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  1. This paper seems to skirt many years of autopsy studies finding that the senile plaques have marginal statistical capacity to distinguish normal from AD patients, such as Davis et al., 1999. Also in 1999, Lue et al. concluded that soluble Aβ posed the greatest toxicity, and that Aβ40 was particularly toxic to synapses. But the issue of deposits seems to pale in the face of new MRI studies concerning gross atrophy of the brain, that is, gross death of brain cells and connectivity. See, for example Stroub and colleagues’ 2006 article on MCI. Is the senile plaque issue becoming a tempest in the teapot?


    . Alzheimer neuropathologic alterations in aged cognitively normal subjects. J Neuropathol Exp Neurol. 1999 Apr;58(4):376-88. PubMed.

    . Soluble amyloid beta peptide concentration as a predictor of synaptic change in Alzheimer's disease. Am J Pathol. 1999 Sep;155(3):853-62. PubMed.

    . Hippocampal disconnection contributes to memory dysfunction in individuals at risk for Alzheimer's disease. Proc Natl Acad Sci U S A. 2006 Jun 27;103(26):10041-5. PubMed.

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