This research applies fluid mechanics, numerical simulations, and machine learning to model the brain’s waste-clearance system during sleep. By investigating how fluid moves through brain tissue and how aging or injury affect this process, the work aims to identify strategies for preventing or slowing neurodegenerative diseases such as Alzheimer's.

This research develops a method to deliver EGCG, a green tea compound known to break apart Alzheimer's-related protein tangles, into the brain. By chemically attaching EGCG to a carrier that can cross the brain's protective barrier, the project aims to create a potential therapeutic strategy for slowing memory loss and disease progression.

This research uses artificial intelligence to predict the progression of Alzheimer’s disease and cancer using medical imaging data. By analyzing brain scans, tumor scans, and treatment responses, AI models can forecast disease development and treatment outcomes, enabling earlier intervention, more personalized care, and improved quality of life for aging populations.

This research investigates whether thallium exposure from 9/11 dust contributes to long-term memory loss in first responders. By linking biological samples with decades of cognitive data, findings suggest higher exposure increases risk of early Alzheimer’s indicators. The study emphasizes early detection and prevention for those exposed to environmental toxins.

This research explores how immune-related cells and molecules, beneficial in wound healing, may become harmful in Parkinson’s disease. Using the fruit fly as a model organism, the study investigates which inflammatory processes contribute to brain damage. Early results suggest that excessive activation worsens degeneration, offering potential targets for future therapies.

This study investigates how immune cells influence Alzheimer’s disease. Using a mouse model, researchers found that removing T cells did not alter amyloid plaque levels but changed microglial behavior, leading to better protection of myelin. The findings suggest T cells may worsen neurodegeneration and highlight new therapeutic possibilities.

Researchers describe a simple strategy to slow Alzheimer’s disease by capping toxic tau protein chains. Inspired by a ring-stacking toy, they engineered spiky molecular “hats” that bind tau, halt aggregation, and reduce spread in cellular and postmortem brain models, suggesting broad potential across neurodegenerative disorders with future therapeutic promise worldwide.

This thesis investigates how gut microbes influence brain health through short-chain fatty acids produced from dietary fibre. Measuring these compounds in stool samples, the research finds lower levels in people at risk for Alzheimer’s disease. The next phase tests whether supplementing short-chain fatty acids can prevent or treat Alzheimer’s in mouse models.

Psychiatric symptoms often precede neurodegenerative diseases, but the biological link remains unclear. This research examines the FMR1 gene using postmortem brain tissue to uncover shared molecular mechanisms, aiming to predict neurodegeneration earlier, improve treatment strategies, and reframe psychiatric symptoms as potential early warning signs.

This research investigates toxic protein fragments involved in amyotrophic lateral sclerosis (ALS). By studying two TDP-43 fragments in mice and neurons, the work shows that specific fragments cause greater movement deficits and protein aggregation. Identifying the most harmful fragments advances understanding of ALS mechanisms and supports development of targeted neuroprotective therapies.