ArticleTranslational psychiatry2026
Cholinergic basal forebrain modulation of glymphatic function: implications for depression.
Article in Translational psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Abnormal resting-state functional connectivity in anhedonia: A systematic review and meta-analysis.Brain imaging and behavior · 2026Pooled it
- From synapse to strategy: a bibliometric map of ionotropic glutamate receptors in depression.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
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Authors and funding
9 authors.
Funding
Abstract
Emerging evidence links glymphatic dysfunction to depression, yet its regulatory mechanisms remain unclear. Through multimodal neuroimaging of two independent cohorts, we tested the hypothesis that the cholinergic basal forebrain (ChBF) modulates glymphatic function and thereby contributes to depression. Glymphatic function was indexed using two indirect MRI markers: the diffusion tensor image analysis along the perivascular space (DTI-ALPS) index and coupling between global blood-oxygen-level-dependent signals and cerebrospinal fluid signals (gBOLD-CSF coupling). In a stroke cohort, we explored ChBF-glymphatic-depression interactions through dual perspectives: acute lesion effects and longitudinal recovery. Baseline lesion network mapping analysis (n = 189) revealed that functional connectivity (FC) between ChBF and lesion predicted glymphatic impairment. Longitudinal resting-state fMRI analysis (n = 71) demonstrated that recovery of ChBF whole-brain FC correlated with glymphatic restoration. Glymphatic dysfunction mediated the association between ChBF damage and post-stroke depression severity. Subsequently, we validated these findings in non-stroke cohort (n = 38) receiving transcranial magnetic stimulation. FC between the stimulation site and ChBF predicted glymphatic improvement, with enhanced ChBF whole-brain FC mediating this association. Furthermore, increased ChBF whole-brain FC was correlated with antidepressant efficacy and glymphatic enhancement mediated this relationship. Our findings identify that ChBF play a regulatory role in glymphatic function, which in turn influences depression. This study provides a theoretical foundation for the development of glymphatic-based therapeutic strategies for depression.
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