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  1. This new report from Kaj Blennow and Oskar Hansson's group appears to support our own findings that soluble α-synuclein levels are increased in brains of subjects with AD (Larson et al., 2012). Whether this elevation corresponds to a "leakage of α-synuclein from degenerating neurons" or to an influx of α-synuclein in the CSF from the periphery remains to be demonstrated. We would favor an alternate hypothesis, i.e., that brain expression of α-synuclein is profoundly increased in AD, resulting in enhanced secretion of the protein into the interstitial fluid (ISF). Another key question relates to the nature of the soluble species of α-synuclein accumulating in AD, whether it is in the ISF, CSF, or neuronal cells. More work is needed to address this question at this time. Overall, this new study and ours highlight the possible involvement of soluble α-synuclein as an important modulator of AD pathophysiology.

    References:

    . Soluble α-synuclein is a novel modulator of Alzheimer's disease pathophysiology. J Neurosci. 2012 Jul 25;32(30):10253-66. PubMed.