SynthesisBMC medical genomics2025
The role of genetic polymorphisms on drug response in Alzheimer's disease: a systematic review.
Synthesis in BMC medical genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Treatment Effects of Cholinesterase Inhibitors in Alzheimer's Disease: a Causal Machine Learning Approach.medRxiv : the preprint server for health sciences · 2026Article
- L-α-GPC in Cognitive Decline: Mechanisms and Clinical Evidence in Neurodegenerative Disorders.Neuropsychiatric disease and treatment · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer’s disease (AD) is the most common neurodegenerative disorder, affecting over 32 million people globally. The variability in treatment response to AD medications is influenced by genetic factors, sex, comorbidities, and medication history. Pharmacogenomics, the study of how an individual’s genetic makeup influences drug response, offers a promising approach to understanding these differences. This systematic review investigated the role of genetic polymorphisms in affecting treatment outcomes in AD. Following PRISMA guidelines, we systematically searched PubMed, Scopus, Cochrane, and PharmGKB databases for studies on AD, pharmacogenomics, and treatment response. Ten researchers independently screened the articles, with two independent reviewers resolving conflicts. A total of 1126 records were identified, and after removing duplicates and screening, 58 studies met inclusion criteria. APOE emerged as the most consistently studied gene, with ε2 and ε3 alleles generally associated with better responses to acetylcholinesterase inhibitors (AChEIs) and NMDA receptor antagonists, while ε4 carriage predicted poorer outcomes. The CYP2D610 allele, common in East Asian populations, was linked to enhanced donepezil response due to slower drug metabolism. Other genes, including ABCA1, A2M, CHRNA7, CHRFAM7A, and CHAT, showed potential associations with treatment response, particularly with AChEIs, though results varied across populations and study designs. Polymorphisms in inflammatory, metabolic, and vascular genes such as IL6, IDE, and ACE were also associated with cognitive outcomes, but findings were largely exploratory. In conclusion, APOE and CYP2D6 remain the most promising pharmacogenetic markers in AD, particularly for guiding donepezil therapy. However, evidence remains inconsistent due to varying study designs, populations, and clinical metrics. Additional genes show potential but require further validation. Larger, multiethnic studies with standardized treatment protocols and outcomes are needed to establish the clinical utility of pharmacogenomics in AD therapy.
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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.