons from Wallerian Degeneration Independently of MEK-ERK Signaling. ... suggesting that MEK-ERK signaling plays a role in delayed Wallerian degeneration, in addition to its established role in ...
Wallerian degeneration) (black star). C) Dorsal root ganglion showing spinal ganglion with satellitosis (arrow) and ...
Targeting Wallerian degeneration slow protein for neuroprotection. *Peripheral neuropathy. *Neuroprotection in diabetic ... Table 12-5: Novel neuroprotective strategies against retinal degeneration. Table 12-6: Clinical trials for retinal ... epilepsy and ischemic optic neuropathy as well as retinal degeneration. Although anesthetics such as propofol are ...
Systemic inflammation switches the inflammatory cytokine profile in CNS Wallerian degeneration, Neurobiology of Disease. , 30, ...
At face value, the form of axon degeneration noted here is similar to the Wallerian degeneration of distal axon segments after ... ATP levels are known to decline during Wallerian degeneration, although a causative role for the decline in the degeneration is ... 2014) Wallerian degeneration: an emerging axon death pathway linking injury and disease. Nat Rev Neurosci 15:394-409. doi: ... Both glycolysis and oxidative phosphorylation are decreased during Wallerian degeneration, and rescue of degeneration by Sarm1 ...
"Natural History and Prognostic Value of Corticospinal Tract Wallerian Degeneration in Intracerebral Hemorrhage." ,i>Journal of ... "Natural History and Prognostic Value of Corticospinal Tract Wallerian Degeneration in Intracerebral Hemorrhage." ,i>Journal of ... "Natural History and Prognostic Value of Corticospinal Tract Wallerian Degeneration in Intracerebral Hemorrhage." ,i>Journal of ... "Natural History and Prognostic Value of Corticospinal Tract Wallerian Degeneration in Intracerebral Hemorrhage." ,i>Journal of ...
8 This cortical atrophy may induce Wallerian degeneration of WM tracts.8 Wallerian degeneration is characterized by a ... Chemistry of Wallerian degeneration: a review of recent studies. Arch Neurol Psychiatry 1950;64:105-21. ... Water diffusion changes in Wallerian degeneration and their dependence on white matter architecture. NeuroImage 2001;13:1174-85 ... Diffusion tensor imaging detects early Wallerian degeneration of the pyramidal tract after ischemic stroke. NeuroImage 2004;22: ...
Llobet Rosell A, Neukomm LJ. Axon death signalling in Wallerian degeneration among species and in disease. Open Biol. 2019 Aug ... Repici M., Borsello T., JNK pathway as therapeutic target to prevent degeneration in the central nervous system. Advances in ... Rossi D., Brambilla L., Valori C. F., Roncoroni C., Crugnola A., Yokota T., Bredesen D. E., Volterra A., Focal degeneration of ... precursor NMN activates dSarm to trigger axon degeneration in Drosophila. Elife. 2022 Dec 23;11:e80245. [Pubmed] ...
Relationship of acute axonal damage, Wallerian degeneration and clinical disability in multiple sclerosis. J Neurinflammation ( ... Wallerian tract degeneration in the human brain is a very slow process, reflected by the presence of degenerating axons even ... a major part of the axonal neurodegeneration in the white matter appears to be due to secondary Wallerian degeneration as a ... An alternative explanation is that these changes reflect Wallerian degeneration, since they are associated with diffuse axonal ...
2001) Water diffusion changes in wallerian degeneration and their dependence on white matter architecture. Neuroimage 13: 1174- ... These unexpected findings may result from degeneration of one pathway, with relatively sparing of the crossing pathway. For ...
A chemically similar drug in this class produced dose-dependent optic nerve degeneration (Wallerian degeneration of ... Wallerian degeneration has not been observed with pitavastatin. Cataracts and lens opacities were seen in dogs treated for 52 ...
Wallerian degeneration, and axonal degeneration.5,6 Segmental demyelination and Wallerian degeneration are repair mechanisms ... 4 Axonotmesis leads to Wallerian degeneration, a process whereby the part of the axon that is separated from the neuronal cell ... neurotmesis initiates Wallerian degeneration, but the prognosis for nerves is poor. Neurotmesis is commonly seen after ... that are relevant to traumatic nerve injury, whereas axonal degeneration is more characteristically seen in metabolic and toxic ...
