Neuroprotection, Growth Factors and BDNF-TrkB Signalling in Retinal Degeneration
AbstractNeurotrophic factors play key roles in the development and survival of neurons. The potent neuroprotective effects of neurotrophic factors, including brain-derived neurotrophic factor (BDNF), ciliary neurotrophic factor (CNTF), glial cell-line derived neurotrophic factor (GDNF) and nerve growth factor (NGF), suggest that they are good therapeutic candidates for neurodegenerative diseases. Glaucoma is a neurodegenerative disease of the eye that causes irreversible blindness. It is characterized by damage to the optic nerve, usually due to high intraocular pressure (IOP), and progressive degeneration of retinal neurons called retinal ganglion cells (RGCs). Current therapy for glaucoma focuses on reduction of IOP, but neuroprotection may also be beneficial. BDNF is a powerful neuroprotective agent especially for RGCs. Exogenous application of BDNF to the retina and increased BDNF expression in retinal neurons using viral vector systems are both effective in protecting RGCs from damage. Furthermore, induction of BDNF expression by agents such as valproic acid has also been beneficial in promoting RGC survival. In this review, we discuss the therapeutic potential of neurotrophic factors in retinal diseases and focus on the differential roles of glial and neuronal TrkB in neuroprotection. We also discuss the role of neurotrophic factors in neuroregeneration. View Full-Text
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Kimura, A.; Namekata, K.; Guo, X.; Harada, C.; Harada, T. Neuroprotection, Growth Factors and BDNF-TrkB Signalling in Retinal Degeneration. Int. J. Mol. Sci. 2016, 17, 1584.
Kimura A, Namekata K, Guo X, Harada C, Harada T. Neuroprotection, Growth Factors and BDNF-TrkB Signalling in Retinal Degeneration. International Journal of Molecular Sciences. 2016; 17(9):1584.Chicago/Turabian Style
Kimura, Atsuko; Namekata, Kazuhiko; Guo, Xiaoli; Harada, Chikako; Harada, Takayuki. 2016. "Neuroprotection, Growth Factors and BDNF-TrkB Signalling in Retinal Degeneration." Int. J. Mol. Sci. 17, no. 9: 1584.