Fibroblast growth factor 21 and autophagy: A complex interplay in Parkinson disease

Violina Kakoty, Sarathlal K C, Ruei Dun Tang, Chih Hao Yang, Sunil Kumar Dubey, Rajeev Taliyan

研究成果: 雜誌貢獻回顧型文獻同行評審

19 引文 斯高帕斯(Scopus)


Parkinson disease (PD) is the second common neurodegenerative disorder after Alzheimer's disease (AD). The predominant pathological hallmark is progressive loss of dopaminergic (DA) neurones in the substantia nigra (SN) complicated by aggregation of misfolded forms of alpha-synuclein (α-syn). α-syn is a cytosolic synaptic protein localized in the presynaptic neuron under normal circumstances. What drives misfolding of this protein is largely unknown. However, recent studies suggest that autophagy might be an important risk factor for contributing towards PD. Autophagy is an evolutionarily conserved mechanism that causes the clearance or degradation of misfolded, mutated and damaged proteins, organelles etc. However, in an aging individual this process might deteriorate which could possibly lead to the accumulation of damaged proteins. Hence, autophagy modulation might provide some interesting cues for the treatment of PD. Additionally, Fibroblast growth factor 21 (FGF21) which is known for its role as a potent regulator of glucose and energy metabolism has also proved to be neuroprotective in various neurodegenerative conditions possibly via mediation of autophagy.
期刊Biomedicine and Pharmacotherapy
出版狀態已發佈 - 7月 2020

ASJC Scopus subject areas

  • 藥理


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