ReviewScientifica2012
The genetics of Alzheimer's disease.
Review in Scientifica, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 2 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
52 citing papers in PubMed, 2 syntheses or guidelines pooled it, 101 citations in OpenAlex.
- Systematic Review on Neurotoxic Implications of Lead-Induced Gene Expression Alterations in the Etiology of Alzheimer's Disease.Cellular and molecular neurobiology · 2025Pooled it
- Dissecting Complex and Multifactorial Nature of Alzheimer's Disease Pathogenesis: a Clinical, Genomic, and Systems Biology Perspective.Molecular neurobiology · 2016Pooled it
- The γ-Secretase Modulator, BMS-932481, Modulates Aβ Peptides in the Plasma and Cerebrospinal Fluid of Healthy Volunteers.The Journal of pharmacology and experimental therapeutics · 2016Trial
- Artificial Intelligence for Alzheimer's Disease Diagnosis: From Traditional Machine Learning to Large Language Models.Biosensors · 2026Review
- Post-translational regulation of human D-3-phosphoglycerate dehydrogenase in Alzheimer's disease.Protein science : a publication of the Protein Society · 2026Article
- Integrative physiology of skeletal muscle for maintaining cognitive health.The Journal of physiology · 2026Review
- Genetic modifiers of APOE-ε4-associated cognitive decline.Nature communications · 2026Article
- Uncovering the Novel Genetic Determinants of Primary Congenital Glaucoma in Pakistani Families.Human mutation · 2026Article
- Whole Genome Variable Number Tandem Repeat Analysis in Alzheimer Disease.Neurology. Genetics · 2025Article
- Review
- Integration of Neuroimaging and Molecular Biomarkers in the Diagnosis of Alzheimer's Disease and Frontotemporal Dementia: The Promise of fMRI.Current Alzheimer research · 2025Review
- Article
- Targeting MS4A4A: A novel pathway to improve immunotherapy responses in glioblastoma.CNS neuroscience & therapeutics · 2024Article
- Article
- Review
- Prominent and conspicuous astrocyte atrophy in human sporadic and familial Alzheimer's disease.Brain structure & function · 2023Article
- Identifying underlying patterns in Alzheimer's disease trajectory: a deep learning approach and Mendelian randomization analysis.EClinicalMedicine · 2023Article
- Early-stage Alzheimer's disease: are skeletal muscle and exercise the key?Journal of applied physiology (Bethesda, Md. : 1985) · 2023Review
- Systemic Inflammation Causes Microglial Dysfunction With a Vascular AD phenotype.Brain, behavior, & immunity - health · 2023Article
- The Role of the JAK/STAT Signaling Pathway in the Pathogenesis of Alzheimer's Disease: New Potential Treatment Target.International journal of molecular sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease is a progressive, neurodegenerative disease that represents a growing global health crisis. Two major forms of the disease exist: early onset (familial) and late onset (sporadic). Early onset Alzheimer's is rare, accounting for less than 5% of disease burden. It is inherited in Mendelian dominant fashion and is caused by mutations in three genes (APP, PSEN1, and PSEN2). Late onset Alzheimer's is common among individuals over 65 years of age. Heritability of this form of the disease is high (79%), but the etiology is driven by a combination of genetic and environmental factors. A large number of genes have been implicated in the development of late onset Alzheimer's. Examples that have been confirmed by multiple studies include ABCA7, APOE, BIN1, CD2AP, CD33, CLU, CR1, EPHA1, MS4A4A/MS4A4E/MS4A6E, PICALM, and SORL1. Despite tremendous progress over the past three decades, roughly half of the heritability for the late onset of the disease remains unidentified. Finding the remaining genetic factors that contribute to the development of late onset Alzheimer's disease holds the potential to provide novel targets for treatment and prevention, leading to the development of effective strategies to combat this devastating disease.
Identifiers
What OpenQuestion 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 OpenQuestion graph.