Whole‐exome sequencing in 20,197 persons for rare variants in Alzheimer's disease
Open accessAbstract
Objective: The genetic bases of Alzheimer's disease remain uncertain. An international effort to fully articulate genetic risks and protective factors is underway with the hope of identifying potential therapeutic targets and preventive strategies. The goal here was to identify and characterize the frequency and impact of rare and ultra‐rare variants in Alzheimer's disease, using whole‐exome sequencing in 20,197 individuals. Methods: We used a gene‐based collapsing analysis of loss‐of‐function ultra‐rare variants in a case–control study design with data from the Washington Heights‐Inwood Columbia Aging Project, the Alzheimer's Disease Sequencing Project and unrelated individuals from the Institute of Genomic Medicine at Columbia University. Results: We identified 19 cases carrying extremely rare SORL 1 loss‐of‐function variants among a collection of 6,965 cases and a single loss‐of‐function variant among 13,252 controls (P = 2.17 × 10−8; OR: 36.2 [95% CI: 5.8–1493.0]). Age‐at‐onset was 7 years earlier for patients with SORL 1 qualifying variant compared with noncarriers. No other gene attained a study‐wide level of statistical significance, but multiple top‐ranked genes, including GRID 2 IP, WDR 76 and GRN, were among candidates for follow‐up studies. Interpretation: This study implicates ultra‐rare, loss‐of‐function variants in SORL 1 as a significant genetic risk factor for Alzheimer's disease and provides a comprehensive dataset comparing the burden of rare variation in nearly all human genes in Alzheimer's disease cases and controls. This is the first investigation to establish a genome‐wide statistically significant association between multiple extremely rare loss‐of‐function variants in SORL 1 and Alzheimer's disease in a large whole‐exome study of unrelated cases and controls.
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SORL1 is a sorting receptor located in neurons, astrocytes, and microglia and is known to direct APP toward non-amyloidogenic processing in the trans-Golgi network.
“SORL1, a sorting receptor located in neurons [152], astrocytes, and microglia [153] is known to direct APP toward non-amyloidogenic processing in the trans-Golgi network [148, 154].”
From Genetic architecture of Alzheimer's disease (2020) · cites this paper as [148]
Rare variants in SORL1 and ABCA7 have been identified in family-based studies of LOAD, each associated with alterations in APP processing.
“For example, rare variants in SORL1 and ABCA7 have been identified in family-based studies of LOAD [147–150], each of which have been associated with alterations in APP processing.”
From Genetic architecture of Alzheimer's disease (2020) · cites this paper as [148]
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- Authors
- Raghavan, N. S., Brickman, A. M., Andrews, H., Manly, J. J., Schupf, N., Lantigua, R., Wolock, C. J., Kamalakaran, S., Petrovski, S., Tosto, G., Vardarajan, B. N., Goldstein, D. B., Mayeux, R., & The Alzheimer's Disease Sequencing Project
- Affiliations
- NewYork–Presbyterian Hospital (US)
- Institute of Genomic Medicine Columbia University The New York Presbyterian Hospital New York New York
- Corresponding author
- Mayeux, Richard
- ORCID
- Venue
- Annals of Clinical and Translational Neurology
- Publisher
- Wiley
- Published
- 2018-05-24
- Volume
- 5
- Issue
- 7
- Pages
- 832-842
- ISSN
- 2328-9503 (ISSN-L)
- PMC
- PMC6043775
- OpenAlex
- W2951968424
- Cited by
- 141
- References
- 33
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 27 · 2023: 21 · 2022: 17 · 2021: 20 · 2020: 13 · 2019: 22 · 2018: 5
- FWCI
- 10.31
- Type
- journal article
- Language
- en
- Update notices
- correction (2019-02-25)
- Open access
- gold
- doi.org
- Licence
- Locations
- Annals of Clinical and Translational Neurology (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Minerva Access (University of Melbourne) (submittedVersion, cc-by-nc-nd)
- Funders
- National Institute on Aging (U01 AG032984, R01 AG033193, UF1AG047133, U01AG049505, U01AG049506, U01AG049507, U01AG049508, U01AG052411, U01AG052410, U54AG052427, R01AG023629, R01AG15928, R01AG20098, U24AG021886, U24 AG056270, NIAGADS, U24AG041689)
- National Institutes of Health (1RF1AG054023, 5R37AG015473, RF1AG015473, R56AG051876, TL1TR001875, RO1HD048805, UL1TR000040)
- National Center for Advancing Translational Sciences
- National Heart, Lung, and Blood Institute (5RC2HL102419, HL105756, HHSN268201100005C, HHSN268201100006C, HHSN268201100007C, HHSN268201100008C, HHSN268201100009C, HHSN268201100010C, HHSN268201100011C, HHSN268201100012C, HHSN268201200036C, HHSN268200800007C, N01HC55222, N01HC85079, N01HC85080, N01HC85081, N01HC85082, N01HC85083, N01HC85086, U01HL080295, U01HL130114)
- National Institute of Neurological Disorders and Stroke (U01NS077303, U01NS053998, U54NS078059)
- Baylor College of Medicine (U54 HG003273)
- National Association for Colitis and Crohn's Disease (U01AG016976)
- U.S. National Library of Medicine
- Biogen
- National Institute of Child Health and Human Development (P01HD080642)
- National Institute of Mental Health (R01MH097971, K01MH098126)
- National Human Genome Research Institute (U01HG007672)
- American Academy of Child and Adolescent Psychiatry
- Ellison Medical Foundation (AG‐NS‐0441‐08)
- Muscular Dystrophy Association
- 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 › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- Alzheimer's disease, rare variants, ultra-rare variants, loss-of-function mutations, SORL1, genetic risk factors, gene regulatory networks, age of onset, exome sequencing
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