| Literature DB >> 33259796 |
Joseph Johnson1, Elizabeth Mercado-Ayon1, Yesica Mercado-Ayon2, Yi Na Dong3, Sarah Halawani3, Lucie Ngaba3, David R Lynch4.
Abstract
In addition to ATP synthesis, mitochondria are highly dynamic organelles that modulate apoptosis, ferroptosis, and inflammasome activation. Through executing these varied functions, the mitochondria play critical roles in the development and progression of neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, and Friedreich ataxia, among others. Impaired mitochondrial biogenesis and abnormal mitochondrial dynamics contribute to mitochondrial dysfunction in these diseases. Additionally, dysfunctional mitochondria play critical roles in signaling for both inflammasome activation and ferroptosis. Therapeutics are being developed to circumvent inflammasome activation and ferroptosis in dysfunctional mitochondria. Targeting these aspects of mitochondrial dysfunction may present viable therapeutic strategies for combatting the neurodegenerative diseases. This review aims to summarize the role of the mitochondria in the development and progression of neurodegenerative diseases and to present current therapeutic approaches that target mitochondrial dysfunction in these diseases.Entities:
Keywords: Ferroptosis; Inflammasome activation; Mitochondrial biogenesis; Mitochondrial dynamics; Mitochondrial dysfunction; Neurodegenerative diseases
Mesh:
Year: 2020 PMID: 33259796 DOI: 10.1016/j.abb.2020.108698
Source DB: PubMed Journal: Arch Biochem Biophys ISSN: 0003-9861 Impact factor: 4.013