Molecular Psychiatry, 2022 · DOI: https://doi.org/10.1038/s41380-022-01644-1 · Published: July 7, 2022
Environmental factors like diet have been linked to depression and/or relapse risk in later life. This could be partially driven by the food metabolome, which communicates with the brain via the circulatory system and interacts with hippocampal neurogenesis (HN), a form of brain plasticity implicated in depression aetiology. Here, we used an in vitro model of HN to test the effects of serum samples from a longitudinal ageing cohort of 373 participants, with or without depressive symptomology. 1% participant serum was applied to human fetal hippocampal progenitor cells, and changes in HN markers were related to the occurrence of depressive symptoms across a 12-year period. These findings potentially suggest that diet and altered HN could subsequently shape the trajectory of late-life depressive symptomology.
Dietary modification in later life could represent a potential therapeutic target for depression.
There may be a metabolic dysregulation of neurodifferentiation in the context of late-life depression.
Hippocampal neurogenesis may play a key role in the pathogenesis and/or progression of depression.