ArticleSchizophrenia bulletin2025
Impact of Relapse in BDNF Receptors Expression in Patients With a First Episode of Schizophrenia.
Article in Schizophrenia bulletin, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
Abstract
background and hypothesisRelapsing after a first episode of schizophrenia (FES) is a main predictor of clinical and functional prognosis. Brain-derived neurotrophic factor (BDNF) plays a critical role in neuronal development and plasticity, and its signaling may be altered by successive relapses.
designWe assessed the impact of first relapse in the expression of the 2 isoforms of the BDNF tropomyosin-related kinase B (TrkB) receptor (active full-length TrkB-F and inactive truncated TrkB-T) in peripheral blood mononuclear cells from 53 FES patients in clinical remission followed up for 3 years.
resultsThe group of participants that relapsed (n = 24) during the follow-up presented a significant decrease in the expression of the active TrkB-F receptor compared to baseline (M = 100 ± 28.13 vs. M = 83.42 ± 33.84, t = 2.5, P = .02), with no changes in the inactive TrkB-T receptor expression nor in BDNF plasma levels. This decrease also led to a significant decline in the F/T ratio (M = 1.13 ± 0.38 vs. 0.94 ± 0.36, t = 2.17, P = .041). No significant differences were found in the receptors' expression nor in plasma levels in the group of cases that remained in remission (n = 29). These results were not associated with baseline differences between the groups in terms of the BDNF signaling pathway biomarkers, clinical or treatment variables.
conclusionsThese findings highlight the biological impact that a relapse produces over the systemic BDNF-TrkB signaling pathway, potentially undermining crucial neuronal functions. Identifying the actors involved can help design specific interventions for relapse prevention and improve the functional prognosis of people in the early stages of schizophrenia.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.