Researchers at New York University School of Medicine have uncovered shared mechanisms that link epilepsy with Alzheimer’s disease, shedding light on how these conditions may share common biological pathways. The study’s findings are published in Acta Neuropathologica.
To reach these conclusions, brain tissue samples from individuals diagnosed with epilepsy or Alzheimer’s disease were analyzed. The team conducted comparative proteomic analyses to measure the expression of specific genes and the corresponding proteins in the samples, providing a comprehensive view of molecular changes across these conditions.
The proteomic dataset revealed that 777 proteins show significantly altered expression in the hippocampus of people with epilepsy. In parallel, data on protein activity in the brains of Alzheimer’s patients were obtained through NeuroPro, a sophisticated approach that integrates protein information from human brain tissue. This analysis identified 5,311 proteins with altered expression in Alzheimer’s disease, painting a broad picture of the proteomic shifts associated with the condition.
Crucially, the researchers found overlapping patterns in how certain proteins are synthesized in both epilepsy and Alzheimer’s disease. This overlap is observed alongside broader pathological changes, including disruptions in mitochondrial function, which governs cellular energy production, and in synaptic activity, the contact points that enable neuronal communication. These shared alterations highlight converging disease processes that may underlie both conditions and suggest potential avenues for therapeutic strategies that address common molecular targets.
A key finding across both disorders is the elevated expression of Tau proteins, particularly the phosphorylated forms pTau217 and pTau231, within the brain. In Alzheimer’s disease, higher levels of Tau are associated with cognitive decline, reduced brain mass, and the development of amyloid plaques. Prior research in animal models has also linked overexpression of specific Tau proteins to an increased susceptibility to convulsive seizures, suggesting a potential mechanistic bridge between these neurological conditions.
Researchers note that lifestyle and physiological factors previously identified by scientists may influence Alzheimer’s risk. While this study emphasizes molecular similarities, it also underscores the importance of a holistic view that considers both genetic and environmental contributors to brain health.