Myelin basic protein

Cambridge Stem Cell Institute. My interdisciplinary research focuses on identifying novel approaches to stimulate central nervous system (CNS) myelin regeneration (remyelination) by endogenous adult neural stem cells. Myelin is a fatty membrane structure around nerve cells and serves to increase the speed of electrical communication between neurons. Myelin is a target of many chronic diseases including, stroke, inflammation, immune disorders, CNS trauma, metabolic disorders, nutritional deficiencies

Fighting Relapsing Multiple Sclerosis with Copaxone Imagine a disease that has the potential to disrupt and ultimately destroy the human nervous system by attacking the myelin sheath. This is not a rare disease. In fact, it affects over 350,000 people in the United States alone (Nordqvist). The ratio of women to men that contract the disease is 2 to 1 and it is a leading cause of disability in young adults (Olek). This disease is not only widespread, it is chronic and has no known cause or cure.

such as deficits in learning and memory. White matter lesions (WML) have also been linked to increasing the risk of post-stroke dementia. Cerebral white matter damage has been widely overlooked. Comprised of oligodendrocytes that form the insulating myelin in the CNS, white matter is evidentially just as vulnerable to ischemia as gray matter.

cytokines and endorsing myelin protection. B.1. English Abstract Multiple sclerosis (MS) is a chronic inflammatory, neurodegenerative disease that affects more than 40,000 individuals in Egypt alone and 2.5 million people worldwide. MS is also categorized as an autoimmune disease in which the immune system instigates an immune response upon encountering the specific myelin antigen and therefore initiating a constant degradation of the myelin sheath. The frequent loss of the myelin leads to irreversible

The immune system of a human body is fascinating and life-saving, when functioning properly. An immune system lacking proper function will consequently lack the ability to protect the human body. Multiple sclerosis (MS) is a chronic, immune-mediated disease of the central nervous system, primarily affecting the brain and spinal cord. There are four types, or courses of the multiple sclerosis disease. The first type is known as relapsing- remitting, the second type is primary progressive, the third

membrane, known as the myelin sheath. In the CNS, myelin is produced by oligodendrocyte. a type of glial cell. (Pfeiffer et al., 1993). These electrical insulating, multilamellar membranes significantly increase the electrical resistance, in which to prevent leakage of electrical currents from the axons, as well as decrease electrical capacitance to reduce the ability of the axons to store electrical energy (Shivane &

Models such as an experimental autoimmune encephalomyelitis have been created to further understand the components of the brain and spinal cord “Spinal cord a role for dendritic cells in the CNS has been demonstrated in multiple sclerosis (MS), experimental autoimmune encephalomyelitis (EAE) delayed-type hypersensitivity infections and after injury” (Jenny S. Henkel, 2004)Experimental autoimmune encephalomyelitis (EAE) is a rat brain model which has been primarily featured in the understanding of

inflammatory, demyelinating, autoimmune neurodegenerative disease characterized by the disruption of the blood brain barrier (BBB), perivascular inflammation, axonal and oligodendrocyte injury, and breakdown of the myelin sheath present in the central nervous system (CNS). The Loss of myelin leads to progressive axonal damage and eventually neuronal death, resulting in neurodegeneration and functional disability in different regions in the brain and the spinal cord. According to the domain which is compromised

Abstract Myelin and oligodendrocyte dysfunctions have been consistently found in patients with schizophrenia. The effect of antipsychotics on myelin disturbances is unknown. The present study examined the effects of quetiapine on oligodendrocyte regeneration and myelin repair in a demyelination animal model. C57BL/6 mice were fed with cuprizone (0.2% w/w) for 12 weeks to induce chronic demyelination and oligodendrocyte degeneration, after which cuprizone was withdrawn to allow recovery. Quetiapine

neuroprotective action mainly through a paracrine-mediated mechanism. In fact, MSCs have the capacity to secret a plethora bioactive factors (secretome), including neurotrophic growth factors, chemokines, interleukins or cytokines, extracellular proteins and extracellular vesicles, which promote injured tissues repair and regeneration (Caplan and Correa, 2011; Maltman, Hardy and Przyborski, 2011; Paul and Anisimov, 2013). Bai et al. demonstrated that MSC’ conditioned medium (MSC-CM), i.e. MSCs’