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.

This talk explains how devastating brain diseases such as Parkinson’s disease and dementia may begin not in the brain, but in the gut. The speaker describes how a protein called alpha-synuclein can change shape, form toxic complexes, and spread from cell to cell, traveling from the gut to the brain via neural connections. Once in the brain, these toxic complexes disrupt movement, memory, and thinking. The research identifies a key protein, FABP2, that promotes this harmful process by interacting with alpha-synuclein. By targeting and breaking this interaction early—at the level of the gut—the work aims to prevent neurodegenerative disease before irreversible brain damage occurs, potentially reducing patient suffering as well as medical and societal costs.

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 talk highlights the lack of ADRD resources and care access for capital-D Deaf communities despite their elevated risk. Through community engagement, sign-language translations, and caregiver-informed guidelines, the research seeks to improve equitable aging and end-of-life support for Deaf individuals until a cure for Alzheimer’s becomes reality.

Prion diseases like CJD are extremely hard to detect early because harmful prions resemble normal brain proteins. This research introduces a new “flashbody” detection tool that binds only disease-causing prions, providing rapid, accurate, equipment-free diagnosis. Early lab results and patient-screening trials are promising, with potential applications to Alzheimer’s and other dementias.

This research develops one of the most advanced human-engineered brain models to better study Alzheimer’s disease and test treatments. Using microfluidic chips containing all key brain cell types, blood-vessel systems, and Alzheimer’s-model neurons, the project enables efficient drug testing, personalised disease modelling, and the possibility of replacing animal testing in the search for a cure.

This research focuses on developing reliable blood-based biomarkers to evaluate new treatments for hereditary frontotemporal dementia. By identifying an imbalance between two key molecules, progranulin and prosaposin, the work aims to provide accurate measures of treatment effectiveness and bring hope to families carrying this devastating genetic condition

This research maps how drugs travel from the cerebrospinal fluid into the brain, offering an alternative to the blood–brain barrier for treating Alzheimer’s disease. Using mouse models, the study identifies specific drug-entry routes and differences in drug penetration, paving the way for targeted, efficient therapies guided by a “Google Brain Map” of delivery pathways.

Learning a new language, even later in life, can boost attention within a single week and support long-term cognitive resilience. Intensive language learners outperform peers in non-language courses, with benefits spanning ages 18–78. Practising five hours weekly maintains gains, offering a promising, accessible strategy for stroke recovery and dementia delay.

My research uses AI and wearable technology to track brain and body signals such as brain waves (EEG), heart rate, and movement. The goal?  Spotting early signs of Alzheimer's and Parkinson's before symptoms show up. Catching these subtle changes could mean helping people sooner, letting them enjoy the everyday moments that matter most