Role of Brain Derived Neurotrophic Factor and Related Therapeutic Strategies in Central Post-Stroke Pain.

Autor: Rajamanickam G; Calcium Signalling Laboratory, National Neuroscience Institute, 11 Jalan Tan Tock Seng, Singapore, 308433, Singapore., Lee ATH; Health and Social Sciences Cluster, Singapore Institute of Technology, Singapore, Singapore., Liao P; Calcium Signalling Laboratory, National Neuroscience Institute, 11 Jalan Tan Tock Seng, Singapore, 308433, Singapore. ping_liao@nni.com.sg.; Health and Social Sciences Cluster, Singapore Institute of Technology, Singapore, Singapore. ping_liao@nni.com.sg.; Duke-NUS Medical School, Singapore, Singapore. ping_liao@nni.com.sg.
Jazyk: angličtina
Zdroj: Neurochemical research [Neurochem Res] 2024 Sep; Vol. 49 (9), pp. 2303-2318. Date of Electronic Publication: 2024 Jun 10.
DOI: 10.1007/s11064-024-04175-z
Abstrakt: Brain-derived neurotrophic factor (BDNF) is vital for synaptic plasticity, cell persistence, and neuronal development in peripheral and central nervous systems (CNS). Numerous intracellular signalling pathways involving BDNF are well recognized to affect neurogenesis, synaptic function, cell viability, and cognitive function, which in turn affects pathological and physiological aspects of neurons. Stroke has a significant psycho-socioeconomic impact globally. Central post-stroke pain (CPSP), also known as a type of chronic neuropathic pain, is caused by injury to the CNS following a stroke, specifically damage to the somatosensory system. BDNF regulates a broad range of functions directly or via its biologically active isoforms, regulating multiple signalling pathways through interactions with different types of receptors. BDNF has been shown to play a major role in facilitating neuroplasticity during post-stroke recovery and a pro-nociceptive role in pain development in the nervous system. BDNF-tyrosine kinase receptors B (TrkB) pathway promotes neurite outgrowth, neurogenesis, and the prevention of apoptosis, which helps in stroke recovery. Meanwhile, BDNF overexpression plays a role in CPSP via the activation of purinergic receptors P2X4R and P2X7R. The neuronal hyperexcitability that causes CPSP is linked with BDNF-TrkB interactions, changes in ion channels and inflammatory reactions. This review provides an overview of BDNF synthesis, interactions with certain receptors, and potential functions in regulating signalling pathways associated with stroke and CPSP. The pathophysiological mechanisms underlying CPSP, the role of BDNF in CPSP, and the challenges and current treatment strategies targeting BDNF are also discussed.
(© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)
Databáze: MEDLINE
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