ReviewMolecular neurobiology2025
Histone Deacetylase 2 in Alzheimer's Disease: A Comprehensive Molecular Blueprint for Therapeutic Targeting.
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 4 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
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- PDE5 Inhibitors as Modulators of Alzheimer's-Associated Inflammation and Oxidative Stress: A Meta-Analytical Assessment of Preclinical Studies.Molecular neurobiology · 2025Pooled it
- 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
- Epigenetic Dysregulation in Neurodegeneration: The Role of Histone Deacetylases and Emerging Inhibitor Strategies.Biomolecules · 2026Review
- The metabolic-epigenetic landscape of aging: interplay between histone acetylation, lactylation, and glycation.Frontiers in aging · 2026Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD), which is known for causing cognitive decline and significant synaptic dysfunction, continues to pose a significant barrier to good health among the aging population worldwide. While there remain major knowledge gaps in the exact molecular framework of this complex and devastating disease, emerging evidence strongly implicates epigenetic dysregulation as having a major influence on the complexity of the various pathological processes, driving this debilitating disease. This comprehensive review meticulously delves into the critical and multifaceted role of histone deacetylase 2 (HDAC2) as a key player in actively driving the various neurotoxic processes closely connected to AD's characteristic pathological hallmarks and features. We extensively point out the diverse interconnected pathways via which dysregulated HDAC2 activity contributes to the initiation and progression of multiple intricate mechanisms responsible for the observed synaptic dysfunction, the marked accumulation of amyloid-beta (Aβ) plaques and the formation of neurofibrillary tau tangles. Furthermore, we explore the intricate interplay between the aberrant HDAC2 activity and resulting neuroinflammation and oxidative stress within the brain's microenvironment. Additionally, the review summarises the current developments towards HDAC inhibition, carefully identifying the existing limitations in this rapidly evolving field of research, and highlighting promising avenues and potential future directions for developing effective and demonstrably safe therapies. Finally, the approaches that can facilitate the selective modulation of this crucial epigenetic enzyme to combat the devastating effects of AD are suggested and elucidated.
Indexed as
Identifiers
40781362What 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.