... and peripheral radiculoneuritis with Wallerian degeneration; findings were consistent with a diagnosis of neuroborreliosis. ...
... showing scattered wallerian degeneration (arrowheads). (b) Low-power view of a paravertebral sympathetic ganglion stained with ... Purkinje cell antibody-2 (PCA-2) frequently causes cerebellar degeneration but can also be associated with autonomic failure. [ ... 19] This antibody is diagnostically useful, but the exact role of humoral immunity in causing neural degeneration remains ...
Axonal degeneration leads to Wallerian degeneration, in which myelin sheaths are phagocytosed, previously myelinating Schwann ... Small fibers resulting from axonal degeneration and regeneration are increased. A variable degree of granular degeneration of ... Axonal degeneration is a prediction of disability. This suggests that, in most cases, axonal damage is the root cause of the ... CMT2B biopsies reveal evidence of degeneration and regeneration, with the presence of occasional onion bulbs. ...
Diffusion tensor magnetic resonance imaging of Wallerian degeneration in rat spinal cord after dorsal root axotomy. J Neurosci ... Visualization of peripheral nerve degeneration and regeneration: monitoring with diffusion tensor tractography. Neuroimage, 44( ...
2009) A dual leucine kinase-dependent axon self-destruction program promotes Wallerian degeneration Nature Neuroscience 12:387- ... 2011) DLK induces developmental neuronal degeneration via selective regulation of proapoptotic JNK activity The Journal of Cell ... 2013) Dual leucine zipper kinase is required for excitotoxicity-induced neuronal degeneration The Journal of Experimental ... 2012) A conditioning lesion protects axons from degeneration via the Wallenda/DLK MAP kinase signaling cascade Journal of ...
  • Axonal degeneration is followed by degradation of the myelin sheath and infiltration by macrophages. (wikipedia.org)
  • Although most injury responses include a calcium influx signaling to promote resealing of severed parts, axonal injuries initially lead to acute axonal degeneration (AAD), which is rapid separation of the proximal (the part nearer the cell body) and distal ends within 30 minutes of injury. (wikipedia.org)
  • The disintegration is dependent on Ubiquitin and Calpain proteases (caused by influx of calcium ion), suggesting that axonal degeneration is an active process and not a passive one as previously misunderstood. (wikipedia.org)
  • Myelin clearance is the next step in Wallerian degeneration following axonal degeneration. (wikipedia.org)
  • Focal infarction without distal axonal degeneration is demonstrated for the 1st month following onset of clinical symptoms. (nih.gov)
  • Peripheral nerves respond to injury or disease in one or more of the following ways: segmental remyelination, Wallerian degeneration, and axonal degeneration. (uspharmacist.com)
  • 5,6 Segmental demyelination and Wallerian degeneration are repair mechanisms that are relevant to traumatic nerve injury, whereas axonal degeneration is more characteristically seen in metabolic and toxic nerve disorders such as diabetes mellitus and renal failure. (uspharmacist.com)
  • Axonal degeneration is a prediction of disability. (medscape.com)
  • 2 - 5 In 1 study from a patient presenting with pure motor GBS, inflammatory demyelination with secondary axonal degeneration was restricted to ventral spinal roots. (ajnr.org)
  • Parson, SH , Mackintosh, CL & Ribchester, RR 1997, ' Elimination of motor nerve terminals in neonatal mice expressing a gene for slow wallerian degeneration (C57Bl/Wlds) ', European Journal of Neuroscience , vol. 9, no. 8, pp. 1586-1592. (elsevierpure.com)
  • Using two mutant murine strains (the slow Wallerian degeneration mouse and a knockout for the chemokine receptors CCR2) we have found that prevention of macrophage accumulation in ganglia significantly inhibits the conditioning lesion response, suggesting that these macrophages play an important role in the response of neurons to injury. (case.edu)
  • Patients with primary Sjögren syndrome show loss of WM microstructural integrity, probably related to both Wallerian degeneration and demyelination. (ajnr.org)
  • Precise inflammatory demyelination of these nerve trunks may imply an increase of endoneurial fluid nerve pressure potentially causing endoneurial ischemia and wallerian-like degeneration. (ajnr.org)
  • Wallerian degeneration is an active process of degeneration that results when a nerve fiber is cut or crushed and the part of the axon distal to the injury (which in most cases is farther from the neuron's cell body) degenerates. (wikipedia.org)
