Meta-analysis of the Association Between Variants in SORL1 and Alzheimer Disease
Open accessAbstract
OBJECTIVE: To reexamine the association between the neuronal sortilin-related receptor gene (SORL1) and Alzheimer disease (AD). DESIGN: Comprehensive and unbiased meta-analysis of all published and unpublished data from case-control studies for the SORL1 single-nucleotide polymorphisms (SNPs) that had been repeatedly assessed across studies. SETTING: Academic research institutions in the United States, the Netherlands, Canada, Belgium, the United Kingdom, Singapore, Japan, Sweden, Germany, France, and Italy. PARTICIPANTS: All published white and Asian case-control data sets, which included a total of 12,464 cases and 17,929 controls. MAIN OUTCOME MEASURES: Alzheimer disease according to the Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition) and the National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer's Disease and Related Disorders Association (now known as the Alzheimer's Association). RESULTS: In the white data sets, several markers were associated with AD after correction for multiple testing, including previously reported SNPs 8, 9, and 10 (P < .001). In addition, the C-G-C haplotype at SNPs 8 through 10 was associated with AD risk (P < .001). In the combined Asian data sets, SNPs 19 and 23 through 25 were associated with AD risk (P < .001). The disease-associated alleles at SNPs 8, 9, and 10 (120,873,131-120,886,175 base pairs [bp]; C-G-C alleles), at SNP 19 (120,953,300 bp; G allele), and at SNPs 24 through 25 (120,988,611 bp; T and C alleles) were the same previously reported alleles. The SNPs 4 through 5, 8 through 10, 12, and 19 through 25 belong to distinct linkage disequilibrium blocks. The same alleles at SNPs 8 through 10 (C-G-C), 19 (G), and 24 and 25 (T and C) have also been associated with AD endophenotypes, including white matter hyperintensities and hippocampal atrophy on magnetic resonance imaging, cerebrospinal fluid measures of amyloid β-peptide 42, and full-length SORL1 expression in the human brain. CONCLUSION: This comprehensive meta-analysis provides confirmatory evidence that multiple SORL1 variants in distinct linkage disequilibrium blocks are associated with AD.
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SORL1 was identified through GWAS as a risk factor for sporadic AD.
“SORL1 was identified through GWAS as a risk factor for sporadic AD (495, 503).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [495]
The paper reports SORL1 variants associated with sporadic AD and confirms an association with AD risk in its meta-analysis (Abstract > Conclusion; Comment; page unavailable). It does not say SORL1 was identified through GWAS; the GWAS it describes found no association for the SORL1 SNPs it examined. (LLM, conf=0.88)
Experimental — accuracy not yet measuredSNPs in SORL1 have also been identified as susceptibility loci in European populations and in a transethnic meta-analysis including South Korean and Caucasian cohorts.
“Importantly, SNPs in SORL1 have also been identified as susceptibility loci in European populations [7, 25], and in a transethnic meta-analysis that included South Korean and Caucasian cohorts.”
From Genetics of Alzheimer’s disease: An East Asian perspective (2023) · cites this paper as [25]
GWAS analysis linked the rs3865444 CD33 SNP to decreased AD risk.
“In 2011, GWAS analysis linked the rs3865444 CD33 SNP to decreased AD risk [445, 474].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [474]
rs668387, rs2070045, rs11218343 and rs3781834 appear protective, whereas other variants such as rs143571823 aggravate AD pathogenesis.
“For instance, rs668387, rs2070045, rs11218343 and rs3781834 appear to be protective [474, 482], whereas other variants of SORL1, such as rs143571823, aggravate AD pathogenesis [483].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [474]
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- Authors
- Reitz, C.
- Affiliations
- Columbia University (US)
- Corresponding author
- Reitz, Christiane
- ORCID
- Reitz, Christiane
- Venue
- Archives of Neurology
- Publisher
- American Medical Association (AMA)
- Published
- 2011-01-01
- Volume
- 68
- Issue
- 1
- Pages
- 99
- ISSN
- 0003-9942 (ISSN-L)
- PMC
- PMC3086666
- OpenAlex
- W2143884110
- Cited by
- 162
- References
- 31
- Citations by year
- 2025: 3 · 2024: 7 · 2023: 3 · 2022: 8 · 2021: 9 · 2020: 7 · 2019: 8 · 2018: 6 · 2017: 11 · 2016: 15 · 2015: 10 · 2014: 19 · 2013: 21 · 2012: 29
- FWCI
- 2.51
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Archives of Neurology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- National University of Singapore (submittedVersion)
- Florence Research (University of Florence) (submittedVersion)
- DZNE Pub (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- Wellcome Trust (089703, 081864, GR082604MA)
- National Institutes of Health (5r37ag015473-15)
- Canadian Institutes of Health Research
- Medical Research Council (MC_G1000734)
- National Institute on Aging (AG 05-133, R37AG15473, R01AG037212, P01AG007232, R01AG018023, P50AG005133, K23AG034550, R37-AG015473, AG 08724, AG028555, R01AG028555, R01AG030653, AG 08861, R01AG018732, R01AG041797, P50AG005681, P01AG003991, R01AG008724, P30AG013846, R01AG025259, R01AG016208, R01AG009029, R01AG017173, U24AG056270, P01AG026276, U24AG021886, AG 030653, P50AG016574)
- 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, single nucleotide polymorphisms, genetic susceptibility, haplotype association, linkage disequilibrium, Asian populations, Caucasian population, amyloid-beta, white matter hyperintensities, hippocampal atrophy, genetic risk factors, case-control study, meta-analysis of genetic association studies, endophenotypes
- MeSH terms
- Alleles, Alzheimer Disease, Humans, Nerve Tissue Proteins, Genetic Variation, Case-Control Studies, Polymorphism, Single Nucleotide, LDL-Receptor Related Proteins, Membrane Transport Proteins
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