Evidence map›Paper›PMID 41858650›Full record

ReviewFrontiers in psychiatry2026

Decreased hippocampal neurogenesis and post-stroke depression.

Xiangyue Tang, Lusen Ran, Wenfei Li

Abstract readReview
In one paragraph

Review in Frontiers in psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Xiangyue TangDepartment of Neurology, Shenzhen Nanshan People's Hospital, Shenzhen, China.
Lusen RanDepartment of Neurology, Shenzhen Nanshan People's Hospital, Shenzhen, China.
Wenfei LiDepartment of Neurology, Shenzhen Nanshan People's Hospital, Shenzhen, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Post-stroke depression (PSD) is a common and serious complication following stroke, affecting approximately one-third of survivors and contributing to poor functional recovery. Its pathophysiology is multifactorial, with recent evidence highlighting decreased hippocampal neurogenesis as a key mechanistic contributor. This review aims to examine the specific role of hippocampal neurogenesis in PSD, focusing on (1) the evidence linking impaired neurogenesis to PSD onset (2), the underlying molecular and cellular mechanisms-including dysregulation of the hypothalamic-pituitary-adrenal(HPA) axis, neuroinflammation, altered neurotrophic signaling, and neurotransmitter disturbances-and (3) current and emerging therapeutic strategies that promote neurogenesis for PSD management. Pharmacological agents (e.g., antidepressants), neuroregulatory interventions, and lifestyle-based approaches show promise in restoring neurogenic activity and alleviating depressive symptoms. In conclusion, impaired hippocampal neurogenesis represents a central pathway in PSD pathogenesis, offering a valuable target for future research and therapeutic development. Further studies are needed to fully elucidate these mechanisms and translate neurogenesis-focused treatments into clinical practice.

Indexed as

Antidepressantshippocampusneurogenesisneuroregulationpost-stroke depressiontreatment

Identifiers

PMID41858650
PMCPMC12996108

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.