Breakthrough in Alzheimer’s Prevention Linked to Decades-Old Seizure Drug

Featured & Cover Breakthrough in Alzheimer's Prevention Linked to Decades Old Seizure Drug

Researchers have discovered that levetiracetam, a decades-old seizure medication, may prevent the progression of Alzheimer’s disease if administered years before symptoms manifest.

A promising breakthrough in Alzheimer’s prevention has emerged from a recent study suggesting that levetiracetam, a medication traditionally used to treat seizures, may help halt the disease’s progression. Originally approved by the FDA in November 1999 under the brand name Keppra, levetiracetam is primarily prescribed for partial-onset seizures in adults, with its use later expanding to include children and various seizure types.

Researchers at Northwestern University have found that levetiracetam can prevent the formation of toxic amyloid beta peptides, which are small protein fragments commonly associated with Alzheimer’s disease. The study, published in Science Translational Medicine, revealed that the medication effectively inhibited the formation of amyloid-beta 42 in both animal models and cultured human neurons. This effect was also observed in post-mortem brain tissue from individuals with Down syndrome, a group at heightened risk for developing Alzheimer’s.

“While many of the Alzheimer’s drugs currently on the market, such as lecanemab and donanemab, are approved to clear existing amyloid plaques, we’ve identified this mechanism that prevents the production of the amyloid-beta 42 peptides and amyloid plaques,” said Jeffrey Savas, the study’s corresponding author and an associate professor of behavioral neurology at Northwestern University Feinberg School of Medicine. “Our new results uncovered new biology while also opening doors for new drug targets.”

Savas explained that the brain is better equipped to avoid the pathways that produce toxic amyloid-beta 42 proteins during younger years. However, as individuals age, this ability diminishes. “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, and that’s when you get amyloid-beta 42 production,” he noted. This accumulation can lead to the formation of tau tangles—abnormal clumps of protein inside brain neurons—which can ultimately kill brain cells, trigger neuroinflammation, and result in dementia.

For levetiracetam to serve as an effective Alzheimer’s preventive, high-risk individuals would need to begin treatment “very, very early,” potentially up to 20 years before elevated levels of amyloid-beta 42 are detected. “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,” Savas cautioned.

The research team also analyzed existing clinical data to assess whether Alzheimer’s patients taking levetiracetam experienced a slower cognitive decline. They found that these patients had a “significant delay” in the time from cognitive decline to death compared to those not on the medication. “Although the magnitude of change was small (on the scale of a few years), this analysis supports the positive effect of levetiracetam to slow the progression of Alzheimer’s pathology,” Savas stated.

Looking ahead, the research team aims to recruit individuals with genetic forms of Alzheimer’s for further testing. However, the study does have limitations, including its reliance on animal models and cultured cells, with no human trials conducted to date. As the study was observational, it cannot definitively prove that levetiracetam caused the prevention of toxic brain proteins.

Savas acknowledged that while levetiracetam shows promise, it is not without its drawbacks. The medication breaks down in the body relatively quickly, prompting the research team to work on developing a “better version” that would have a longer duration of action and more effectively target the mechanism responsible for preventing plaque production.

Common side effects of levetiracetam include drowsiness, weakness, dizziness, irritability, headache, loss of appetite, and nasal congestion. The medication has also been associated with potential mood and behavior changes, such as anxiety, depression, agitation, and aggression. In rare cases, it may lead to severe allergic reactions, skin reactions, blood disorders, and suicidal ideation.

Funding for this study was provided by the National Institutes of Health and the Cure Alzheimer’s Fund. For further details, Fox News Digital reached out to both the drug manufacturer and the researchers for additional comments.

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