Accumulation of cellular prion protein within β-amyloid oligomer plaques in aged human brains.

ABSTRACT: Alzheimer's disease (AD) is the main cause of dementia, and β-amyloid (Aβ) is a central factor in the initiation and progression of the disease. Different forms of Aβ have been identified as monomers, oligomers, and amyloid fibrils. Many proteins have been implicated as putative receptors of respective forms of Aβ. Distinct forms of Aβ oligomers are considered to be neurotoxic species that trigger the pathophysiology of AD. It was reported that cellular prion protein (PrP^C ) is one of the most selective and high-affinity binding partners of Aβ oligomers. The interaction of Aβ oligomers with PrP^C is important to synaptic dysfunction and loss. The binding of Aβ oligomers to PrP^C has mostly been studied with synthetic peptides, cell culture, and murine models

SUBMITTER: Takahashi RH 

PROVIDER: S-EPMC8412093 | biostudies-literature | 2021 Sep

REPOSITORIES: biostudies-literature