SynthesisArchives of neurology2011
Meta-analysis of the association between variants in SORL1 and Alzheimer disease.
Synthesis in Archives of neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 95 papers, 6 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
95 citing papers in PubMed, 6 syntheses or guidelines pooled it, 166 citations in OpenAlex.
- Genetic Variability in Molecular Pathways Implicated in Alzheimer's Disease: A Comprehensive Review.Frontiers in aging neuroscience · 2021Pooled it
- Microglial Phagocytosis: A Disease-Associated Process Emerging from Alzheimer's Disease Genetics.Trends in neurosciences · 2020Pooled it
- Association between ABCB1 polymorphisms and haplotypes and Alzheimer's disease: a meta-analysis.Scientific reports · 2016Pooled it
- A comprehensive study of the genetic impact of rare variants in SORL1 in European early-onset Alzheimer's disease.Acta neuropathologica · 2016Pooled it
- Pooled it
- SORL1 is genetically associated with late-onset Alzheimer's disease in Japanese, Koreans and Caucasians.PloS one · 2013Pooled it
- Domain mapping of disease mutations reveals pathogenic SORL1 variants in Alzheimer's disease.Molecular neurodegeneration · 2025Article
- Cardiovascular Risk Factors, Alzheimer's Disease, and the MIND Diet: A Narrative Review from Molecular Mechanisms to Clinical Outcomes.Nutrients · 2025Review
- Limbic-predominant age-related TDP-43 encephalopathy (LATE-NC): Co-pathologies and genetic risk factors provide clues about pathogenesis.Journal of neuropathology and experimental neurology · 2024Review
- Revealing third-order interactions through the integration of machine learning and entropy methods in genomic studies.BioData mining · 2024Article
- A familial missense variant in the Alzheimer's disease gene SORL1 impairs its maturation and endosomal sorting.Acta neuropathologica · 2024Article
- Potentially PathogenicCells · 2023Article
- A familial missense variant in the Alzheimer's Disease genebioRxiv : the preprint server for biology · 2023Article
- Altered DNA methylome profiles of blood leukocytes in Chinese patients with mild cognitive impairment and Alzheimer's disease.Frontiers in genetics · 2023Article
- Recent Advances Towards Diagnosis and Therapeutic Fingerprinting for Alzheimer's Disease.Journal of molecular neuroscience : MN · 2022Review
- Article
- Endophenotypic effects of theFrontiers in aging neuroscience · 2022Article
- Mutations in SORL1 and MTHFDL1 possibly contribute to the development of Alzheimer's disease in a multigenerational Colombian Family.PloS one · 2022Article
- Alzheimer's Disease and Frontotemporal Dementia: A Robust Classification Method of EEG Signals and a Comparison of Validation Methods.Diagnostics (Basel, Switzerland) · 2021Article
- Epigenetic Regulation of Alternative Splicing: How LncRNAs Tailor the Message.Non-coding RNA · 2021Review
35 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
32 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTo reexamine the association between the neuronal sortilin-related receptor gene (SORL1) and Alzheimer disease (AD).
designComprehensive 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.
settingAcademic research institutions in the United States, the Netherlands, Canada, Belgium, the United Kingdom, Singapore, Japan, Sweden, Germany, France, and Italy.
participantsAll published white and Asian case-control data sets, which included a total of 12,464 cases and 17,929 controls.
main outcome measuresAlzheimer 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).
resultsIn 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.
conclusionThis comprehensive meta-analysis provides confirmatory evidence that multiple SORL1 variants in distinct linkage disequilibrium blocks are associated with AD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.