  • Prior to degeneration, the distal section of the axon tends to remain electrically excitable. (wikipedia.org)
  • A condition caused by degeneration, atrophy, and destruction of the distal part of a nerve fiber''s axon and myelin, when continuity with the neural cell nucleus has been severed due to injury. (nih.gov)
  • In the absence of NGF, inhibition of glycolysis along distal axons results in axon degeneration independent of cell death. (jneurosci.org)
  • 3,4 Axonotmesis leads to Wallerian degeneration , a process whereby the part of the axon that is separated from the neuronal cell body disintegrates distal to the injury. (uspharmacist.com)
  • Degeneration of motor terminals after nerve section occurs much more slowly than normal in young adult mice of the C57Bl/Wlds strain. (elsevierpure.com)
  • B) Nerve showing disruptive changes of axons (Wallerian degeneration) (black star). (cdc.gov)
  • a) Peripheral nerve in longitudinal section stained with Luxol fast blue-periodic acid-Schiff (PAS) showing scattered wallerian degeneration (arrowheads). (medscape.com)
  • In the late 1960s, neurophysiologic testing allowed the classification of CMT into 2 groups, one with slow nerve conduction velocities and histologic features of a hypertrophic demyelinating neuropathy (hereditary motor and sensory neuropathy type 1 or CMT1) and another with relatively normal velocities and axonal and neuronal degeneration (hereditary motor and sensory neuropathy type 2 or CMT2). (medscape.com)
  • Sciatic nerve transection, early after birth, results in significant degeneration of spinal motoneurons as well as sensory neurons present in the dorsal root ganglia. (hindawi.com)
  • I study the role of immune cells in nerve degeneration and regeneration, and compare nerve regeneration in different types of sensory neurons. (case.edu)
  • Histograms evaluating large portions of tissue reveal significant increases in MD in individuals with Alzheimer's disease when compared with controls as well as a significant reduction in regional peak MD heights, which indicates nerve loss in gray matter and Wallerian degeneration in white matter. (diagnosticimaging.com)
  • Wallerian degeneration occurs after axonal injury in both the peripheral nervous system (PNS) and central nervous system (CNS). (wikipedia.org)
  • We are primarily concerned with neurotoxicants that produce Wallerian-type degeneration of the axon and myelin of the central and peripheral nervous systems. (duke.edu)
  • We conclude (i) that the Wlds gene has no direct impact on the normal rate of postnatal synapse elimination, (ii) that Wallerian degeneration and synapse elimination must occur by distinct and different mechanisms, and (iii) that muscle fibres are able to sustain polyneuronal synaptic inputs even after motor axons have become disconnected from their cell bodies. (elsevierpure.com)
  • Combined MBK and EPN exposure caused Wallerian type degeneration and paranodal axonal swelling in the spinal cord. (cdc.gov)
  • The macrophages, accompanied by Schwann cells, serve to clear the debris from the degeneration. (wikipedia.org)
  • The dynamic signal intensity changes at magnetic resonance (MR) imaging in active and chronic wallerian degeneration in the corticospinal tract were evaluated. (nih.gov)
  • Chronic inflammation can result in edema, wallerian degeneration, and fibrotic changes to the neural tissues. (medscape.com)
  • In research and clinical settings, DTI has generated information on tissue infrastructure and indications of inflammation, tissue degeneration, and neurodevelopmental abnormalities, said Dr. Marco Bozzali from Don C. Gnocchi Foundation in Milan. (diagnosticimaging.com)
  • A related process of dying back or retrograde degeneration known as 'Wallerian-like degeneration' occurs in many neurodegenerative diseases, especially those where axonal transport is impaired such as ALS and Alzheimer's disease. (wikipedia.org)
  • I. An analysis in tissue culture of proliferation during development, Wallerian degeneration, and direct injury. (rupress.org)
  • This observation prompted us to re-examine the possible role of degeneration and intrinsic axon withdrawal during neonatal synapse elimination. (elsevierpure.com)
  • Specifically, YFP-labeled axons are present in regions beyond those with anterogradely labeled CST axons, most YFP-labeled axons beyond established CST locations do not undergo Wallerian degeneration following a large lesion of the sensorimotor cortex, some rubrospinal and reticulospinal neurons are labeled with YFP, and some YFP-labeled cells in the spinal gray matter have YFP-labeled projections into the spinal cord white matter. (nih.gov)
