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September 17, 2025Open Access

Neuronal HDAC9: A key regulator of cognitive and synaptic aging, rescuing Alzheimer's disease-related phenotypes

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Authors

YLYun LeiYCYuting ChenMGMing‐Lei Guo

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Overview

Observational analysis reveals hdac9's role in cognitive aging and alzheimer's disease, suggesting potential for therapeutic targeting.

Key Points

  • Overexpression of hdac9 preserves cognitive function in aged mice, indicating its protective role.
  • Hdac9 deficiency leads to impaired cognitive function and synaptic plasticity in young mice, supporting its importance.
  • Selective deletion of hdac9 in hippocampal neurons induces cognitive impairment, further emphasizing its critical function.
  • Neuronal overexpression of hdac9 reduces amyloid-beta deposition in brain models of alzheimer's disease, hinting at therapeutic potential.

Cite This Study

Lei et al. (2025) studied this question.

synapsesocial.com/papers/68d42725713b0b5dfea6dc46https://doi.org/10.1101/2025.09.13.675847
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1HDACs in the Brain: From Chromatin Remodeling to Neurodegenerative Disease2025
  2. 2Histone Deacetylases in Neurodegenerative Diseases and Their Potential Role as Therapeutic Targets: Shedding Light on Astrocytes2025
  3. 3Advancing histone deacetylase 6 (HDAC6) as a promising therapeutic target for Alzheimer’s disease: from molecular insights to clinical prospects2025
  4. 4Epigenetic manipulation of anterior insular cortex alters neural signals and cognitive control2025 · 1 citations
  5. 5Epigenetic Regulation in Ischemic Neuroprotection: The Dual Role of HDACs and HATs in Neuroinflammation and Recovery2025