What's Happening?
Researchers at Northwestern University have discovered that levetiracetam, an FDA-approved anti-seizure drug, can prevent the formation of amyloid plaques associated with Alzheimer's disease. The study, published in Science Translational Medicine, reveals
that levetiracetam stops the production of amyloid-beta 42 peptides, which are toxic protein fragments linked to Alzheimer's. The drug's effectiveness is contingent on early administration, potentially up to 20 years before symptoms appear, making it particularly beneficial for individuals at high genetic risk, such as those with Down syndrome. The research highlights a new mechanism that could open doors for additional drug targets.
Why It's Important?
This discovery is significant as it offers a potential preventive measure for Alzheimer's, a disease that affects millions and currently lacks a cure. By targeting the production of amyloid-beta 42 peptides early, levetiracetam could delay or prevent the onset of Alzheimer's symptoms, particularly in genetically predisposed individuals. This could lead to a shift in how Alzheimer's is managed, focusing on prevention rather than treatment of symptoms. The findings also suggest that existing drugs could be repurposed, potentially accelerating the availability of new treatments and reducing the time and cost associated with drug development.
What's Next?
The research team plans to identify patient populations with genetic forms of Alzheimer's to test the drug's preventive capabilities further. They are also working on developing a more effective version of levetiracetam that lasts longer in the body. These efforts could lead to clinical trials and, eventually, a new preventive treatment for Alzheimer's. The study's findings may prompt further research into other existing drugs that could be repurposed for Alzheimer's prevention.
