The research subjects were the rodent equivalent of casual drinkers - the type who enjoy a glass of wine with dinner or chitchat at a party, rather than getting blackout drunk.
Just like their human counterparts, some were male and others female. Some had a genetic vulnerability to developing Alzheimer's disease later in life, and others did not.
Working on her dissertation under Binghamton University Psychology Professor Terrence Deak, Paige Marsland PhD '23, expected to find that even moderate alcohol use increased the risk of neurodegenerative disease. The actual results came as a surprise: The transgenic rats who drank moderate amounts of alcohol developed less amyloid beta plaques and other indications of Alzheimer's disease, rather than more.
"In some ways, it looks like the alcohol model we were using was almost protective, which is a very controversial take," said Marsland, now a researcher in Assistant Professor of Psychology Florence Varodayan's lab. "We know that a lot of alcohol will lead to neurodegeneration, but more moderate amounts could be neuroprotective in some ways."
Originally from Seattle and raised in the Rochester, N.Y., area, Marsland earned a bachelor's of science in psychology at the University at Buffalo. She came to Binghamton to study with Deak, following her interests in neuroimmunology.
Her dissertation focused on the impact of lifelong alcohol exposure on the development of neurodegenerative disease. She presented her findings at the Research Society on Alcohol's June conference in Minneapolis, where she won the Enoch Gordis Research Recognition Award.
"I was really happy with how the project turned out, even if it was the total opposite of what we expected to see," she reflected. "I think the fun part of science is being shown that you're wrong and having to put new information into a different framework."
Much remains unknown about Alzheimer's disease, although science has uncovered contributing factors, such as genetic vulnerabilities. Marsland believes that it may ultimately be inflammatory in nature; factors that increase inflammation - for example, an autoimmune disorder, such as rheumatoid arthritis - may increase the risk of developing it.
"One of the things we're really looking into isn't just why inflammation contributes to Alzheimer's disease, but how we can treat that inflammation and reduce our risk in the long run," she said.
In Varodaryan's lab, she plans to research the effect of glucagon-like peptide-1 (GLP1) receptor agonists on alcohol use, and the influence of prior alcohol use on the effectiveness of GLP1 agonists and neuroinflammation. Also known as semaglutides, this class of drugs includes the popular diabetes and weight loss medications Ozempic and Wegovy.
In a way, the proposed project hearkens back to Marsland's undergraduate research, which focused on the impact of GLP1 on water balance and intake in elderly populations - years before the drugs entered the public spotlight.
These drugs appear to affect the satiety system in the brain, which reduces appetite and the motivation to obtain substances that individuals find rewarding, whether drugs, alcohol or food, she said.
Overall, Marsland's research highlights the need for individualized medicine in healthcare, particularly throughout aging.
"My research shows that it's not just about whether you currently drink alcohol or not that matters; your history with alcohol, even in the past, can impact future development of disease and how your body responds to treatment," she explained. "This is why I've transitioned into GLP-1 research; we know a lot about how GLP1 affects the brain, but we know a lot less about how a past history of alcohol will change the response to GLP1."
