الفهرس 
Title : Genetic and Epigenetic Mechanisms Controlling Biological Clock Genes in Multiple Sclerosis
AbstractOnly 14 pages are availabe for public view
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Abstract
Multiple sclerosis (MS) is a central nervous system (CNS) autoimmune disorder represented by demyelination, chronic inflammation, and neuronal loss. MS is the major cause of disability in young adults, especially young women aged between 20 and 40 years. Exceeding 80% of patients present initially with the course of relapsing-remitting MS (RRMS) having recurrent episodes of neurological deficits followed by full or partial recovery. RRMS patients ultimately join the secondary progressive MS (SPMS) type. Circadian rhythm deregulation was observed in several neurodegenerative disorders like MS, Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease.The study of circadian rhythms performance is prominent in chronic diseases such as MS. In addition, microRNAs fine-tune the core clock genes and are key pathogenic elements in MS pathogenesis.
As far as we know this is the discrete study evaluating the association between genetic variability and expression of key circadian rhythm regulators, ARNTL/BMAL-1 and CLOCK genes, along with their targeting miRNAs inEgyptian populations with MS, and the unique study to evaluate miR-182-5p level in serum of adult MS patients.
ARNTL/BMAL-1 and CLOCK genes wereselected because they are the core circadian clock-regulating genes. The current study explored whether the genetic polymorphisms in these clock genes may be ascribed to the development of MS and the functional role of such polymorphisms in influencing the expression of the molecular components of these core clock genes. Theaim of the study also was to add links that associate epigenetics to clock-targeting miRNAs, which may represent a reasonable future therapeutic choice for MS