SynthesisMolecular psychiatry2025
The habenula in mood disorders: A systematic review of human studies.
Synthesis in Molecular psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- Rapid antidepressant potential of nitrous oxide: current state and major questions.Molecular psychiatry · 2026Review
- Habenular structural-functional dysconnectivity in bipolar disorder: evidence from multimodal imaging and transcriptomic integration.BMC psychiatry · 2026Article
- The lateral habenula as a master regulator of innate and learned social behaviors.Psychopharmacology · 2026Review
- NMDA receptors are not necessary for burst firing of lateral habenula neurons in mice.Frontiers in psychiatry · 2026Article
- Neural signaling mechanisms in depression: bridging classical monoamine hypotheses, animal models, and emerging antidepressant strategies.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
4 authors.
Funding
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Abstract
backgroundIn animal models, the habenula has been identified as a key structure involved in mood disorders (MDs). Thanks to recent technological advancements, a burgeoning body of work has also investigated the habenula in the context of human MDs.
objectiveThis systematic review aims to synthesize findings from human studies concerning the habenula and its relationship with MDs. The review was conducted according to PRISMA guidelines. The literature search yielded 93 articles, of which 50 articles were included in the review.
resultsWe found that the evidence for baseline habenular hyperactivity in human depression is mixed. Although the finding of baseline habenular hyperactivity is widely replicated in animal models of depression, the available evidence is not sufficient to either conclude the presence or the absence of this hyperactivity in human depression. As for findings from resting-state functional connectivity (RSFC) studies, they were mainly inconsistent across studies. Nevertheless, a notable observation is that alterations in connectivity between the habenula and regions of the default mode network (DMN) were overrepresented in the results, suggesting that connections between the habenula and DMN regions may play a role in MDs. Lastly, we found no evidence indicating that MDs are linked to changes in habenular volume.
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