Suppression of follistatin by spontaneous seizures dysregulates neurogenesis in a model of Alzheimer’s disease neuropathology
Researchers identified that the protein follistatin is suppressed by spontaneous seizures in Alzheimer's disease models, which in turn disrupts neurogenesis. Restoring follistatin levels was shown to normalize neurogenesis dynamics in these models.
Why it matters
This discovery provides a potential new therapeutic target for addressing cognitive decline and neurogenesis issues in Alzheimer's patients who experience seizures.
Communications Biology ( 2026 ) Cite this article
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