Our research focuses on why the brain’s blood vessels and nerve cells are damaged in Alzheimer’s disease (AD), cerebral amyloid angiopathy (CAA) and related dementias.  

We are working on several projects, including: 

• Investigating the impact of cardiovascular risk factors on cerebral vascular dysfunction and development of AD and CAA. 
• Researching how mitochondrial dysfunction (damage to the cell’s energy center), oxidative stress (cell damage from unstable molecules), metabolic changes and cell death pathways cause brain cell damage. 
• Exploring carbonic anhydrase enzymes and other novel targets to learn how they trigger mitochondrial dysfunction, apoptosis, and inflammation in brain neural and vascular cells.  
• Discovering new biomarkers in body fluid for AD, TBI and related disorders. 
• Studying how AD and vascular risk factors affect endothelial cells (which line blood vessels) and the blood–brain barrier (which protects the brain).

Using biochemical, molecular, and imaging techniques, cultured cells, animal models and human AD or CAA brain cells, we are finding new ways to understand and possibly treat these diseases.

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Our lab investigates how aging affects synapses — the brain connections that support memory, thinking, and emotion. These changes can  lead to late-life depression and Alzheimer’s dementia (AD). Our goal is to turn these discoveries into targeted treatments that improve patients’ lives.  

Our integrative approach includes: 

1. Studying older mice to identify the core behaviors that have remained the same for all species, including humans, throughout evolution, 
2. Using physiology and molecular biology tools to uncover how these behaviors are linked to synaptic changes in both males and females, and  
3. Exploring possible gene manipulation and behavioral pharmacology treatments. 

Through collaborations with researchers inside and outside of ACT, we are studying: 

• How synapses respond positively or negatively to cardiovascular risks and other cellular pathologies seen in Alzheimer's disease.  
• Stress resilience 
• Spatial memories. 
• Learning from experience (plasticity) 
• Impact of substance abuse. 
• How brain cells interact with tumors. 
• Development of new tools to watch and control synapses in real time. 
• Modeling how calcium moves in brain networks. 

Our team studies how imbalances in fat — a condition known as lipid homeostasis — may lead to Alzheimer’s disease (AD) or age-related macular degeneration (AMD).  

About 60% of the brain contains fats, including phospholipids, essential fatty acids and other types.  These fats play an important role in how brain cells work. Large genetic studies in people have shown that problems with these proteins are linked to diseases like AD or AMD.  

We are focusing on several key proteins that move fats into and out of cells and between layers of the cell’s outer membrane. These include: 

• Adenosine triphosphate (ATP)-binding cassette transporter subfamily A member 1 and 7 (ABCA1 and ABCA7, respectively). 

• A P-type ATPase in subfamily IV called ATPase phospholipid transporting 8B4 (ATP8B4) and the proteins encoded in the p13.2 band of chromosome 17. ABCA1, ABCA7, ATP8B4. 

• One or more proteins at chr17 p13.2 that modulate the risk of AD. ABCA1 also affects the risk of AMD. ABCA1 and ABCA7 mediate cell lipid export in lipoprotein particles stabilized by apolipoproteins, such as apolipoprotein E. ATP8B4 is thought to flip phospholipid from one leaflet of the cell lipid membrane into the other.

By better understanding how these fat-moving proteins work, we hope to find new ways to prevent or treat AD and AMD.

Our lab studies how brain diseases like Alzheimer’s disease, Parkinson’s disease, tauopathies (such as Pick’s disease and Progressive Supranuclear Palsy), and Down syndrome develop. We focus on a field called oxidative neurobiology, which explores how damage from unstable, oxygen-related molecules (oxidative stressors) can harm brain cells over time and lead to disease. Our research, which is part of clinical pharmacology, looks at how these changes affect memory, behavior, and thinking. 

To do this, we study small molecules, enzymes, and cell pathways that are involved in creating or responding to this damage. We also study additional factors such as inflammation, lifestyle, diet, and environmental exposures. We focus on how cells manage proteins and fats — called proteostasis and lipidostasis — and how problems in these systems may lead to amyloid buildup, tau tangles, and neurodegeneration. We use cell cultures, transgenic mice, and human tissue samples, along with tools from biochemistry, molecular biology, and neuroanatomy. 

We also mentor young scientists and work with other labs to support collaborative, high-quality research.