ReviewThe neurologist2009
Genetic aspects of Alzheimer disease.
Review in The neurologist, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 135 citations in OpenAlex.
- Pooled it
- Unraveling the Mysteries of Alzheimer's Disease Using Artificial Intelligence.Reviews on recent clinical trials · 2025Review
- Neuroinflammation and nutrition in Alzheimer's disease.Frontiers in neurology · 2025Review
- Examining the Performance of Polygenic Risk Scores for Alzheimer Disease Within and Across Populations UsingNeurology. Genetics · 2024Article
- Genetic analysis of cognitive preservation in the midwestern Amish reveals a novel locus on chromosome 2.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Exploring Heparan Sulfate Proteoglycans as Mediators of Human Mesenchymal Stem Cell Neurogenesis.Cellular and molecular neurobiology · 2024Review
- From the Mind to the Spine: The Intersecting World of Alzheimer's and Osteoporosis.Current osteoporosis reports · 2024Review
- Genetic analysis of cognitive preservation in the midwestern Amish reveals a novel locus on chromosome 2.medRxiv : the preprint server for health sciences · 2023Article
- The genetic architecture of Alzheimer disease risk in the Ohio and Indiana Amish.HGG advances · 2022Article
- The relationship of early- and late-onset Alzheimer's disease genes with COVID-19.Journal of neural transmission (Vienna, Austria : 1996) · 2022Review
- Nanotherapeutics for Nose-to-Brain Drug Delivery: An Approach to Bypass the Blood Brain Barrier.Pharmaceutics · 2021Review
- ACells · 2021Review
- Artificial Intelligence for Alzheimer's Disease: Promise or Challenge?Diagnostics (Basel, Switzerland) · 2021Review
- Endocytosis-pathway polygenic scores affects the hippocampal network connectivity and individualized identification across the high-risk of Alzheimer's disease.Brain imaging and behavior · 2021Article
- Review
- An Open Question: Is the AFrontiers in pharmacology · 2021Article
- MicroRNAs Dysregulation and Mitochondrial Dysfunction in Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
- PET Radiopharmaceuticals for Alzheimer's Disease and Parkinson's Disease Diagnosis, the Current and Future Landscape.Molecules (Basel, Switzerland) · 2020Review
- Xenobiotics, Trace Metals and Genetics in the Pathogenesis of Tauopathies.International journal of environmental research and public health · 2020Review
- Improving predictive models for Alzheimer's disease using GWAS data by incorporating misclassified samples modeling.PloS one · 2020Article
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 at 1 institution in 1 country.
Funding
Abstract
backgroundAlzheimer disease (AD) is a genetically complex disorder. Mutations in 3 genes, presenilin 1, amyloid precursor protein, and presenilin 2, lead to early-onset familial AD in rare families with onset of disease occurring prior to age 65. Specific polymorphisms in apolipoprotein E are associated with the more common, late-onset AD occurring after age 65. In this review, we discuss current advances in AD genetics, the implications of the known AD genes, presenilin 1, presenilin 2, amyloid precursor protein, and apolipoprotein E, and other possible genes on the clinical diagnosis, treatment, and genetic counseling of patients and families with early- and late-onset AD. REVIEW SUMMARY: In addition to the mutations in 4 known genes associated with AD, mutations in other genes may be implicated in the pathogenesis of the disease. Most recently, 2 different research groups have reported genetic association between 2 genes, sortilin-related receptor and GAB2, and AD. These associations have not changed the diagnostic and medical management of AD.
conclusionsNew research in the genetics of AD have implicated novel genes as having a role in the disease, but these findings have not been replicated nor have specific disease causing mutations been identified. To date, clinical genetic testing is limited to familial early-onset disease for symptomatic individuals and asymptomatic relatives and, although not recommended, amyloid precursor protein apolipoprotein E testing as an adjunct to diagnosis of symptomatic individuals.
Indexed as
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.