Research

My research with the ADRIFT Lab focuses on understanding how plastic consumption harms wildlife, from visible tissue damage through to the molecular signals that predict disease. Working across pathology, histology, and biomarker discovery, we examine how ingested plastics interact with the gut and internal organs to trigger inflammation, scarring, and disrupted tissue function. We pair classical pathology (gross examinations, histopathology, lesion scoring, and organ-level assessment) with molecular approaches such as proteomics and targeted marker panels to identify the biological pathways most affected by plastic exposure.

My dementia research spans three complementary scales: whole organisms, cell biology, and population-level epidemiology. Using animal models, I investigate how immune dysregulation and chronic inflammation shape cognitive decline and neurodegenerative pathology, with a focus on the pathways that convert an initially protective inflammatory response into one that becomes maladaptive and tissue-damaging over time. These models allow us to test causality and to explore how environmental and metabolic stressors can accelerate disease-relevant phenotypes.

At the cellular level, my work examines how dementia-related protein aggregates interact with neurons and glial cells, particularly astrocytes and microglia. I am interested in how these aggregates are handled, how they propagate stress signals, and how innate immune signalling can amplify neuronal dysfunction. This includes probing inflammatory mediators and upstream triggers that prime or activate microglia, and identifying molecular signatures that distinguish adaptive clearance and repair from harmful, self-sustaining neuroinflammation.

In parallel, I apply epidemiological methods to human health data to understand how these mechanisms translate to real-world risk and trajectories. Using longitudinal and time-series approaches, I study patterns of cognitive decline and the factors that modify them, including inflammation-related exposures and medication use. By integrating mechanistic insights from animal and cellular work with epidemiological evidence, my research aims to produce a coherent, translational picture of dementia risk and progression, and to identify practical intervention points that can be tested experimentally and evaluated at scale.