ReviewFrontiers in cellular neuroscience2015
Mitochondrial dynamism and the pathogenesis of Amyotrophic Lateral Sclerosis.
Review in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Rasagiline for amyotrophic lateral sclerosis: A randomized, controlled trial.Muscle & nerve · 2019Trial
- Mitochondrial Aging in the CNS: Unravelling Implications for Neurological Health and Disease.Biomolecules · 2025Review
- Preliminary Analysis of Potentially Overlapping Differentially Expressed Proteins in Both the Spinal Cord and Brain of SOD1 G93A Mice.Current protein & peptide science · 2025Article
- Review
- Potential Applications for Growth Hormone Secretagogues Treatment of Amyotrophic Lateral Sclerosis.Current neuropharmacology · 2023Article
- Site-specific mitochondrial dysfunction in neurodegeneration.Mitochondrion · 2022Article
- Interplay between Mitochondrial Protein Import and Respiratory Complexes Assembly in Neuronal Health and Degeneration.Life (Basel, Switzerland) · 2021Review
- The Overlapping Genetics of Amyotrophic Lateral Sclerosis and Frontotemporal Dementia.Frontiers in neuroscience · 2020Review
- Exploring the Extended Biological Functions of the Human Copper Chaperone of Superoxide Dismutase 1.The protein journal · 2019Review
- Dysregulated mitochondrial CaArchives of biochemistry and biophysics · 2019Review
- Loss of MICOS complex integrity and mitochondrial damage, but not TDP-43 mitochondrial localisation, are likely associated with severity of CHCHD10-related diseases.Neurobiology of disease · 2018Article
- Expression and Distribution of Arylsulfatase B are Closely Associated with Neuron Death in SOD1 G93A Transgenic Mice.Molecular neurobiology · 2018Article
- Amyotrophic lateral sclerosis as a protein level, non-genomic disease: Therapy with S2RM exosome released molecules.World journal of stem cells · 2017Review
- Mutation Screening of the CHCHD10 Gene in Chinese Patients with Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2017Article
- Loss of function CHCHD10 mutations in cytoplasmic TDP-43 accumulation and synaptic integrity.Nature communications · 2017Article
- Dysregulated axonal RNA translation in amyotrophic lateral sclerosis.Wiley interdisciplinary reviews. RNA · 2016Review
- Neuroprotective Effect of Human Adipose Stem Cell-Derived Extract in Amyotrophic Lateral Sclerosis.Neurochemical research · 2016Article
- New ALS-Related Genes Expand the Spectrum Paradigm of Amyotrophic Lateral Sclerosis.Brain pathology (Zurich, Switzerland) · 2016Review
- Adducin at the Neuromuscular Junction in Amyotrophic Lateral Sclerosis: Hanging on for Dear Life.Frontiers in cellular neuroscience · 2016Review
- Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Research on mitochondria in the last years has been characterized by the fundamental finding that the morphology of mitochondria is deeply connected to the regulation of a vast number of different processes, including oxidative phosphorylation and ATP production, calcium buffering, and apoptosis. This has immediately focused the attention of the neuroscience community to the possible involvement of mitochondrial dynamism, the process underlying morphological features of mitochondria, in neurodegeneration, where mitochondrial dysfunction is believed to represent an important contributing event, or even a primary causative factor. Amyotrophic Lateral Sclerosis (ALS), a disease of motor neurons and their neighboring cells, has long been considered as a neurodegenerative disease with an important mitochondrial issue. Yet, whether mitochondria have a causative, primary role in the pathogenic process has always been debated, and the specific defects which account for this role are elusive. Here we discuss recent genetic advances suggesting that defective mitochondrial dynamism is primarily involved in the pathogenic mechanisms of ALS, and that foster the longstanding concept that disruption of mitochondrial function is a vulnerable factor for motor neurons.
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