ArticleThe American journal of psychiatry2012
Effect of Alzheimer's disease risk genes on trajectories of cognitive function in the Cardiovascular Health Study.
Article in The American journal of psychiatry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 6 syntheses or guidelines pooled it, 67 citations in OpenAlex.
- Genome-wide association identifies the first risk loci for psychosis in Alzheimer disease.Molecular psychiatry · 2021Pooled it
- PICALM rs3851179 Variant Confers Susceptibility to Alzheimer's Disease in Chinese Population.Molecular neurobiology · 2017Pooled it
- CR1 rs3818361 Polymorphism Contributes to Alzheimer's Disease Susceptibility in Chinese Population.Molecular neurobiology · 2016Pooled it
- CLU rs9331888 Polymorphism Contributes to Alzheimer's Disease Susceptibility in Caucasian But Not East Asian Populations.Molecular neurobiology · 2016Pooled it
- CLU rs2279590 polymorphism contributes to Alzheimer's disease susceptibility in Caucasian and Asian populations.Journal of neural transmission (Vienna, Austria : 1996) · 2015Pooled it
- An Updated Analysis with 85,939 Samples Confirms the Association Between CR1 rs6656401 Polymorphism and Alzheimer's Disease.Molecular neurobiology · 2015Pooled it
- Dissecting Alzheimer's disease heterogeneity by cross-trait polygenic prediction.bioRxiv : the preprint server for biology · 2026Article
- Article
- Sex differences in APOE- and PICALM-related cognitive profiles in healthy middle-aged adults.Frontiers in aging · 2025Article
- Molecular Imaging of Neuroinflammation in Alzheimer's Disease and Mild Cognitive Impairment.Advances in experimental medicine and biology · 2023Article
- Review
- Heterogeneity in Alzheimer's Disease Diagnosis and Progression Rates: Implications for Therapeutic Trials.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Review
- Article
- Single Nucleotide Polymorphism rs11136000 of CLU Gene (Clusterin, ApoJ) and the Risk of Late-Onset Alzheimer's Disease in a Central European Population.Neurochemical research · 2021Article
- The Relationship ofFrontiers in neurology · 2021Article
- Genetic Association Between Alzheimer's Disease Risk Variant of theFrontiers in neuroscience · 2020Article
- High-dimensional longitudinal classification with the multinomial fused lasso.Statistics in medicine · 2019Article
- Genome-wide analysis of genetic predisposition to Alzheimer's disease and related sex disparities.Alzheimer's research & therapy · 2019Article
- Complement Receptor 1 (CR1, CD35) Polymorphisms and Soluble CR1: A Proposed Anti-inflammatory Role to Quench the Fire of "Fogo Selvagem" Pemphigus Foliaceus.Frontiers in immunology · 2019Article
- Clusterin in Alzheimer's Disease: Mechanisms, Genetics, and Lessons From Other Pathologies.Frontiers in neuroscience · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThe trajectory of cognitive decline in patients with late-onset Alzheimer's disease varies widely. Genetic variations in CLU, PICALM, and CR1 are associated with Alzheimer's disease, but it is unknown whether they exert their effects by altering cognitive trajectory in elderly individuals at risk for the disease.
methodThe authors developed a Bayesian model to fit cognitive trajectories in a cohort of elderly subjects and test for genetic effects. They first validated the model's ability to detect the previously established effects of APOE ε4 alleles on age at cognitive decline and of psychosis on the rate of cognitive decline in 802 subjects from the Cardiovascular Health Cognition Study who did not have dementia at study entry and developed incident dementia during follow-up. The authors then evaluated the effects of CLU, PICALM, and CR1 on age and rate of decline in 1,831 subjects who did not have dementia at study entry and then did or did not develop incident dementia by study's end.
resultsThe model generated robust fits to the observed cognitive trajectory data, and validation analysis supported the model's utility. CLU and CR1 were associated with more rapid cognitive decline. PICALM was associated with an earlier age at midpoint of cognitive decline. Associations remained after accounting for the effects of APOE and demographic factors.
conclusionsEvaluation of cognitive trajectories provides a powerful approach to dissecting genetic effects on the processes leading to cognitive deterioration and Alzheimer's 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 OpenQuestion graph.