Seizure Drug May Halt Alzheimer's Before It Starts

Researchers have identified a potential new avenue for Alzheimer's disease prevention using levetiracetam, a medication historically prescribed for seizures. A recent Northwestern University study indicated that this drug can inhibit the development of toxic amyloid beta peptides, which are commonly found in the brains of Alzheimer's patients. The research demonstrated that levetiracetam's effect was observed in both animal models and human neuron cultures. This preventative mechanism also showed promise in post-mortem human brain tissue from individuals with Down syndrome, a group at higher risk for Alzheimer's.

Unlike current Alzheimer's treatments that clear existing amyloid plaques, this mechanism focuses on preventing the initial production of harmful peptides. Scientists noted that the brain's ability to manage this process diminishes with age, leading to increased amyloid-beta 42 production in individuals developing Alzheimer's. For levetiracetam to be effective as an Alzheimer's preventative, high-risk individuals would need to begin treatment much earlier, potentially up to two decades before elevated amyloid-beta 42 levels appear, as it cannot counteract irreversible brain changes or cell death once dementia has set in.

Further analysis of existing human clinical data suggested that patients taking levetiracetam experienced a slower cognitive decline. While this effect was noted to be modest, it supports the drug's potential to slow Alzheimer's pathology. The research team plans to investigate levetiracetam's effects in individuals with genetic forms of Alzheimer's. Limitations of the study include its reliance on animal and cell models, and the observational nature of the human data, which cannot definitively prove causation. The researchers are working to develop an improved version of the drug that would be more stable in the body and more effectively target the plaque-production pathway.