ReviewDialogues in clinical neuroscience2014
The epigenetic dimension of Alzheimer's disease: causal, consequence, or curiosity?
Review in Dialogues in clinical neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- The Role of Hydrogen Sulfide (HInternational journal of molecular sciences · 2023Pooled it
- Brain 5-hydroxymethylcytosine alterations are associated with Alzheimer's disease neuropathology.Nature communications · 2025Article
- Epigenetics Modulators as Therapeutics for Neurological Disorders.Current pharmaceutical design · 2025Review
- Deciphering Early and Progressive Molecular Signatures in Alzheimer's Disease through Integrated Longitudinal Proteomic and Pathway Analysis in a Rodent Model.International journal of molecular sciences · 2024Article
- An Epigenetic Manifestation of Alzheimer's Disease: DNA Methylation.Actas espanolas de psiquiatria · 2024Review
- The oDGal Mouse: A Novel, Physiologically Relevant Rodent Model of Sporadic Alzheimer's Disease.International journal of molecular sciences · 2023Article
- A Review of the Recent Advances in Alzheimer's Disease Research and the Utilization of Network Biology Approaches for Prioritizing Diagnostics and Therapeutics.Diagnostics (Basel, Switzerland) · 2022Review
- Profile ofInternational journal of molecular sciences · 2022Article
- Apoptotic Pathways and Alzheimer's Disease: Probing Therapeutic Potential.Neurochemical research · 2021Review
- Gender-Dependent Deregulation of Linear and Circular RNA Variants of HOMER1 in the Entorhinal Cortex of Alzheimer's Disease.International journal of molecular sciences · 2021Article
- Gut Microbiota Composition and Epigenetic Molecular Changes Connected to the Pathogenesis of Alzheimer's Disease.Journal of molecular neuroscience : MN · 2021Review
- Neuroprotective effects of some epigenetic modifying drugs' on Chlamydia pneumoniae-induced neuroinflammation: A novel model.PloS one · 2021Article
- Therapeutic Targeting of Histone Deacetylation to Prevent Alzheimer's Disease.eMedical research · 2021Article
- Molecular mechanisms underlying actions of certain long noncoding RNAs in Alzheimer's disease.Metabolic brain disease · 2020Review
- Epigenetic mechanisms of neurodegenerative diseases and acute brain injury.Neurochemistry international · 2020Review
- A Comparative Study on 5hmC Targeting Regulation of Neurons in AD Mice by Several Natural Compounds.BioMed research international · 2020Article
- Cerebrovascular miRNAs correlate with the clearance of Aβ through perivascular route in younger 3xTg-AD mice.Brain pathology (Zurich, Switzerland) · 2020Article
- Targeted Downregulation ofJournal of Korean medical science · 2019Article
- Significant association between GPR50 hypomethylation and AD in males.Molecular medicine reports · 2019Article
- Inhibition of EHMT1/2 rescues synaptic and cognitive functions for Alzheimer's disease.Brain : a journal of neurology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Early-onset, familial Alzheimer's disease (AD) is rare and may be attributed to disease-causinq mutations. By contrast, late onset, sporadic (non-Mendelian) AD is far more prevalent and reflects the interaction of multiple genetic and environmental risk factors, together with the disruption of epigenetic mechanisms controlling gene expression. Accordingly, abnormal patterns of histone acetylation and methylation, as well as anomalies in global and promoter-specific DNA methylation, have been documented in AD patients, together with a deregulation of noncoding RNA. In transgenic mouse models for AD, epigenetic dysfunction is likewise apparent in cerebral tissue, and it has been directly linked to cognitive and behavioral deficits in functional studies. Importantly, epigenetic deregulation interfaces with core pathophysiological processes underlying AD: excess production of Aβ42, aberrant post-translational modification of tau, deficient neurotoxic protein clearance, axonal-synaptic dysfunction, mitochondrial-dependent apoptosis, and cell cycle re-entry. Reciprocally, DNA methylation, histone marks and the levels of diverse species of microRNA are modulated by Aβ42, oxidative stress and neuroinflammation. In conclusion, epigenetic mechanisms are broadly deregulated in AD mainly upstream, but also downstream, of key pathophysiological processes. While some epigenetic shifts oppose the evolution of AD, most appear to drive its progression. Epigenetic changes are of irrefutable importance for AD, but they await further elucidation from the perspectives of pathogenesis, biomarkers and potential treatment.
Indexed as
Identifiers
25364287PMC4214179W2156676300What 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.