General fitness, health and nutrition · Public discussion

Cerebral Ass Load

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General fitness, health and nutrition
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22 June 2007
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22 June 2007
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  1. PLoS ONE. 2007 Jun 20;2:e536.
    Mitochondrial oxidative stress causes hyperphosphorylation of tau.
    Melov S, Adlard PA, Morten K, Johnson F, Golden TR, Hinerfeld D,
    Schilling B, Mavros C, Masters CL, Volitakis I, Li QX, Laughton K,
    Hubbard A, Cherny RA, Gibson B, Bush AI.
    Buck Institute for Age Research, Novato, California, United States of
    America.

    Age-related neurodegenerative disease has been mechanistically linked
    with mitochondrial dysfunction via damage from reactive oxygen species
    produced within the cell. We determined whether increased
    mitochondrial oxidative stress could modulate or regulate two of the
    key neurochemical hallmarks of Alzheimer's disease (AD): tau
    phosphorylation, and ss-amyloid deposition. Mice lacking superoxide
    dismutase 2 (SOD2) die within the first week of life, and develop a
    complex heterogeneous phenotype arising from mitochondrial dysfunction
    and oxidative stress. Treatment of these mice with catalytic
    antioxidants increases their lifespan and rescues the peripheral
    phenotypes, while uncovering central nervous system pathology. We
    examined sod2 null mice differentially treated with high and low doses
    of a catalytic antioxidant and observed striking elevations in the
    levels of tau phosphorylation (at Ser-396 and other phospho-epitopes
    of tau) in the low-dose antioxidant treated mice at AD-associated
    residues. This hyperphosphorylation of tau was prevented with an
    increased dose of the antioxidant, previously reported to be
    sufficient to prevent neuropathology. We then genetically combined a
    well-characterized mouse model of AD (Tg2576) with heterozygous sod2
    knockout mice to study the interactions between mitochondrial
    oxidative stress and cerebral Ass load. We found that mitochondrial
    SOD2 deficiency exacerbates amyloid burden and significantly reduces
    metal levels in the brain, while increasing levels of Ser-396
    phosphorylated tau. These findings mechanistically link mitochondrial
    oxidative stress with the pathological features of AD.

    PMID: 17579710 [PubMed - in process]

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