Abstract
Parkinson’s disease (PD) is a neurodegenerative disease associated with severe disability and adverse effects on life quality. In PD, motor dysfunction can occur, such as quiescence, muscle stiffness, and postural instability. PD is also associated with autonomic nervous dysfunction, sleep disorders, psychiatric symptoms, and other non-motor symptoms. Degeneration of dopaminergic neurons in the substantia nigra compact (SNPC), Lewy body, and neuroinflammation are the main pathological features of PD. The death or dysfunction of dopaminergic neurons in the dense part of the substantia nigra leads to dopamine deficiency in the basal ganglia and motor dysfunction. The formation of the Lewy body is associated with the misfolding of α-synuclein, which becomes insoluble and abnormally aggregated. Astrocytes and microglia mainly cause neuroinflammation, and the activation of a variety of pro-inflammatory transcription factors and regulatory proteins leads to the degeneration of dopaminergic neurons. At present, PD is mainly treated with drugs that increase dopamine concentration or directly stimulate dopamine receptors. Fibroblast growth factor (FGF) is a family of cellular signaling proteins strongly associated with neurodegenerative diseases such as PD. FGF and its receptor (FGFR) play an essential role in the development and maintenance of the nervous system as well as in neuroinflammation and have been shown to improve the survival rate of dopaminergic neurons. This paper summarized the mechanism of FGF and its receptors in the pathological process of PD and related signaling pathways, involving the development and protection of dopaminergic neurons in SNPC, α-synuclein aggregation, mitochondrial dysfunction, and neuroinflammation. It provides a reference for developing drugs to slow down or prevent the potential of PD.
Highlights
Parkinson’s disease (PD) is considered the most common neurodegenerative disease after Alzheimer’s disease (Feigin et al, 2017)
These findings indicate that endoplasmic reticulum stress in dopaminergic neurons is positively correlated with misfolded α-synuclein
Experiments have demonstrated that Fibroblast growth factor (FGF)-21 ameliorates dopaminergic neuron loss and α-synuclein pathological abnormalities in vivo and in vitro models of PD, and the SIRT1-autophagy axis plays an essential role in fibroblast growth factor 21 (FGF-21) induced α-synuclein clearance (Chen et al, 2020)
Summary
Parkinson’s disease (PD) is considered the most common neurodegenerative disease after Alzheimer’s disease (Feigin et al, 2017). In PD model, FGF can provide effective protection against dopaminergic neuron loss, promote the development and survival of nervous system, relieve neurological symptoms and exert neurotrophic activity on DA neurons in vivo and in vitro. These findings indicate the importance of FGF in the differentiation and survival of dopamine neurons, and the etiology and treatment of PD (Ye et al, 1998; Tanaka et al, 2001; Timmer et al, 2007; Mäkelä et al, 2014). This review will provide an overview of this growth factor family, summarize its significance in the pathophysiology of PD, and discuss possible opportunities for targets to obtain new treatment strategies
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