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UCSF Identifies Iron-Storage Protein That Reverses Memory Decline in Aged Mice

The mouse findings point to mitochondrial metabolism as a promising lever for restoring hippocampal function.

Overview

  • Published in Nature Aging, the UCSF study pinpointed ferritin light chain 1 as elevated in aged hippocampal neurons using RNA sequencing, transcriptomics and mass spectrometry.
  • Genetically boosting FTL1 in young mice simplified neuronal wiring, reduced synaptic markers, and impaired learning and memory.
  • Reducing FTL1 in older mice restored dendritic complexity, strengthened hippocampal connectivity, and improved performance on memory tasks.
  • Mechanistic assays implicated mitochondrial suppression and lower ATP production, and metabolic stimulation with NADH blocked FTL1-driven defects in cell models.
  • Researchers stress the results are preclinical in mice and cells, with human relevance, safety, sex differences, broader brain effects, and disease models still to be tested.