Brain-Derived Neurotrophic Factor in Schizophrenia Pathophysiology
Summary
Brain-Derived Neurotrophic Factor (BDNF) is a pivotal regulator of neuronal survival, differentiation and synaptic plasticity. In schizophrenia, alterations in BDNF expression and signalling through its high-affinity receptor TrkB have been implicated in the neurodevelopmental disturbances and cortical connectivity deficits that typify the disorder. Reduced BDNF levels have been detected in both central and peripheral compartments of affected individuals, correlating with hippocampal volume loss, impaired cognitive performance and severity of negative and depressive symptoms. Genetic variants such as the Val66Met polymorphism influence intracellular trafficking and activity-dependent secretion of BDNF, thereby modulating susceptibility to psychosis and treatment response. Dysregulation of downstream cascades—particularly the PI3K/AKT, MAPK/ERK and CREB pathways—further compromises synaptic maintenance and neuronal resilience. Efforts to restore BDNF function encompass pharmacological agents, nutritional interventions and cognitive or physical training. As a biomarker, BDNF offers promise for early detection, stratification of clinical subtypes and monitoring of therapeutic efficacy, with significant implications for personalised medicine and global mental health strategies.
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Brain-Derived Neurotrophic Factor in Schizophrenia Pathophysiology publication trend
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Technical terms
Brain-Derived Neurotrophic Factor (BDNF): A protein essential for neuronal growth, survival and synaptic plasticity.
TrkB: The high-affinity receptor for BDNF that activates intracellular signalling cascades.
Synaptic Plasticity: The ability of synapses to strengthen or weaken over time, critical for learning and memory.
PI3K/AKT Pathway: An intracellular signalling route promoting cell survival and growth downstream of TrkB activation.
CREB: A transcription factor regulated by BDNF-mediated signalling, involved in long-term synaptic changes.
Val66Met Polymorphism: A common genetic variant in the BDNF gene affecting activity-dependent secretion of the protein.
References
- TNF receptor 2 knockout mouse had reduced lung cancer growth and schizophrenia-like behavior through a decrease in TrkB-dependent BDNF level. Archives of Pharmacal Research (2024).
- The month of walking alone and BDNF level differ between drug-naive first-episode schizophrenia patients and healthy controls. Frontiers in Molecular Neuroscience (2023).
- Study on correlations of BDNF, PI3K, AKT and CREB levels with depressive emotion and impulsive behaviors in drug-naïve patients with first-episode schizophrenia. BMC Psychiatry (2023).
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