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Alzheimer’s disease (AD) is characterized by deposition of beta-amyloid as senile plaques and cerebral amyloid angiopathy. The principal component of AD amyloid is the amyloid beta peptide (A beta). Although production and deposition of A beta appear closely related to the pathogenesis of AD, current evidence suggest that A beta alone is not sufficient to cause neuronal death and symptoms of dementia. A component of senile plaque (SP), CLAC (collagen-like Alzheimer amyloid plaque component ) and its precursor CLAC-P are deposited with extracellular beta-amyloid and have been recently implicated in cell toxicity of beta-amyloid in AD brains. CLAC-P is a unique, membrane-bound collagen-like structure containing three Gly-X-Y repeat motifs and may define a novel class of neuronal collagens.
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Protein Aliases: Alzheimer disease amyloid-associated protein; AMY; CLAC-P; col25a1; Collagen alpha-1(XXV) chain; collagen, type XXV, alpha 1; collagen-like Alzheimer amyloid plaque component; collagenous Alzheimer amyloid plaque component; procollagen, type XXV, alpha 1
Gene Aliases: 2700062B08Rik; AMY; CFEOM5; CLAC; CLAC-P; CLACP; COL25A1
UniProt ID: (Human) Q9BXS0, (Mouse) Q99MQ5
Entrez Gene ID: (Human) 84570, (Rat) 687064, (Mouse) 77018
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