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New perspectives on cytoskeletal dysregulation and mitochondrial mislocalization in amyotrophic lateral sclerosis

Translational Neurodegeneration 2021年第4期10卷 595-610页

作者： Frances Theunissen Phillip K.West Samuel Brennan Bojan Petrovic Kosar Hooshmand P.Anthony Akkari Matt Keon boris guennewig Perron Institute for Neurological and Translational Science NedlandsWAAustralia Centre for Molecular Medicine and Innovative Therapeutics Murdoch UniversityMurdochWAAustralia GenieUs Genomics Pty Ltd SydneyNSWAustralia Brain and Mind Centre and Central Clinical School Faculty of Medicine and Healththe University of SydneyamperdownNSWAustralia Division of Neurology Duke University Medical CentreDuke UniversityDurhamNCUSA

Amyotrophic lateral sclerosis(ALS)is a progressive neurodegenerative disease characterized by selective,early degeneration of motor neurons in the brain and spinal cord.Motor neurons have long axonal projections,which rely on the integrity of neuronal cytoskeleton and mitochondria to regulate energy requirements for maintaining axonal stability,anterograde and retrograde transport,and signaling between neurons.The formation of protein aggregates which contain cytoskeletal proteins,and mitochondrial dysfunction both have devastating effects on the function of neurons and are shared pathological features across several neurodegenerative conditions,including ALS,Alzheimer's disease,Parkinson's disease,Huntington's disease and Charcot-Marie-Tooth disease.Furthermore,it is becoming increasingly clear that cytoskeletal integrity and mitochondrial function are intricately linked.Therefore,dysregulations of the cytoskeletal network and mitochondrial homeostasis and localization,may be common pathways in the initial steps of neurodegeneration.Here we review and discuss known contributors,including variants in genetic loci and aberrant protein activities,which modify cytoskeletal integrity,axonal transport and mitochondrial localization in ALS and have overlapping features with other neurodegenerative diseases.Additionally,we explore some emerging pathways that may contribute to this disruption in ALS.

关键词： Cytoskeleton Neurofilament Mitochondria Amyotrophic lateral sclerosis Neurodegeneration Axonal transport Gut microbiome

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