ArticleJournal of molecular histology2014
Expression of full-length and truncated trkB in human striatum and substantia nigra neurons: implications for Parkinson's disease.
Article in Journal of molecular histology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- TrkB Truncated Isoform Receptors as Transducers and Determinants of BDNF Functions.Frontiers in neuroscience · 2022Pooled it
- Redefining Parkinson's Disease management: the synergistic role of neurotrophic factors and mitochondria.Cellular and molecular life sciences : CMLS · 2026Review
- The Intricate Relationship of Trk Receptors in Brain Diseases and Disorders.Molecular neurobiology · 2025Review
- BDNF/proBDNF Interplay in the Mediation of Neuronal Apoptotic Mechanisms in Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- Development of Pleiotropic TrkB and 5-HTMolecules (Basel, Switzerland) · 2024Article
- DAT1 and BDNF polymorphisms interact to predict Aβ and tau pathology.Neurobiology of aging · 2024Article
- Hypothalamic TrkB.FL overexpression improves metabolic outcomes in the BTBR mouse model of autism.PloS one · 2023Article
- An Ultra-Low Dose of ∆9-Tetrahydrocannabinol Alleviates Alzheimer's Disease-Related Cognitive Impairments and Modulates TrkB Receptor Expression in a 5XFAD Mouse Model.International journal of molecular sciences · 2022Article
- New Frontiers in Neurodegeneration and Regeneration Associated with Brain-Derived Neurotrophic Factor and the rs6265 Single Nucleotide Polymorphism.International journal of molecular sciences · 2022Review
- RNA and neuronal function: the importance of post-transcriptional regulation.Oxford open neuroscience · 2022Review
- Review
- Parkinson's Disease-Associated Changes in the Expression of Neurotrophic Factors and their Receptors upon Neuronal Differentiation of Human Induced Pluripotent Stem Cells.Journal of molecular neuroscience : MN · 2020Article
- Regulation of BDNF-TrkB Signaling and Potential Therapeutic Strategies for Parkinson's Disease.Journal of clinical medicine · 2020Review
- Chaperone Sigma1R mediates the neuroprotective action of afobazole in the 6-OHDA model of Parkinson's disease.Scientific reports · 2019Article
- Rbfox1 up-regulation impairs BDNF-dependent hippocampal LTP by dysregulating TrkB isoform expression levels.eLife · 2019Article
- NT-4/5 antagonizes the BDNF modulation of corticostriatal transmission: Role of the TrkB.T1 receptor.CNS neuroscience & therapeutics · 2019Article
- Electro-Acupuncture Ameliorated MPTP-Induced Parkinsonism in Mice via TrkB Neurotrophic Signaling.Frontiers in neuroscience · 2019Article
- Inhibiting TRK Proteins in Clinical Cancer Therapy.Cancers · 2018Review
- Integral Characterization of Defective BDNF/TrkB Signalling in Neurological and Psychiatric Disorders Leads the Way to New Therapies.International journal of molecular sciences · 2017Review
- Neurotrophin signalling: novel insights into mechanisms and pathophysiology.Clinical science (London, England : 1979) · 2017Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain derived neurotrophic factor (BDNF) is a potent mediator of cell survival and differentiation and can reverse neuronal injury associated with Parkinson's disease (PD). Tropomyosin receptor kinase B (trkB) is the high affinity receptor for BDNF. There are two major trkB isoforms, the full-length receptor (trkB.tk(+)) and the truncated receptor (trkB.t1), that mediate the diverse, region specific functions of BDNF. Both trkB isoforms are widely distributed throughout the brain, but the isoform specific distribution of trkB.t1 and trkB.tk(+) to human neurons is not well characterized. Therefore, we report the regional and neuronal distribution of trkB.tk(+) and trkB.t1 in the striatum and substantia nigra pars compacta (SNpc) of human autopsy tissues from control and PD cases. In both PD and control tissues, we found abundant, punctate distribution of trkB.tk(+) and trkB.t1 proteins in striatum and SNpc neurons. In PD, trkB.tk(+) is decreased in striatal neurites, increased in striatal somata, decreased in SNpc somata and dendrites, and increased in SNpc axons. TrkB.t1 is increased in striatal somata, decreased in striatal axons, and increased in SNpc distal dendrites. We believe changes in trkB isoform distribution and expression levels may be markers of pathology and affect the neuronal response to BDNF.
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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.