SynthesisTranslational psychiatry2021
Genetically regulated expression in late-onset Alzheimer's disease implicates risk genes within known and novel loci.
Synthesis in Translational psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 4 of them syntheses that pooled it.
What it found
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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.
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Who cites it
27 citing papers in PubMed, 4 syntheses or guidelines pooled it, 38 citations in OpenAlex.
- Proteome-wide Mendelian randomization identifies causal plasma proteins in frontotemporal dementia.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Pooled it
- Alzheimer disease is (sometimes) highly heritable: Drivers of variation in heritability estimates for binary traits, a systematic review.PLoS genetics · 2025Pooled it
- Hippocampal transcriptome-wide association study and pathway analysis of mitochondrial solute carriers in Alzheimer's disease.Translational psychiatry · 2024Pooled it
- A haptoglobin (HP) structural variant alters the effect of APOE alleles on Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Pooled it
- Multi-ancestry transcriptome-wide association study reveals shared and population-specific genetic effects in Alzheimer disease.American journal of human genetics · 2026Article
- Comprehensive adjudication identifies 111 high-confidence loci for Alzheimer's disease and related dementias.medRxiv : the preprint server for health sciences · 2026Article
- Functional Analysis of Late-Onset Alzheimer's Disease Risk Genes inbioRxiv : the preprint server for biology · 2026Article
- Neuroimaging PheWAS and molecular phenotyping implicate PSMC3 in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Distinct Regulatory Genomic Architectures Distinguish Early-Onset from Late-Onset Alzheimer's Disease.Genes · 2026Article
- Challenges and Opportunities in Characterizing the Genetics of Stuttering: From Sample Acquisition to Functional Interpretation of the Genome.Journal of speech, language, and hearing research : JSLHR · 2025Review
- Multi-ancestry Transcriptome-Wide Association Study Reveals Shared and Population-Specific Genetic Effects in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2025Article
- Integrated Multi-Omics Analysis and Cross-Model Validation Reveal Mitochondrial Signatures in Alzheimer's Disease.CNS neuroscience & therapeutics · 2025Article
- Neuroimaging PheWAS and molecular phenotyping implicatemedRxiv : the preprint server for health sciences · 2025Article
- Identifying Alzheimer's disease-related pathways based on whole-genome sequencing data.Computational and structural biotechnology journal · 2025Article
- Serum proteomics reveal APOE-ε4-dependent and APOE-ε4-independent protein signatures in Alzheimer's disease.Nature aging · 2024Article
- Heterogeneity of factors associated with cognitive decline and cortical atrophy in early- versus late-onset Alzheimer's disease.Scientific reports · 2024Article
- Article
- Serum proteomics reveals APOE dependent and independent protein signatures in Alzheimer's disease.Research square · 2024Article
- Enhancing of cerebral Abeta clearance by modulation of ABC transporter expression: a review of experimental approaches.Frontiers in aging neuroscience · 2024Review
- Serum proteomics revealsmedRxiv : the preprint server for health sciences · 2023Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Late-onset Alzheimer disease (LOAD) is highly polygenic, with a heritability estimated between 40 and 80%, yet risk variants identified in genome-wide studies explain only ~8% of phenotypic variance. Due to its increased power and interpretability, genetically regulated expression (GReX) analysis is an emerging approach to investigate the genetic mechanisms of complex diseases. Here, we conducted GReX analysis within and across 51 tissues on 39 LOAD GWAS data sets comprising 58,713 cases and controls from the Alzheimer's Disease Genetics Consortium (ADGC) and the International Genomics of Alzheimer's Project (IGAP). Meta-analysis across studies identified 216 unique significant genes, including 72 with no previously reported LOAD GWAS associations. Cross-brain-tissue and cross-GTEx models revealed eight additional genes significantly associated with LOAD. Conditional analysis of previously reported loci using established LOAD-risk variants identified eight genes reaching genome-wide significance independent of known signals. Moreover, the proportion of SNP-based heritability is highly enriched in genes identified by GReX analysis. In summary, GReX-based meta-analysis in LOAD identifies 216 genes (including 72 novel genes), illuminating the role of gene regulatory models in LOAD.
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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.