Common drug may stop Alzheimer's process before it begins

Northwestern researchers report that the anti‑seizure drug levetiracetam can block early production of the amyloid‑beta 42 protein in laboratory models, and the team says the effect would require treatment long before symptoms appear.

Researchers at Northwestern University report that the anti‑seizure drug levetiracetam can prevent neurons from producing the amyloid‑beta 42 protein linked to Alzheimer's in laboratory models. The study combined experiments in genetically engineered mice, lab‑grown human neurons, and brain tissue from people with Down syndrome to examine where the toxic peptide forms. The team found amyloid‑beta 42 accumulates inside synaptic vesicles and showed levetiracetam alters synaptic vesicle recycling through the SV2A protein. Investigators describe the drug's action as preventive rather than restorative, and say it would need to be given well before clinical symptoms appear. Key findings: - Levetiracetam binds the SV2A protein and slightly slows synaptic vesicle recycling, which keeps amyloid precursor protein (APP) on the cell surface longer and reduces routing that leads to amyloid‑beta 42 production. - Evidence came from genetically engineered mice, cultured human neurons, and brain tissue from people with Down syndrome, who are at high genetic risk of early Alzheimer's. - The team analyzed existing clinical records and found patients who had taken levetiracetam showed a longer interval between onset of cognitive decline and death, but investigators described this as a correlative finding rather than results from a controlled trial. - Researchers say levetiracetam would be unlikely to help people with established dementia because the study targets an early step in pathology rather than existing damage. - The investigators noted levetiracetam breaks down quickly and are working on longer‑lasting compounds that better target the same mechanism. Summary: The study identifies a mechanism that appears to prevent production of the toxic amyloid‑beta 42 peptide rather than clearing existing plaques, which could shift research attention toward earlier intervention strategies. The human data cited are correlative and not from randomized clinical trials, and investigators are developing longer‑lasting versions of the compound to act on the same pathway. Undetermined at this time.