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Article

ADAM10 missense mutations potentiate β-amyloid accumulation by impairing prodomain chaperone function.

Neuron - 16 Oct 2013

Suh Jaehong, Choi Se Hoon, Romano Donna M, Gannon Moira A, Lesinski Andrea N, Kim Doo Yeon, Tanzi Rudolph E

Abstract excerpt

The generation of Aβ, the main component of senile plaques in Alzheimer's disease (AD), is precluded by α-secretase cleavage within the Aβ domain of the amyloid precursor protein (APP). We identified two rare mutations (Q170H and R181G) in the prodomain of the metalloprotease, ADAM10, that cosegregate with late-onset AD (LOAD). Here, we addressed the pathogenicity of these mutations in transgenic mice expressing...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 24055016
DOI: 10.1016/j.neuron.2013.08.035
PMCID: PMC4105199

Genes

ADAM10
APP

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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