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Oxidative stress and mitochondrial dysfunction-linked neurodegenerative disorders.

Md Torequl Islam1,2

  • 1a Northeast Biotechnology Network (RENORBIO), Postgraduate Program in Biotechnology , Federal University of Piauí (UFPI) , Teresina , Brazil.

Neurological Research
|November 5, 2016
PubMed
Summary

Oxidative stress from overproduced reactive oxygen and nitrogen species damages cells and mitochondria. This imbalance is linked to neurodegenerative diseases like Alzheimer's and Parkinson's.

Keywords:
AD: Alzheimer’s diseaseALS: Amyotrophic lateral sclerosisAP-1: activator protein 1APP: Aβ precursor proteinAβ: amyloid-βBBB: blood–brain barrierBER: base excision repairBSE: Bovine Spongiform EncephalopathyCAA: cerebral amyloid angiopathyCAT: catalaseCBF: cerebral blood flowCJD: Creutzfeldt-Jakob diseaseCNS: central nervous systemCOX: cyclooxygenaseCRP: C-reactive proteinCyt-c: cytochrome cDA: dopamineDAG: diacylglycerolDJ-1: protein deglycase 1DNMT: DNA methyltransferaseDOPAC: 3, 4-dihydroxyphenylacetic acidDRG: dorsal root gangliaDSBs: double strand breaksEPCs: endothelial progenitor cellsFFI: Fatal Familial InsomniaFRDA: Friedreich’s ataxiaGPx: glutathione peroxidaseGSH: glutathioneGSS: Gerstmann-Straussler-Scheinker syndromeHD: Huntington’s diseaseHIF-1α: hypoxia-inducible factor-1 alphaHNE: 4- hydroxynonenalHVA: homovanillic acidIL: interleukinIR: ionizing radiationJAK: Janus kinaseMAO-B: monoamine oxidase BMDA: malondialdehydeMMPs: matrix metalloproteinsNADP: nicotinamide adenine dinucleotide phosphateNDDs: neurodegenerative diseasesNF-κB: nuclear factor kappa BNFTs: neurofibrillary tanglesNHEJ: non-homologous end joiningNHR: nucleotide excision repairNeurodegenerative diseasesPD: Parkinson’s diseasePG: prostaglandinPGC-1α: peroxisome proliferator-activated receptor-γ co-activator-1αPPL: phospholipasePrP: prion proteinRNS: reactive nitrogen speciesROS: reactive oxygen speciesSC: spinal cordSMCs: smooth muscle cellsSOD: superoxide dismutaseSSBs: single strand breaksTGF-β: tumor growth factor-betaTNF-α: tumor necrosis factor-alphaTOMM40: a gene associated with ADTSEs: Transmissible Spongiform EncephalopathiesVEGF: vascular endothelial growth factoriNOS: inducible nitric oxide synthasemitochondrial dysfunctionmtDNA: mitochondrial DNAmtMP: mitochondrial membrane permeability/potentialoxidative stress

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Neuroscience

Background:

  • Reactive species (ROS/RNS) are crucial in physiology but their overproduction disrupts cellular balance.
  • Antioxidant enzyme systems can fail, leading to oxidative damage to cellular components and DNA.
  • Mitochondrial dysfunction exacerbates ROS/RNS levels, causing further oxidative damage.

Purpose of the Study:

  • To review the link between oxidative stress, mitochondrial dysfunction, and neurodegenerative diseases (NDDs).
  • To summarize the role of oxidative stress in the etiology of various NDDs.
  • To provide an overview of NDDs associated with oxidative stress and mitochondrial dysfunction.

Main Methods:

  • Literature review of studies on oxidative stress and NDDs.
  • Analysis of the mechanisms linking reactive species to cellular damage.
  • Synthesis of information on mitochondrial roles in oxidative stress and disease pathogenesis.

Main Results:

  • Overproduction of ROS/RNS leads to oxidative damage to lipids, proteins, DNA, and RNA.
  • Mitochondrial dysfunction significantly contributes to increased ROS/RNS levels.
  • Oxidative stress is implicated in the pathogenesis of numerous NDDs, including Alzheimer's, Parkinson's, and prion diseases.

Conclusions:

  • Oxidative stress and mitochondrial dysfunction are key factors in the development of neurodegenerative diseases.
  • Understanding these mechanisms is crucial for developing therapeutic strategies for NDDs.
  • This review highlights the broad impact of oxidative stress on neurological health.