Biomechanistic insights into the roles of oxidative stress in generating complex neurological disorders.
Mohammad YusufMaria KhanMajed A RobaianRiaz A KhanPublished in: Biological chemistry (2018)
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.
Keyphrases
- mesenchymal stem cells
- oxidative stress
- amyotrophic lateral sclerosis
- cell therapy
- cerebral ischemia
- diabetic rats
- bone marrow
- reactive oxygen species
- dna damage
- ischemia reperfusion injury
- induced apoptosis
- traumatic brain injury
- single cell
- lipopolysaccharide induced
- cognitive decline
- depressive symptoms
- multiple sclerosis
- subarachnoid hemorrhage
- hydrogen peroxide
- binding protein
- heat shock
- endoplasmic reticulum stress
- blood brain barrier
- nitric oxide
- cell proliferation
- amino acid
- mild cognitive impairment
- lps induced
- fatty acid
- bone regeneration
- anti inflammatory
- heat stress