Overview
- An UCSF-led study published as a Letter in Nature Aging identifies FTL1 as uniquely elevated with age in the hippocampus and linked to poorer memory performance.
- Increasing FTL1 in young animals reduced synaptic connectivity and impaired performance on hippocampal-dependent tasks such as the Y maze and novel object recognition.
- Reducing FTL1 in aged animals restored synaptic markers and dendritic complexity and improved memory, demonstrating bidirectional control over age-related deficits.
- Mechanistic assays showed excess FTL1 suppresses mitochondrial ATP production, and NADH supplementation rescued neurite outgrowth and mitigated cognitive impairments.
- Findings are preclinical and based on male animals focused on the hippocampus, with authors noting the need for studies in females, broader brain regions, long-term safety, and human validation.