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J. Neurochem. (2011) 117, 538–553.
AbstractIn Alzheimer’s disease, the amyloid‐β peptide (Aβ) interacts with distinct proteins at the cell surface to interfere with synaptic communication. Recent data have implicated the prion protein (PrPC) as a putative receptor for Aβ. We show here that Aβ oligomers signal in cells in a PrPC‐dependent manner, as might be expected if Aβ oligomers use PrPC as a...
J. Neurochem. (2011) 117, 359–374.
AbstractCurrent evidence suggests that Alzheimer’s disease (AD) is a multi‐factorial disease that starts with accumulation of multiple proteins. We have previously proposed that inhibition of γ‐secretase may impair membrane recycling causing neurodegeneration starting at synapses (Sambamurti K., Suram A., Venugopal C., Prakasam A., Zhou Y., Lahiri D. K. and Greig...
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