ReviewInternational journal of molecular sciences2025
Recent Advances and Future Directions in Alzheimer's Disease Genetic Research.
Review in International journal of molecular sciences, 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
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
2 citing papers in PubMed.
- Electrochemical Detection of miR-29a and miR-34a Using AuNPs Immobilized by a Silsesquioxane Polyelectrolyte: Potential Early Alzheimer's Disease Biomarkers Detection.Sensors (Basel, Switzerland) · 2026Article
- Investigating the Impact of ABCB1 3435C>T (rs1045642) Variant on Severity and Cognitive Decline in Egyptian Alzheimer's Disease Patients.Molecular neurobiology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Alzheimer's disease (AD) is a complex neurodegenerative condition which, despite its high prevalence and socioeconomic impact on the world, has an etiology that remains poorly understood. The genetic causes of AD are complex and have been continuously studied for decades. They range from rare pathogenic, highly penetrant mutations in early-onset (EOAD) forms, which account for 5% of the cases to multiple-risk alleles across different genes in late-onset (LOAD) forms. Monogenic causes of EOAD allocate within
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Identifiers
What Socratic 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 Socratic graph.