ArticleAnnals of neurology2012
Multiple loci influencing hippocampal degeneration identified by genome scan.
Article in Annals of neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 4 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
46 citing papers in PubMed, 4 syntheses or guidelines pooled it, 68 citations in OpenAlex.
- Meta-analysis of genome-wide association studies identifies ancestry-specific associations underlying circulating total tau levels.Communications biology · 2022Pooled it
- Genetic Variability in Molecular Pathways Implicated in Alzheimer's Disease: A Comprehensive Review.Frontiers in aging neuroscience · 2021Pooled it
- Genetic Markers of ADHD-Related Variations in Intracranial Volume.The American journal of psychiatry · 2019Pooled it
- Genetic analysis of quantitative phenotypes in AD and MCI: imaging, cognition and biomarkers.Brain imaging and behavior · 2014Pooled it
- Landscape of copy number variants in Spanish people with dementia.NPJ genomic medicine · 2026Article
- Article
- Novel Genes Associated With Working Memory Are Identified by Combining Connectome, Transcriptome, and Genome.Human brain mapping · 2025Article
- Cell type-specific functions of Alzheimer's disease endocytic risk genes.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Review
- Clenching the Strings of Bruxism Etiopathogenesis: Association Analyses on Genetics and Environmental Risk Factors in a Deeply Characterized Italian Cohort.Biomedicines · 2024Article
- Genetics of Alzheimer's Disease in the African American Population.Journal of clinical medicine · 2023Review
- Review
- A missense variant in SHARPIN mediates Alzheimer's disease-specific brain damages.Translational psychiatry · 2021Article
- Effect of longevity genetic variants on the molecular aging rate.GeroScience · 2021Article
- Genetic Risk Factors for Alzheimer's Disease in Racial/Ethnic Minority Populations in the U.S.: A Scoping Review.Frontiers in public health · 2021Article
- Single Nucleotide Polymorphisms in Alzheimer's Disease Risk Genes Are Associated with Intrinsic Connectivity in Middle Age.Journal of Alzheimer's disease : JAD · 2020Article
- Mouse genome-wide association and systems genetics identifies Lhfp as a regulator of bone mass.PLoS genetics · 2019Article
- Clusterin in Alzheimer's Disease: Mechanisms, Genetics, and Lessons From Other Pathologies.Frontiers in neuroscience · 2019Review
- Early Life Stress and Epigenetics in Late-onset Alzheimer's Dementia: A Systematic Review.Current genomics · 2018Review
- Genetic Overlap Between Schizophrenia and Volumes of Hippocampus, Putamen, and Intracranial Volume Indicates Shared Molecular Genetic Mechanisms.Schizophrenia bulletin · 2018Article
- Genetic associations with childhood brain growth, defined in two longitudinal cohorts.Genetic epidemiology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 5 institutions in 1 country.
Funding
Abstract
objectiveLarge genome-wide association studies (GWASs) have identified many novel genes influencing Alzheimer disease (AD) risk, but most of the genetic variance remains unexplained. We conducted a 2-stage GWAS for AD-related quantitative measures of hippocampal volume (HV), total cerebral volume (TCV), and white matter hyperintensities (WMH).
methodsBrain magnetic resonance imaging measures of HV, TCV, and WMH were obtained from 981 Caucasian and 419 African American AD cases and their cognitively normal siblings in the MIRAGE (Multi Institutional Research in Alzheimer's Genetic Epidemiology) Study, and from 168 AD cases, 336 individuals with mild cognitive impairment, and 188 controls in the Alzheimer's Disease Neuroimaging Initiative Study. A GWAS for each trait was conducted in the 2 Caucasian data sets in stage 1. Results from the 2 data sets were combined by meta-analysis. In stage 2, 1 single nucleotide polymorphism (SNP) from each region that was nominally significant in each data set (p < 0.05) and strongly associated in both data sets (p < 1.0 × 10(-5)) was evaluated in the African American data set.
resultsTwenty-two markers (14 for HV, 3 for TCV, and 5 for WMH) from distinct regions met criteria for evaluation in stage 2. Novel genome-wide significant associations (p < 5.0 × 10(-8)) were attained for HV with SNPs in the APOE, F5/SELP, LHFP, and GCFC2 gene regions. All of these associations were supported by evidence in each data set. Associations with different SNPs in the same gene (p < 1 × 10(-5) in Caucasians and p < 2.2 × 10(-4) in African Americans) were also observed for PICALM with HV, SYNPR with TCV, and TTC27 with WMH.
interpretationOur study demonstrates the efficacy of endophenotypes for broadening our understanding of the genetic basis of AD.
Indexed as
Identifiers
What OpenQuestion holds
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.