Levetiracetam, a common anti-seizure drug, prevents Alzheimer’s plaques in lab and human samples
Northwestern researchers report that levetiracetam stops neurons from making toxic amyloid-beta 42 by altering APP trafficking, based on mouse models, cultured human neurons and brains from people with Down syndrome, study published Feb 11 in Science Translational Medicine.
- Levetiracetam binds the synaptic protein SV2A and slows synaptic vesicle recycling so APP stays on the neuron surface and is diverted away from producing amyloid-beta 42.
- The effect was observed in genetically engineered mouse models, cultured human neurons and brain tissue from people with Down syndrome, who are at high risk of early Alzheimer’s.
- Levetiracetam is an FDA-approved, decades-old anti-seizure drug and analysis of clinical data found patients on the drug had a modest delay from cognitive decline to death compared with lorazepam or no/other anti-epileptics.
- Researchers emphasize the drug would likely need to be started very early, potentially decades before symptoms, and would not reverse established dementia.
- The team is working on longer lasting versions of levetiracetam to better target the mechanism and improve therapeutic potential.