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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...