Multiple Sclerosis: Re-expression of a developmental pathway
Multiple sclerosis (MS) is an autoimmune disease that affects a part of the body known as the central nervous system or CNS. The CNS consists mainly of the brain and spinal cord. Surrounding and protecting the CNS nerve fibers is a tissue known as myelin, which protects and quickens the nerve impulses sent along those fibers. This myelin is created by glial cells known as oligodendrocytes which reside on the axon itself. In MS, the nerve fibers demyelinate, causing a scar tissue known as sclerosis to form in areas that a called plaques or lesions. The symptoms of this disease are varied and include vertigo and dizziness, cognitive problems, emotional instability, fatigue, numbness, spasticity, vision problems, and many more. As the authors point out, there are well documented cases of remyelination of the CNS in MS patients, but unfortunately it is not well understood. This article seeks to explain how remyelination of the CNS is prohibited in this disease by the re-expression of a pathway that is normally only used in the human body very early in development. During mammalian CNS development, a receptor on oligodendrocyte precursors known as Notch1 are contact mediated into activation by the ligand Jagged1. Jagged1 is
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Some common words found in the essay are:
TGF-beta1 Hes5, Jagged1 Notch1, CNS CNS, TGF-beta1 Western, CNS MS, TGF-beta1 Blocking, Notch1 Hes5, , Jagged1 Jagged1, Genbank R70685, expression profile, gene expression profile, nerve fibers, gene expression, mature humans, cytokines tgf-beta1, demyelinating remyelinating, remyelination cns, central nervous, nervous system, ms patients, central nervous system,
Approximate Word count = 885
Approximate Pages = 4 (250 words per page double spaced)
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