ReviewMolecular biology reports2026
BDNF and GSK-3β signaling in depression: molecular mechanisms underlying neural plasticity dysfunction.
Review in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Depression, a complicated psychiatric condition, is characterized by persistent low mood, disrupted emotional regulation, and cognitive impairment. Attenuated brain-derived neurotrophic factor (BDNF) and dysregulated glycogen synthase kinase-3 beta (GSK-3β) activity promote synaptic deterioration, oxidative imbalance, neuroinflammatory responses, and hippocampal dysfunction, hallmark features of depressive pathology. This review provides an overview of current preclinical and clinical findings explaining the independent and interactive roles of BDNF and GSK-3β in depression. It further illustrates emerging therapeutic approaches targeting this axis, such as metformin, famotidine, tideglusib, lithium, and ketamine. Collectively, the altered crosstalk between BDNF and GSK-3β contributes to the impaired neuroplasticity observed in depression, suggesting that this signaling axis is a promising therapeutic target.
Indexed as
Identifiers
42417900What Socratic holds
Registered trials
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.