Investigating the pathological mechanisms of Aβ and tau protein aggregation, synaptic dysfunction, and cognitive decline in Alzheimer's disease
Updated on April 1, 2024

Alzheimer's disease is the most common form of dementia, characterized by progressive cognitive decline and memory loss. Our research investigates the complex molecular mechanisms underlying neuronal death, including Aβ plaque formation, tau protein aggregation, and synaptic dysfunction.
Using advanced genetic tools, computational modeling, and neuroimaging techniques, we aim to understand how these pathological processes interact and develop targeted therapeutic interventions to prevent or slow disease progression.
Studying Aβ and tau protein misfolding and aggregation mechanisms
Investigating synaptic dysfunction and neurotransmitter system alterations
Developing novel therapies targeting multiple pathological pathways
Understanding Aβ plaque formation and its role in neurodegeneration
Investigating tau protein hyperphosphorylation and neurofibrillary tangle formation
Studying the relationship between brain pathology and cognitive symptoms
Investigating how epigenetic modifications regulate gene expression patterns in Alzheimer's disease and identifying potential targets for therapeutic intervention.
Computational biology approach
Utilizing artificial intelligence and machine learning algorithms to identify novel therapeutic compounds that target multiple pathological pathways in Alzheimer's disease.
Collaborative computational project
Developing therapeutic approaches to protect synapses from Alzheimer's-related damage and preserve cognitive function in early-stage disease.
Translational research initiative