Developing Extracellular Vesicle Blood Biomarkers for Early Detection of Parkinson’s Disease

Parkinson’s disease (PD) is a progressive neurodegenerative disorder that affects more than 100,000 Canadians and is expected to rise to more than 163,700 by 2031. Although it may begin as a movement disorder, it is associated with early and progressive cognitive decline, with nearly 50% of patients developing dementia within 10 years.
Without a reliable blood test, early diagnosis remains extremely difficult.

My research aims to fill this gap by developing a rapid blood-based biomarker system that complements current diagnostic methods and brings PD detection closer to everyday clinical practice. I will focus on measuring proteins carried by extracellular vesicles (EVs), which are tiny particles released by brain cells that travel into the bloodstream. A key protein linked to PD is α-synuclein, which can misfold and build up in the brain.Using nanoscale flow cytometry, an emerging technology for measuring EVs, it can sensitively detect EVs that carry α-synuclein and other PD-related markers.

This research will help identify EV biomarkers that clearly distinguish individuals with PD and Parkinson’s disease dementia from healthy individuals, while also reflecting disease severity. By analyzing patient samples and confirming the findings from a large national study of aging and neurodegenerative diseases, the aim is to develop a reliable and affordable blood test for PD. This test has the potential to reduce long wait times and high costs in diagnosing PD, enabling timely care, better treatment planning, and an improved quality of life for patients.

Designing Next-Generation Hybrid MAO-B Inhibitors as Disease-Modifying Therapeutics for Parkinson’s Disease

Parkinson’s disease (PD) is the second most common brain disorder after Alzheimer’s disease. It mainly affects movement, and people with PD often experience tremors, stiff muscles, slow movement, and problems with balance and walking. These symptoms occur because certain brain cells that produce dopamine, a neurotransmitter responsible for smooth and coordinated movement, gradually stop working or die.

Current treatments can help manage symptoms and improve quality of life, but they do not cure the disease or stop it from progressing.

Scientists now understand that Parkinson’s disease is complex and caused by several interacting factors. One key feature is the buildup of harmful substances in the brain. For example, iron can accumulate in certain brain regions, potentially damaging cells. In addition, a protein called alpha-synuclein can clump together to form abnormal, toxic deposits that harm brain cells. These changes contribute to damage in energy-producing structures within cells and increase the production of harmful molecules, ultimately leading to the loss of dopamine-producing neurons and ongoing neurodegeneration.

Most current treatments focus on replacing dopamine or improving its function, which helps with symptoms but does not address the underlying causes of the disease. This work aims to go beyond symptom control by developing new drugs that target multiple harmful processes at the same time. These compounds are designed to enter the brain and act on key drivers of Parkinson’s disease, with the goal of not only relieving symptoms but also slowing or potentially stopping disease progression.

Understanding How Exercise-Mediated Changes to the Peripheral Immune System Affect Neuropathology in Parkinson’s Disease

People living with Parkinson’s disease (PD) experience a range of motor and non-motor symptoms because certain brain cells gradually become damaged, destroyed, and eventually die. Current medications are unable to prevent damage to these cells, and while they can help manage symptoms, they often come with side effects and become less effective at advanced stages of the disease.

To overcome these limitations, research is increasingly focused on disease-modifying approaches. One promising intervention for people with PD is exercise, particularly aerobic exercise such as cycling or running. It is safe, can reduce chronic inflammation, improve symptoms, and may even slow disease progression when performed regularly. Although the mechanisms behind these benefits are not yet fully understood, it is known that exercise influences the immune system. This is especially important because inflammation begins early in PD and is linked to the loss of vulnerable brain cells.

My research explores how aerobic exercise affects inflammation, communication between the brain and blood, and brain cell health. More specifically, we will collect blood samples from people with PD before and after a single cycling session to examine immune cell composition. These samples will then be tested using a cell culture model of the human blood-brain barrier (BBB), a key interface between the brain and the blood, to determine whether exercise-induced changes in inflammation influence BBB function and neuronal health.

By improving our understanding of how exercise impacts immune cells, the BBB, and brain cells in PD, we hope to refine exercise recommendations and identify therapeutic targets that help restore BBB function. Working alongside Parkinson Society Southwestern Ontario, our goal is to better inform healthcare professionals, people with PD, and their families about the biological effects of aerobic exercise and ultimately improve the lives of those living with this neurodegenerative disease.

Characterizing the Structural and Functional Perturbations of Parkinson’s Under Oxidative Stress

Parkinson’s disease (PD) patients struggle with motor symptoms such as bradykinesia, tremors, and stiffness, which significantly impact daily life. These difficulties worsen as neurodegeneration progresses in the brain’s substantia nigra. The neurons in this region produce dopamine, a neurotransmitter that enables communication between the brain and muscles to coordinate movement. As these neurons die, dopamine levels decrease, impairing this communication pathway.

Currently, the most effective treatments focus on dopamine replacement therapy to manage symptoms, but none can stop or slow the underlying neurodegeneration. Addressing this challenge requires investigating key conditions that contribute to neuron death, particularly oxidative stress and mitochondrial dysfunction.

Oxidative stress occurs when levels of reactive oxygen species (ROS) exceed the cell’s antioxidant defence capacity, leading to damage of cellular components. Neurons are especially vulnerable because their constant activity requires high energy, which is produced in mitochondria and also generates ROS as a byproduct. Over time, this creates a damaging cycle where ROS build-up impairs mitochondrial function, leading to further oxidative stress and eventually neuronal death.

During this process, the protein parkin helps clear damaged mitochondria and protect cells. However, parkin itself is sensitive to oxidation, which can affect its protective function. This study will investigate how oxidation modifies parkin and contributes to Parkinson’s disease, with the goal of identifying ways to improve its resilience and potentially slow neuronal damage.