ADAM10 Prodomain Mutations Cause Late-Onset Alzheimer’s Disease: Not Just the Latest FAD
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In this issue of Neuron, Suh et al. (2013) describe two rare ADAM10 prodomain mutations that cause late-onset Alzheimer's disease by impairing prodomain chaperone function, attenuating α-secretase activity, and reducing adult hippocampal neurogenesis. These results support both ADAM10 as a therapeutic target and the amyloid hypothesis of Alzheimer's disease.
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ACE and ADAM10 were previously reported as Alzheimer's disease candidate genes but were not replicated in some subsequent studies.
“ACE and ADAM10 were previously reported as Alzheimer’s disease candidate genes18–22 but were not replicated in some subsequent studies23–25.”
From Genetic meta-analysis of diagnosed Alzheimer’s disease identifies new risk loci and implicates Aβ, tau, immunity and lipid processing (2019) · cites this paper as [18]
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Cites
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Research works printed but not linked: 1
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Cited by
Sorted by citations
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- Authors
- Vassar, R.
- Affiliations
- Northwestern University (US)
- Corresponding author
- Vassar, Robert
- ORCID
- Vassar, Robert
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2013-10
- Volume
- 80
- Issue
- 2
- Pages
- 250-253
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC4090694
- OpenAlex
- W2088025160
- Cited by
- 32
- References
- 16
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 2 · 2022: 2 · 2021: 8 · 2020: 1 · 2019: 3 · 2018: 3 · 2017: 2 · 2016: 3 · 2015: 3 · 2014: 2
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (RF1AG022560, R01AG022560)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- ADAM10, late-onset Alzheimer's disease, familial Alzheimer's disease, adult hippocampal neurogenesis, amyloid hypothesis, therapeutic target
- MeSH terms
- ADAM10 Protein, Animals, Female, Humans, Male, Membrane Proteins, Amyloid beta-Peptides, Molecular Chaperones, Genetic Predisposition to Disease, Mutation, Missense, ADAM Proteins, Amyloid Precursor Protein Secretases
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