| Literature DB >> 27809706 |
Md Torequl Islam1,2.
Abstract
Reactive species play an important role in physiological functions. Overproduction of reactive species, notably reactive oxygen (ROS) and nitrogen (RNS) species along with the failure of balance by the body's antioxidant enzyme systems results in destruction of cellular structures, lipids, proteins, and genetic materials such as DNA and RNA. Moreover, the effects of reactive species on mitochondria and their metabolic processes eventually cause a rise in ROS/RNS levels, leading to oxidation of mitochondrial proteins, lipids, and DNA. Oxidative stress has been considered to be linked to the etiology of many diseases, including neurodegenerative diseases (NDDs) such as Alzheimer diseases, Amyotrophic lateral sclerosis, Friedreich's ataxia, Huntington's disease, Multiple sclerosis, and Parkinson's diseases. In addition, oxidative stress causing protein misfold may turn to other NDDs include Creutzfeldt-Jakob disease, Bovine Spongiform Encephalopathy, Kuru, Gerstmann-Straussler-Scheinker syndrome, and Fatal Familial Insomnia. An overview of the oxidative stress and mitochondrial dysfunction-linked NDDs has been summarized in this review.Entities:
Keywords: AD: Alzheimer’s disease; ALS: Amyotrophic lateral sclerosis; AP-1: activator protein 1; APP: Aβ precursor protein; Aβ: amyloid-β; BBB: blood–brain barrier; BER: base excision repair; BSE: Bovine Spongiform Encephalopathy; CAA: cerebral amyloid angiopathy; CAT: catalase; CBF: cerebral blood flow; CJD: Creutzfeldt-Jakob disease; CNS: central nervous system; COX: cyclooxygenase; CRP: C-reactive protein; Cyt-c: cytochrome c; DA: dopamine; DAG: diacylglycerol; DJ-1: protein deglycase 1; DNMT: DNA methyltransferase; DOPAC: 3, 4-dihydroxyphenylacetic acid; DRG: dorsal root ganglia; DSBs: double strand breaks; EPCs: endothelial progenitor cells; FFI: Fatal Familial Insomnia; FRDA: Friedreich’s ataxia; GPx: glutathione peroxidase; GSH: glutathione; GSS: Gerstmann-Straussler-Scheinker syndrome; HD: Huntington’s disease; HIF-1α: hypoxia-inducible factor-1 alpha; HNE: 4- hydroxynonenal; HVA: homovanillic acid; IL: interleukin; IR: ionizing radiation; JAK: Janus kinase; MAO-B: monoamine oxidase B; MDA: malondialdehyde; MMPs: matrix metalloproteins; NADP: nicotinamide adenine dinucleotide phosphate; NDDs: neurodegenerative diseases; NF-κB: nuclear factor kappa B; NFTs: neurofibrillary tangles; NHEJ: non-homologous end joining; NHR: nucleotide excision repair; Neurodegenerative diseases; PD: Parkinson’s disease; PG: prostaglandin; PGC-1α: peroxisome proliferator-activated receptor-γ co-activator-1α; PPL: phospholipase; PrP: prion protein; RNS: reactive nitrogen species; ROS: reactive oxygen species; SC: spinal cord; SMCs: smooth muscle cells; SOD: superoxide dismutase; SSBs: single strand breaks; TGF-β: tumor growth factor-beta; TNF-α: tumor necrosis factor-alpha; TOMM40: a gene associated with AD; TSEs: Transmissible Spongiform Encephalopathies; VEGF: vascular endothelial growth factor; iNOS: inducible nitric oxide synthase; mitochondrial dysfunction; mtDNA: mitochondrial DNA; mtMP: mitochondrial membrane permeability/potential; oxidative stress
Mesh：
Year: 2016 PMID： 27809706 DOI： 10.1080/01616412.2016.1251711
Source DB: PubMed Journal: Neurol Res ISSN： 0161-6412 Impact factor: 2.448