review · Journal of Cellular and Molecular Medicine
Parkinson's disease is a neurodegenerative condition causing motor and non-motor symptoms through the loss of dopaminergic neurons in the substantia nigra. The disease mechanisms involve mitochondrial dysfunction, oxidative damage, and programmed cell death. Brain-derived neurotrophic factor, known as BDNF, and its receptor, tropomyosin receptor kinase type B or TrkB, play critical protective roles in these brain areas. BDNF supports the survival of dopaminergic neurons and boosts the function of striatal neurons. Conversely, a deficiency in TrkB leads to the degeneration of dopaminergic cells and the buildup of alpha-synuclein. Signalling through the BDNF and TrkB pathway decreases during the early stages of Parkinson's disease and corresponds with disease severity and long-term complications. Using specific activators to stimulate this pathway offers a potential therapeutic strategy to reduce Parkinson's disease neuropathology.
Parkinson's disease causes debilitating physical and neurological symptoms through progressive neuronal loss. Identifying biological targets that halt or reverse this damage is vital for developing better treatments. Understanding how BDNF and TrkB signalling protects vulnerable brain cells highlights a promising route for designing therapies aimed at preserving neurons, curbing toxic protein accumulation, and slowing disease progression.
The abstract points towards the development of specific BDNF and TrkB activators as potential therapeutic agents for pharmaceutical companies tackling Parkinson's disease. As a conceptual review examining biological pathways and disease mechanisms, the work sits at an early discovery stage. Significant pre-clinical validation and clinical drug development will be required before any commercial or clinical application can be realised.
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Parkinson's disease (PD) is a neurodegenerative disorder of the brain and is manifested by motor and non-motor symptoms because of degenerative changes in dopaminergic neurons of the substantia nigra. PD neuropathology is associated with mitochondrial dysfunction, oxidative damage and apoptosis. Thus, the modulation of mitochondrial dysfunction, oxidative damage and apoptosis by growth factors could be a novel boulevard in the management of PD. Brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin receptor kinase type B (TrkB) are chiefly involved in PD neuropathology. BDNF promotes the survival of dopaminergic neurons in the substantia nigra and enhances the functional activity of striatal neurons. Deficiency of the TrkB receptor triggers degeneration of dopaminergic neurons and accumulation of α-Syn in the substantia nigra. As well, BDNF/TrkB signalling is reduced in the early phase of PD neuropathology. Targeting of BDNF/TrkB signalling by specific activators may attenuate PD neuropathology. Thus, this review aimed to discuss the potential role of BDNF/TrkB activators against PD. In conclusion, BDNF/TrkB signalling is decreased in PD and linked with disease severity and long-term complications. Activation of BDNF/TrkB by specific activators may attenuate PD neuropathology.
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DOI: 10.1111/jcmm.18368
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