ArticlemicroPublication biology2021
Changes in Histone H3 Acetylation on Lysine 9 Accompany Aβ 1-40 Overexpression in an Alzheimer's Disease Yeast Model.
Article in microPublication biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 4 citations in OpenAlex.
- Modifications on histone tails in psychiatric disorders.EC psychology and psychiatry · 2026Article
- Review
- Histone post-translational modification and heterochromatin alterations in neurodegeneration: revealing novel disease pathways and potential therapeutics.Frontiers in molecular neuroscience · 2024Review
- Gut microbiota defined epigenomes of Alzheimer's and Parkinson's diseases reveal novel targets for therapy.Epigenomics · 2024Review
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's Disease (AD), the most common type of dementia, is a neurodegenerative disease characterized by plaques of amyloid-beta (Aβ) peptides found in the cerebral cortex of the brain. The pathological mechanism by which Aβ aggregation leads to neurodegeneration remains unknown. Interestingly, genetic mutations do not explain most AD cases suggesting that other mechanisms are at play. Epigenetic mechanisms, such as histone post-translational modifications (PTMs), may provide insight into the development of AD. Here, we exploit a yeast Aβ overexpression model to map out the histone PTM landscape associated with AD. We find a modest decrease in the acetylation levels on lysine 9 of histone H3 in the context of Aβ 1-40 overexpression. This change is accompanied by a decrease in RNA levels. Our results support a potential role for H3K9ac in AD pathology and allude to the role of epigenetics in AD and other neurodegenerative diseases.
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.