ReviewGenes2020
The Role of BMI1 in Late-Onset Sporadic Alzheimer's Disease.
Review in Genes, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 9 citations in OpenAlex.
- Biomarker profiling to determine clinical impact of microRNAs in cognitive disorders.Scientific reports · 2024Article
- Distinct CSF biomarker-associated DNA methylation in Alzheimer's disease and cognitively normal subjects.Alzheimer's research & therapy · 2023Article
- Distinct CSF biomarker-associated DNA methylation in Alzheimer's disease and cognitively normal subjects.Research square · 2023Article
- Role of primary aging hallmarks in Alzheimer´s disease.Theranostics · 2023Review
- Toxicoepigenetics and Environmental Health: Challenges and Opportunities.Chemical research in toxicology · 2022Review
- Non-Canonical Functions of the ARF Tumor Suppressor in Development and Tumorigenesis.Biomolecules · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Late-onset sporadic Alzheimer's disease (LOAD) seems to contain a "hidden" component that cannot be explained by classical Mendelian genetics, with advanced aging being the strongest risk factor. More surprisingly, whole genome sequencing analyses of early-onset sporadic Alzheimer's disease cohorts also revealed that most patients do not present classical disease-associated variants or mutations. In this short review, we propose that
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.