  • 2015 ) Laser-Mediated Microlesions in Mouse Neocortex to Investigate Neuronal Degeneration and Regeneration. (neurotree.org)
  • Axotomised neuromuscular junctions in Wld(S) mutant mice offer favourable experimental opportunities for examining developmental mechanisms of synaptic regression, that may also benefit our understanding of how degeneration in the synaptic compartment of a neuron is initiated, and its role in progressive, whole-cell neuronal degeneration. (ed.ac.uk)
  • In this study, we hypothesized that higher Aß oligomerization in the blood are associated with the neuronal degeneration of the brain in the form of AD. (biomedcentral.com)
  • 2. Longitudinal investigations on the anterograde and retrograde degeneration in the pyramidal tract following pontine infarction with diffusion tensor imaging. (nih.gov)
  • 4. Diffusion tensor imaging detects early Wallerian degeneration of the pyramidal tract after ischemic stroke. (nih.gov)
  • An assessment of the correlation between early postinfarction pyramidal tract Wallerian degeneration and nerve function recovery using diffusion tensor imaging. (geneticsmr.com)
  • This study aimed to evaluate the clinical significance of diffusion tensor imaging (DTI) in the early diagnosis of pyramidal tract Wallerian degeneration (WD) and assessment of neurological recovery following cerebral infarction. (geneticsmr.com)
  • A related process of dying back or retrograde degeneration known as 'Wallerian-like degeneration' occurs in many neurodegenerative diseases, especially those where axonal transport is impaired such as ALS and Alzheimer's disease. (wikipedia.org)
  • Degeneration and regeneration of nerve fiber BY PANDIAN MTHIS PPT ONLY FIOR. (slideshare.net)
  • shows axon degeneration with a typical "digestion chamber," containing axonal fragments (arrow). (nih.gov)
  • SARM1 is now recognized as the primary axon killer through its NAD + -consuming enzymatic activity, and SARM1 inhibitors that protect against axon degeneration in pre-clinical studies are generating great excitement (2, 3). (genetex.com)
  • GeneTex is expanding its inventory of antibodies for axon degeneration research with the addition of new recombinant rabbit antibodies against SARM1 (see below). (genetex.com)
  • Wallerian degeneration occurred in the dorsal funiculus where the white discoloration was observed on gross examination. (cdc.gov)
  • Dorsal root ganglia neuronal cell bodies will be the principal target of proteasome inhibition, with peripheral nerve degeneration occurring later. (ack1inhibitor.com)
  • dblp: Search for 'The acute phase of Wallerian degeneration: Longitudinal diffusion tensor imaging of the fornix following temporal lobe surgery. (dblp.org)
  • When the neurons themselves die, Wallerian degeneration takes place, resulting in muscle weakness in those muscles once innervated by the now dead neurons. (cdc.gov)
  • 1. Retrograde Wallerian degeneration of cranial corticospinal tracts in cervical spinal cord injury patients using diffusion tensor imaging. (nih.gov)
  • 5. Corticospinal tract degeneration and possible pathogenesis in ALS evaluated by MR diffusion tensor imaging. (nih.gov)
  • 6. Wallerian degeneration in lateral cervical spinal cord detected with diffusion tensor imaging in four chronic stroke patients. (nih.gov)
  • 14. [Diffusion tensor MRI of Wallerian degeneration: a case report]. (nih.gov)
  • 18. Focal Wallerian degeneration of the corpus callosum in large middle cerebral artery stroke: serial diffusion tensor imaging. (nih.gov)
  • This work identified key players that dictate the fate of axons, including the pro-survival factors NMNAT2 and STMN2 and the degeneration-promoting factors DLK and SARM1 (1). (genetex.com)
  • Next, I showed that Sarm1, a key effector of Wallerian degeneration, is not required for structural plasticity of Merkel cell-neurite complexes in young adulthood. (columbia.edu)
  • Research that began with investigations into the mechanism underlying Wallerian degeneration of damaged axons has revealed the crucial importance of NAD + metabolism in axon survival. (genetex.com)
  • Autopsy studies have shown Wallerian-like degeneration of motor fibers. (qxmd.com)
  • Adult lifespan maturation and degeneration patterns in gray and white matter: A mean apparent propagator (MAP) MRI study. (nih.gov)
  • 2020 ) In vivo imaging of injured cortical axons reveals a rapid onset form of Wallerian degeneration. (neurotree.org)