The Alzheimer's Association International Conference (AAIC) 2026, held July 12-15, 2026, at Excel London, features sessions on epigenetic mechanisms in Alzheimer's disease. While specific session abstracts are not publicly available prior to the conference, the Basic Science Track includes sessions on molecular mechanisms of neurodegeneration, genetic risk factors, and neuroimmune pathways—areas where epigenetic research is prominently featured.
The Basic Science Track covers several areas directly relevant to epigenetic mechanisms:
- Molecular mechanisms of neurodegeneration — including DNA methylation, histone modifications, and chromatin remodeling
- Genetic risk factors and protective variants — including epigenetic GWAS and eQTL studies
- Glial biology — microglia and astrocyte epigenetic regulation in neuroinflammation
- Neuroimmune pathways — TREM2, complement system, and inflammasome regulation through epigenetic modifications
ISTAART (International Society to Advance Alzheimer's Research and Treatment) sessions include:
- Epigenetics PIA — focusing on DNA methylation, histone modifications, and non-coding RNA
- Bioinformatics and Data Science — covering multi-omics integration approaches
- Neuronal-Glial Interactions — epigenetic regulation of glial function
Genome-wide studies have identified widespread DNA methylation changes in AD brain and blood. Key findings include:
- ANK1 hypermethylation — consistently observed in hippocampus and entorhinal cortex
- Blood-based biomarkers — DNA methylation signatures correlate with AD pathology
- Epigenetic age acceleration — where DNA methylation-based age exceeds chronological age, associated with increased AD risk
Recent meta-analysis by Smith et al. (2024) identified novel differentially methylated loci across cortex in AD brains.
Histone acetylation and methylation changes are prominent in AD:
- HDAC2 overexpression — represses synaptic plasticity genes
- H4K16ac loss — leads to chromatin compaction and gene silencing
- H3K9me3 alterations — leads to epigenetic derepression and cell cycle re-entry
Multiple non-coding RNA classes are dysregulated in AD:
- miR-132 — most consistently downregulated, targets tau kinases
- miR-146a — upregulated, promotes neuroinflammation
- circular RNAs — emerging as biomarkers
- m6A RNA methylation — significantly altered in AD hippocampus
Recent research by Deng et al. (2024) revealed that m6A modification of promoter-antisense RNAs is profoundly rewired in AD, affecting 3D chromatin organization.
Epigenetic therapies represent a promising approach for AD:
- HDAC inhibitors — selective compounds targeting HDAC2 or HDAC6
- DNMT modulators — low-dose approaches for BDNF promoter demethylation
- Epigenome editing — CRISPR-based tools for targeted epigenetic modification
- miRNA therapeutics — miR-132 mimics and anti-miRNA oligonucleotides
- Lifestyle interventions — exercise, diet, and stress reduction modify epigenetic marks