ReviewMolecular neurobiology2025
HDAC3 as an Emerging Therapeutic Target for Alzheimer's Disease and other Neurological Disorders.
Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed.
- Article
- HDAC11 as a potential therapeutic target for Alzheimer's disease.Drug discovery today · 2026Review
- HDAC3 in Alzheimer's Disease: established evidence, unresolved questions, and translational priorities.Molecular biology reports · 2026Review
- Qishen Yiqi Dripping Pills Activate HDAC3-Mediated Nrf2-PITX2 Signaling Pathway to Reduce Oxidative Stress and Alleviate Myocardial Infarction Injury in Mice.Chinese journal of integrative medicine · 2026Article
- Discovery of a CI-994 derivative as a dual modulator of class I HDACs and Wnt/β- catenin signaling for Alzheimer's disease therapy.bioRxiv : the preprint server for biology · 2026Article
- Aerobic exercise facilitates p300 nuclear translocation via ADRB2-AMPKα signaling, leading to enhanced histone acetylation and mitigation of cognitive decline in APP/PS1 mice.Alzheimer's research & therapy · 2026Article
- Implications of pentose phosphate metabolism and astrocyte co-expression patterns in the pathogenesis of Alzheimer's disease: evidence from artificial intelligence-driven omics and clinical validation.Frontiers in neuroscience · 2026Article
- Biosynthesized nanoparticles of Tibetan medicine mercuric sulfide preparation to promote endocytosis and realize drug crossing through blood brain barrier.Journal of nanobiotechnology · 2025Article
- Targeting HDAC3 Suppresses Ferroptosis and Demyelination in White Matter Injury by Restoring PDK4-Mediated Iron Homeostasis.CNS neuroscience & therapeutics · 2025Article
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 the most common cause of dementia in the aged population. Histone acetylation is a major epigenetic mechanism linked to memory formation and cognitive function. Histone deacetylases (HDACs) are responsible for the deacetylation of lysine residues in histone proteins. Although pan-HDAC inhibitors are effective in ameliorating AD phenotypes in preclinical models, they are associated with potential unfavorable adverse effects and barely translated into clinical trials. Therefore, the development of novel HDAC inhibitors with a well isoform-selectivity has been desired in AD drug discovery. Among various HDAC isoforms, HDAC3 is highly expressed in neurons and exhibits detrimental effects on synaptic plasticity and cognitive function. Moreover, HDAC3 provokes neuroinflammation and neurotoxicity and contributes to AD pathogenesis. In this review, we highlight HDAC3 as an attractive therapeutic target for disease-modifying therapy in AD. In addition, we discuss the therapeutic potential of HDAC3 inhibitors in other neurological disorders.
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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.