ArticleJournal of affective disorders2011
Tyrosine kinase B protein expression is reduced in the cerebellum of patients with bipolar disorder.
Article in Journal of affective disorders, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Manic switching from depression is affected by adult hippocampal neurogenesis.Animal cells and systems · 2026Article
- Exploration of interaction interface of TRKβ/BDNF through fingerprint analysis to disinter potential agonists.Molecular diversity · 2024Article
- Review
- Supra-second interval timing in bipolar disorder: examining the role of disorder sub-type, mood, and medication status.International journal of bipolar disorders · 2023Article
- Emotional and Spontaneous Locomotor Behaviors Related to cerebellar Daidzein-dependent TrkB Expression Changes in Obese Hamsters.Cerebellum (London, England) · 2023Article
- Supra-second interval timing in bipolar disorder: examining the role of disorder sub-type, mood, and medication status.Research square · 2023Article
- Building better brains: the pleiotropic function of neurotrophic factors in postnatal cerebellar development.Frontiers in molecular neuroscience · 2023Review
- Aberrant cerebellar connectivity in bipolar disorder with psychosis.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2017Article
- BDNF and NGF Signalling in Early Phases of Psychosis: Relationship With Inflammation and Response to Antipsychotics After 1 Year.Schizophrenia bulletin · 2016Article
- Intracerebral Administration of BDNF Protects Rat Brain Against Oxidative Stress Induced by Ouabain in an Animal Model of Mania.Molecular neurobiology · 2015Article
- Dysregulation of miR-34a links neuronal development to genetic risk factors for bipolar disorder.Molecular psychiatry · 2015Article
- Expression of full-length and truncated trkB in human striatum and substantia nigra neurons: implications for Parkinson's disease.Journal of molecular histology · 2014Article
- Decreased BDNF and TrkB mRNA expression in multiple cortical areas of patients with schizophrenia and mood disorders.Translational psychiatry · 2014Article
- Cis-acting regulation of brain-specific ANK3 gene expression by a genetic variant associated with bipolar disorder.Molecular psychiatry · 2013Article
- TrkB receptor signalling: implications in neurodegenerative, psychiatric and proliferative disorders.International journal of molecular sciences · 2013Review
- BDNF-TrkB signaling and neuroprotection in schizophrenia.Asian journal of psychiatry · 2013Review
- Neurobiology of bipolar disorders: a review of genetic components, signaling pathways, biochemical changes, and neuroimaging findings.Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999)Review
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThe role of the cerebellum in coordinating mental activity is supported by its connections with cerebral regions involved in cognitive/affective functioning, with decreased activities on functional neuroimaging observed in the cerebellum of schizophrenia patients performing mental tasks. Brain-derived neurotrophic factor (BDNF)-induced activation of tyrosine kinase B (TrkB) is essential to synaptic plasticity. We hypothesized that alterations in BDNF and TrkB expression in the cerebellum were associated with schizophrenia and affective disorders.
methodsWe employed immunohistochemistry and immunoblotting to quantify protein expression of BDNF and TrkB in the cerebellum of patients with schizophrenia, bipolar disorder, and major depression compared to controls (n=15 each).
resultsWhile TrkB immunoreactivity in each of the molecular and granule-cell layers was reduced in all 3 disease groups (12-34%) compared to the control (P=0.018 and 0.038, respectively, ANOVA), only the reduction in bipolar disorder remained statistically significant upon Tukey-Kramer post hoc analyses (P=0.019 and 0.021, respectively). Apparent decreases in BDNF immunoreactivity in all 3 disease groups (12-30%) compared to the control were not statistically significant. TrkB immunoreactivity was not significantly associated with any of the demographic, clinical, and postmortem variables. Immunoblotting displayed an 85-kDa TrkB-immunoreactive band, consistent with a truncated isoform, in all 60 cases. LIMITATIONS: On immunoblotting, apparent decreases in 85-kDa-TrkB levels in all 3 disease groups compared to the control were not statistically significant.
conclusionsOur finding of reduced TrkB expression in bipolar disorder suggests that dysregulation of TrkB-mediated neurotrophin signaling in the cerebellum may play a role in the pathophysiology of this disease.
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Registered trials
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