ArticleNature communications2022
The causes and consequences of Alzheimer's disease: phenome-wide evidence from Mendelian randomization.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis 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
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Hippocampal transcriptome-wide association study and pathway analysis of mitochondrial solute carriers in Alzheimer's disease.Translational psychiatry · 2024Pooled it
- The potential effect and pathway of valsartan: genome-wide and phenome-wide association study from UK Biobank data.Pharmacogenetics and genomics · 2026Article
- Article
- Aging beyond diagnosis: the MRI brain age gap across disorders.GeroScience · 2026Review
- Genetic susceptibility to Alzheimer's disease and cardiometabolic risk from childhood.Pediatric research · 2026Article
- An evaluation of age-varying genetic effects underlying body-mass index and blood pressure in the UK Biobank.PLoS genetics · 2026Article
- Molecular Crossroads: Shared and Divergent Molecular Signatures in Alzheimer's Disease and Dementia with Lewy Bodies.International journal of molecular sciences · 2025Review
- Immune, blood-brain barrier, and metabolic biomarkers mediate gut-brain axis crosstalk in alzheimer's disease.Biomarker research · 2025Article
- Polygenic risk for Alzheimer's disease in healthy aging: age-related and APOE-driven effects on brain structures and cognition.Genome medicine · 2025Article
- The causal relationship between 91 inflammatory cytokines and chronic pancreatitis, and the mediating role of 1400 metabolites.Medicine · 2025Article
- Intervention on Modifiable Lifestyle and Physiological Factors via Variational Autoencoder Reveals Changes in Functional Connectivity-Mediated Risk for Alzheimer's Disease.medRxiv : the preprint server for health sciences · 2025Article
- Exploring the effect of pre-clinical Alzheimer's disease on blood pressure using Mendelian randomisation and parental dementia as an instrumental variable in UK Biobank.BMC medicine · 2025Article
- Reductions in brainstem volume as a key macrostructural indicator in at-risk populations for Alzheimer's disease.Alzheimer's research & therapy · 2025Article
- Genetically proxied blood pressure, vascular brain injury, and Alzheimer's disease pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Hearing impairment and dementia: cause, catalyst or consequence?Journal of neurology · 2025Review
- Genetic predisposition to adiposity, and type 2 diabetes: the role of lifestyle and phenotypic adiposity.European journal of endocrinology · 2025Article
- Viruses and neurodegeneration: a growing concern.Journal of translational medicine · 2025Review
- Brain change trajectories in healthy adults correlate with Alzheimer's related genetic variation and memory decline across life.Nature communications · 2024Article
- AN INTEGRATIVE NETWORK-BASED MEDIATION MODEL (NMM) TO ESTIMATE MULTIPLE GENETIC EFFECTS ON OUTCOMES MEDIATED BY FUNCTIONAL CONNECTIVITY.The annals of applied statistics · 2024Article
- Causal effect of the age at first birth with depression: a mendelian randomization study.BMC medical genomics · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
Abstract
Alzheimer's disease (AD) has no proven causal and modifiable risk factors, or effective interventions. We report a phenome-wide association study (PheWAS) of genetic liability for AD in 334,968 participants of the UK Biobank study, stratified by age. We also examined the effects of AD genetic liability on previously implicated risk factors. We replicated these analyses in the HUNT study. PheWAS hits and previously implicated risk factors were followed up in a Mendelian randomization (MR) framework to identify the causal effect of each risk factor on AD risk. A higher genetic liability for AD was associated with medical history and cognitive, lifestyle, physical and blood-based measures as early as 39 years of age. These effects were largely driven by the APOE gene. The follow-up MR analyses were primarily null, implying that most of these associations are likely to be a consequence of prodromal disease or selection bias, rather than the risk factor causing the disease.
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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 Socratic graph.