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Conditional Deletion of <i>Prnp</i> Rescues Behavioral and Synaptic Deficits after Disease Onset in Transgenic Alzheimer's Disease

21 Aug 2017

Abstract excerpt

Biochemical and genetic evidence implicate soluble oligomeric amyloid-β (Aβo) in triggering Alzheimer's disease (AD) pathophysiology. Moreover, constitutive deletion of the Aβo-binding cellular prion protein (PrP C ) prevents development of memory deficits in APP swe /PS1ΔE9 mice, a model of familial AD. Here, we define the role of PrP C to rescue or halt established AD endophenotypes in a therapeutic...

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PMID: 28842420
DOI: 10.1523/jneurosci.0722-17.2017

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