Mitochondrial Abeta: a potential focal point for neuronal metabolic dysfunction in Alzheimer's disease.

@article{Caspersen2005MitochondrialAA,
  title={Mitochondrial Abeta: a potential focal point for neuronal metabolic dysfunction in Alzheimer's disease.},
  author={Casper S Caspersen and Ning Wang and Jun Yao and Alexander A. Sosunov and Xi Chen and Joyce W. Lustbader and Hong Wei Xu and David Stern and Guy McKhann and Shirley ShiDu Yan},
  journal={FASEB journal : official publication of the Federation of American Societies for Experimental Biology},
  year={2005},
  volume={19 14},
  pages={
          2040-1
        }
}
Although amyloid-beta peptide (Abeta) is the neurotoxic species implicated in the pathogenesis of Alzheimer's disease (AD), mechanisms through which intracellular Abeta impairs cellular properties, resulting in neuronal dysfunction, remain to be clarified. Here we demonstrate that intracellular Abeta is present in mitochondria from brains of transgenic mice with targeted neuronal overexpression of mutant human amyloid precursor protein and AD patients. Abeta progressively accumulates in… CONTINUE READING

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