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Spinal muscular atrophy counteracted by Agrin biological NT-1654

Published on: 20th April, 2018

OCLC Number/Unique Identifier: 7671782483

Spinal muscular atrophy (SMA) is a genetic and gravely disease, portrayed by motor neuron (MN) death, thereby leading to progressive and accelerating muscle fragility, respiratory collapse, and, in the most severe cases, it even pave the way to death. At the neuromuscular junction (NMJ), abnormally have been reported in SMA, including neurofilament (NF) aggregation at presynaptic terminals, immature and smaller endplates, lowered transmitter release, and, eventually, muscle denervation. In this review the role of Agrin in SMA is studied. This review highlights the antagonizing role of Agrin in SMA
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Discrepancy in Microglia and Peripheral Monocytic Cells - A scope in the Pathophysiology of Psychiatric maladies

Published on: 29th June, 2018

Broad medleys of research have recognized the microglial activation in perilous psychiatric maladies such as schizophrenia, bipolar disorder, and major depressive disorder. There is a scenario of enlivening of peripheral monocytic cells along with the microglial interactions within the body while considering the Pathogenesis of psychiatric disorders. this review, epitomize and discuss the activation of microglia and monocytic cells in psychiatric disorders, thereby showcasing the potential association between these cell types and the Pathogenisis of the ailment , and proffer perspectives for future research on these processes.
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Vigour of CRISPR/Cas9 Gene Editing in Alzheimer’s Disease

Published on: 5th October, 2018

Ailment repairing regiments has turn out to be arduous, despite a plenty of understanding and knowledge acquired in the past relating to the molecular underpinnings of Alzheimer’s disease (AD. Umpteen clinical experiments targeting the fabrication and accumulation have been turned fruitless to fit potency standards. The tests aiming beta-amyloid hypothesis also turned futile making it exigent for further handling tactics. The new emanation of a comparably candid, economical, and punctilious system known as gene editing have showed light in path of cure for AD by CRISPR/Cas9 gene editing. Being a straight approach this procedure has already shown assurance in other neurological disorders too such as Huntington’s disease. This review standpoint the immanent service of CRISPR/Cas9 as a remedial option for AD by aiming on specific genes inclusive of those that induce early-onset AD, as well as those that are substantial risk components for late-onset AD such as the apolipoprotein E4 (APOE4) gene.
Cite this ArticleCrossMarkPublonsHarvard Library HOLLISGrowKudosResearchGateBase SearchOAI PMHAcademic MicrosoftScilitSemantic ScholarUniversite de ParisUW LibrariesSJSU King LibrarySJSU King LibraryNUS LibraryMcGillDET KGL BIBLiOTEKJCU DiscoveryUniversidad De LimaWorldCatVU on WorldCat
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