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Publication Detail
Activation of PARP by oxidative stress induced by β-amyloid: implications for Alzheimer's disease.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Abeti R, Duchen MR
  • Publication date:
    11/2012
  • Pagination:
    2589, 2596
  • Journal:
    Neurochem Res
  • Volume:
    37
  • Issue:
    11
  • Status:
    Published
  • Country:
    United States
  • Language:
    eng
  • Keywords:
    Alzheimer Disease, Amyloid beta-Peptides, Animals, Enzyme Activation, Humans, Oxidative Stress, Poly(ADP-ribose) Polymerases, Reactive Oxygen Species
Abstract
Alzheimer's disease (AD) is a major neurodegenerative disease of old age, characterised by progressive cognitive impairment, dementia and atrophy of the central nervous system. The pathological hallmarks include the accumulation of the peptide β-amyloid (Aβ) which itself is toxic to neurons in culture. Recently, it has been discovered that Aβ activates the protein poly(ADP-ribosyl) polymerase-1 (PARP-1) specifically in astrocytes, leading indirectly to neuronal cell death. PARP-1 is a DNA repair enzyme, normally activated by single strand breaks associated with oxidative stress, which catalyses the formation of poly ADP-ribose polymers from nicotinamide adenine dinucleotide (NAD(+)). The pathological over activation of PARP-1 causes depletion of NAD(+) and leads to cell death. Here we review the relationship between AD and PARP-1, and explore the role played by astrocytes in neuronal death. AD has so far proven refractory to any effective treatment. Identification of these pathways represents a step towards a greater understanding of the pathophysiology of this devastating disease with the potential to explore novel therapeutic targets.
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