Journal
COLD SPRING HARBOR PERSPECTIVES IN MEDICINE
Volume 7, Issue 5, Pages -Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/cshperspect.a024075
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Funding
- National Institutes of Health
- BrightFocus Foundation
- Alzheimer's Association
- Falk Medical Research Trust
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In Alzheimer's disease (AD), insoluble and fibrillary amyloid-beta (A beta) peptide accumulates in plaques. However, soluble A beta oligomers are most potent in creating synaptic dysfunction and loss. Therefore, receptors for A beta oligomers are hypothesized to be the first step in a neuronal cascade leading to dementia. A number of cell-surface proteins have been described as A beta binding proteins, and one or more are likely to mediate A beta oligomer toxicity in AD. Cellular prion protein (PrPC) is a high-affinity A beta oligomer binding site, and a range of data delineates a signaling pathway leading from A beta complexation with PrPC to neuronal impairment. Further study of A beta binding proteins will define the molecular basis of this crucial step in AD pathogenesis.
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