摘要
Due to their intense electrical activity,neurons have high energy demands.This requirement makes them particularly sensitive to mitochondrial dysfunction.Like all eukaryotic cells,neurons have intrinsic mechanisms to mitigate the impact of mitochondrial dysfunction and its consequent production of toxic substances.Among such(neuro)protective mechanisms,mitochondrial autophagy(mitophagy)is responsible for the removal of dysfunctional mitochondria.Pathological inhibition of mitophagy,together with insufficient mitochondrial activity,results in a shortage of adenosine triphosphate(ATP)and the accumulation of reactive oxygen species(ROS)(Simmons et al.,2020).
基金
financed by the European Regional Development Fund(ERDF),through the COMPETE 2020-Operational Programme for Competitiveness and Internationalization,under the project POCI-01-0145-FEDER-029391(Mito4ALS)
by Portuguese national funds via FCT-Fundação para a Ciência e a Tecnologia,under the projects UIDB/04539/2020,UIDP/04539/2020,LA/P/0058/2020,and UIDB/00081/2020
by the European Social Fund,through the DL57/2016-SFRH/BPD/84473/2012 to AID.
