Alzheimers Disease & Dementia

Genomic & Epigenomic Drivers of Alzheimer’s Progression

Genomic and epigenomic research is uncovering the underlying factors that shape Alzheimer’s susceptibility, onset, and progression. Key genetic contributors, including APOE variants, TREM2 mutations, and polygenic risk factors, help explain individual differences in disease vulnerability. Epigenomic changes such as DNA methylation, histone modification, and chromatin remodeling alter gene expression patterns linked to inflammation, synaptic health, and metabolic dysfunction. Environmental influences including stress, lifestyle, and toxin exposure can further modify epigenetic signatures, accelerating neurodegenerative processes. Advances in single-cell sequencing and spatial transcriptomics reveal cell-specific regulatory changes occurring in neurons, astrocytes, and microglia during disease evolution. Understanding these mechanisms enables precision profiling and supports development of targeted therapies that modulate gene expression pathways. Gene-editing tools, epigenetic modulators, and personalized risk assessment models hold promise for predicting progression and designing individualized treatment strategies rooted in genetic and regulatory biology.