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Biomechanistic insights into the roles of oxidative stress in generating complex neurological disorders

Journal

BIOLOGICAL CHEMISTRY
Volume 399, Issue 4, Pages 305-319

Publisher

WALTER DE GRUYTER GMBH
DOI: 10.1515/hsz-2017-0250

Keywords

Alzheimer's disease; biomechanistics; epilepsy; Huntington's disease; neurological disorders; oxidative stress; parkinsonism, pathogenesis

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Neurological diseases like Alzheimer's disease, epilepsy, parkinsonism, depression, Huntington's disease and amyotrophic lateral sclerosis prevailing globally are considered to be deeply influenced by oxidative stress-based changes in the biochemical settings of the organs. The excess oxygen concentration triggers the production of reactive oxygen species, and even the intrinsic antioxidant enzyme system, i.e. SOD, CAT and GSHPx, fails to manage their levels and keep them under desirable limits. This consequently leads to oxidation of protein, lipids and nucleic acids in the brain resulting in apoptosis, proteopathy, proteasomes and mitochondrion dysfunction, glial cell activation as well as neuroinflammation. The present exploration deals with the evidence-based mechanism of oxidative stress towards development of key neurological diseases along with the involved biomechanistics and biomaterials.

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