Common Seizure Medication Could Halt Alzheimer's Onset, Study Reveals
Groundbreaking research from Northwestern Medicine has identified a common seizure medication that may prevent the development of Alzheimer's disease symptoms. The study, published in Science Translational Medicine, suggests that levetiracetam—a drug used clinically for decades—can stop the accumulation of toxic proteins in the brain that leads to Alzheimer's.
The Critical Timing Challenge
Scientists have discovered a significant catch in this potential breakthrough. To be effective, the medication might need to be administered nearly two decades before current tests can detect elevated protein levels in the brain. This means individuals at high risk for Alzheimer's could require treatment in their 30s, 40s, or 50s—long before any cognitive symptoms emerge.
"You couldn't take this when you already have dementia because the brain has already undergone a number of irreversible changes and a lot of cell death," explained Jeffrey Savas, PhD, the study's corresponding author and associate professor at Northwestern University Feinberg School of Medicine.
How Levetiracetam Works Differently
Current Alzheimer's medications primarily work by clearing out existing protein fragments in the brain. Levetiracetam represents a fundamentally different approach by preventing the initial buildup from occurring. The research team discovered precisely when and where these toxic protein fragments begin to accumulate, revealing the drug's preventive potential.
"In our 30s, 40s and 50s, our brains are generally able to steer proteins away from harmful pathways," Savas noted. "As we age, that protective ability gradually weakens. This is not a statement of disease; this is just a part of aging. But in brains developing Alzheimer's, too many neurons go astray."
Targeting High-Risk Populations
The study's findings suggest that people with rare genetic forms of Alzheimer's would be the primary beneficiaries of this preventive approach. This includes individuals with Down syndrome, more than 95% of whom will develop Alzheimer's during their lifetime.
The research utilized multiple approaches including:
- Genetically engineered mouse models
- Cultured human neurons
- Human brain tissue from deceased Down syndrome patients who died in their 20s or 30s
"By obtaining Down syndrome patient brains from people who died in their 20s or 30s, we know they would have eventually developed Alzheimer's, so it gives us an opportunity to study the very initial early changes in the human brain," Savas explained.
Developing Improved Formulations
Researchers identified a practical challenge with levetiracetam: it breaks down quickly in the body. The Northwestern team is now working to develop a modified version of the drug that would last longer and more effectively target the prevention of plaque buildup.
"Conceivably, if you started giving these patients levetiracetam in their teenage years, it could actually have a preventative therapeutic benefit," Savas suggested, referring to the potential application for Down syndrome patients.
Opening New Research Pathways
This discovery has created new avenues for understanding Alzheimer's disease progression and developing treatments. The research highlights what scientists call the "paradoxical stage" of Alzheimer's—the period before synapses are lost and dementia sets in, when presynaptic proteins first begin to accumulate.
The Northwestern study represents a significant shift in Alzheimer's research, moving from treatment of existing symptoms to prevention of the disease's underlying mechanisms. While practical implementation faces timing challenges, the findings offer hope for at-risk populations and open new possibilities for early intervention strategies.
