. Functional mitochondria are required for amyloid beta-mediated neurotoxicity. FASEB J. 2001 Jun;15(8):1439-41. PubMed.

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  1. Mitochondria, Amyloid-β, and Metabolism

    Studies of amyloid-β (Aβ) cellular toxicity using cells with the full complement of organelles have implicated various sites of action but have primarily focused on the plasma membrane (Mark et al., 1997). Indeed, an intracellular organellar site of Aβ action seemed at variance with plasma membrane effects involving Ca2+ entry thereby relegating mitochondrial abnormalities to secondary events.

    However, in an elegant study, Cardoso and colleagues (2001) show that Aβ toxicity is strictly dependent on functional mitochondria such that Aβ has no effect on neuroblastoma cells lacking mitochondria (r0). When seen in light of the strict dependence of Ab toxicity on iron (Rottkamp et al., 2001) and altered Ab metabolism in cells populated by mitochondria from cases of Alzheimer disease (AD) (Khan et al., 2000), there appears to be a compelling case for a mitochondria-Aβ link. In fact, given that reduced brain metabolism is one of the earliest events in AD (Small et al., 2000), an important role of Aβ might be related to metabolic function. Therefore, instead of mediating toxicity, Aβ could serve to regulate metabolic state as compensation to a catastrophic disease process. - George Perry and Mark Smith, Institute of Pathology, Case Western Reserve University

    References:

    . Functional mitochondria are required for amyloid beta-mediated neurotoxicity. FASEB J. 2001 Jun;15(8):1439-41. PubMed.

    . Alzheimer's disease cybrids replicate beta-amyloid abnormalities through cell death pathways. Ann Neurol. 2000 Aug;48(2):148-55. PubMed.

    . Amyloid beta-peptide impairs glucose transport in hippocampal and cortical neurons: involvement of membrane lipid peroxidation. J Neurosci. 1997 Feb 1;17(3):1046-54. PubMed.

    . Redox-active iron mediates amyloid-beta toxicity. Free Radic Biol Med. 2001 Feb 15;30(4):447-50. PubMed.

    . Cerebral metabolic and cognitive decline in persons at genetic risk for Alzheimer's disease. Proc Natl Acad Sci U S A. 2000 May 23;97(11):6037-42. PubMed.

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