Purpose Of Review: To review the role of brain-derived neurotrophic factor (BDNF) in neuroplasticity related to schizophrenia and the recent findings that have been reported on the status of BDNF in patients with schizophrenia and its association with the clinical measures.
Recent Findings: Peripheral BDNF levels have been found altered in first-episode patients with psychosis and also in chronic schizophrenia patients. A few studies have reported changes in peripheral BDNF levels following antipsychotic treatment. The role of Val66Met polymorphism in BDNF has been shown to play an important role in structural and functional plasticity in schizophrenia.
Summary: Although peripheral BDNF levels hold promise for providing new perspectives for the development of novel therapeutic strategies for the treatment of schizophrenia, additional studies including efforts to prove its potential as a biomarker are warranted.
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http://dx.doi.org/10.1097/YCO.0b013e3283436eb7 | DOI Listing |
Neuroscience
January 2025
Center of Health Sciences, Department of Physiology and Pharmacology, Federal University of Santa Maria, Santa Maria, RS, Brazil; Center of Health Sciences, Postgraduate Program in Pharmacology, Federal University of Santa Maria, Santa Maria, RS, Brazil. Electronic address:
Major depressive disorder (MDD) is a complex neuropsychiatric disorder potentially influenced by factors such as stress and inflammation. Chronic stress can lead to maladaptive brain changes that may trigger immune hyperactivation, contributing to MDD's pathogenesis. While the involvement of inflammation in MDD is well established, the effects of inflammatory preconditioning in animals subsequently exposed to chronic stress remain unclear.
View Article and Find Full Text PDFBrain Behav
January 2025
Biggs Institute, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
Background: This systematic review and meta-analysis evaluates peripheral and CNS BDNF levels in glioma patients.
Methods: Following PRISMA guidelines, we systematically searched databases for studies measuring BDNF in glioma patients and controls. After screening and data extraction, we conducted quality assessment, meta-analysis, and meta-regression.
Nutrients
December 2024
The Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences, 05-110 Jabłonna, Poland.
Although physical activity and balanced diet may increase peripheral brain-derived neurotrophic factor (BDNF) concentration, little is known about whether these factors modify BDNF content in physically active individuals and whether the serum fatty acid (FA) profile is related. This study aimed to evaluate quality of diet, identify specific dietary patterns and assess their influence on BDNF and FA levels in serum. It is hypothesized that there is a correlation between diet quality and the concentrations of BDNF and FA in the serum of physically active male individuals.
View Article and Find Full Text PDFbioRxiv
December 2024
Center for Pain Therapeutics and Addiction Research, School of Dentistry, University of Texas Health San Antonio, Texas, 78229, USA.
Truncated TrkB (TrkBT1), traditionally considered a dominant-negative regulator of full-length TrkB (TrkBTK+), remains poorly understood in peripheral sensory neurons, particularly nociceptors. Furthermore, sensory neuronal TrkB expression and function has been traditionally associated with non-nociceptive neurons, particularly Aδ low-threshold mechanoreceptors. This study challenges prevailing assumptions by demonstrating that TrkBT1 is the predominant TrkB isoform expressed in sensory neurons and plays a functional role in modulating neuronal activity.
View Article and Find Full Text PDFeNeuro
January 2025
Department of Cell Biology, School of Medicine, Emory University, Atlanta, Georgia 30322
Brain-derived neurotrophic factor (BDNF) and tropomyosin receptor kinase B (TrkB) are known to contribute to both protective and pronociceptive processes. However, their contribution to neuropathic pain after spinal cord injury (SCI) needs further investigation. In a recent study utilizing TrkB mice, it was shown that systemic pharmacogenetic inhibition of TrkB signaling with 1NM-PP1 (1NMP) immediately after SCI delayed the onset of pain hypersensitivity, implicating maladaptive TrkB signaling in pain after SCI.
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