Targeting epigenetic mechanisms in amyloid-β-mediated Alzheimer's pathophysiology: unveiling therapeutic potential.

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  • Author(s): Li JZ;Li JZ; Ramalingam N; Li S
  • Source:
    Neural regeneration research [Neural Regen Res] 2025 Jan 01; Vol. 20 (1), pp. 54-66. Date of Electronic Publication: 2024 Mar 01.
  • Publication Type:
    Journal Article
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Wolters Kluwer Health, Medknow Country of Publication: India NLM ID: 101316351 Publication Model: Print-Electronic Cited Medium: Print ISSN: 1673-5374 (Print) Linking ISSN: 16735374 NLM ISO Abbreviation: Neural Regen Res Subsets: PubMed not MEDLINE
    • Publication Information:
      Publication: 2013 - : Mumbai : Wolters Kluwer Health, Medknow
      Original Publication: Shenyang : Editorial Board of Neural Regeneration Research
    • Abstract:
      Alzheimer's disease is a prominent chronic neurodegenerative condition characterized by a gradual decline in memory leading to dementia. Growing evidence suggests that Alzheimer's disease is associated with accumulating various amyloid-β oligomers in the brain, influenced by complex genetic and environmental factors. The memory and cognitive deficits observed during the prodromal and mild cognitive impairment phases of Alzheimer's disease are believed to primarily result from synaptic dysfunction. Throughout life, environmental factors can lead to enduring changes in gene expression and the emergence of brain disorders. These changes, known as epigenetic modifications, also play a crucial role in regulating the formation of synapses and their adaptability in response to neuronal activity. In this context, we highlight recent advances in understanding the roles played by key components of the epigenetic machinery, specifically DNA methylation, histone modification, and microRNAs, in the development of Alzheimer's disease, synaptic function, and activity-dependent synaptic plasticity. Moreover, we explore various strategies, including enriched environments, exposure to non-invasive brain stimulation, and the use of pharmacological agents, aimed at improving synaptic function and enhancing long-term potentiation, a process integral to epigenetic mechanisms. Lastly, we deliberate on the development of effective epigenetic agents and safe therapeutic approaches for managing Alzheimer's disease. We suggest that addressing Alzheimer's disease may require distinct tailored epigenetic drugs targeting different disease stages or pathways rather than relying on a single drug.
      (Copyright © 2025 Copyright: © 2025 Neural Regeneration Research.)
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    • Grant Information:
      P50 AG005134 United States AG NIA NIH HHS
    • Publication Date:
      Date Created: 20240520 Latest Revision: 20240715
    • Publication Date:
      20240715
    • Accession Number:
      PMC11246147
    • Accession Number:
      10.4103/NRR.NRR-D-23-01827
    • Accession Number:
      38767476