ArticleFrontiers in cellular neuroscience2014
Dysfunctional mitochondrial Ca(2+) handling in mutant SOD1 mouse models of fALS: integration of findings from motor neuron somata and motor terminals.
Article in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Genetic ablation of neuronal mitochondrial calcium uptake impedes Alzheimer's disease progression.The EMBO journal · 2026Article
- Spinal Cord Injury Model Mitochondria Connect Altered Function with Defects of Mitochondrion Morphology: an Ultrastructural Study.Molecular neurobiology · 2024Article
- How neurons maintain their axons long-term: an integrated view of axon biology and pathology.Frontiers in neuroscience · 2023Review
- Structure and Function of the Mammalian Neuromuscular Junction.Comprehensive Physiology · 2022Article
- Mitochondrial Calcium: Effects of Its Imbalance in Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Mitophagy Modulation, a New Player in the Race against ALS.International journal of molecular sciences · 2021Review
- Functional Importance of Transient Receptor Potential (TRP) Channels in Neurological Disorders.Frontiers in cell and developmental biology · 2021Review
- Review
- Dysregulated mitochondrial CaArchives of biochemistry and biophysics · 2019Review
- Activity-dependent degeneration of axotomized neuromuscular synapses in Wld S mice.Neuroscience · 2015Article
- Compartment-dependent mitochondrial alterations in experimental ALS, the effects of mitophagy and mitochondriogenesis.Frontiers in cellular neuroscience · 2015Article
- Homocysteine aggravates ROS-induced depression of transmitter release from motor nerve terminals: potential mechanism of peripheral impairment in motor neuron diseases associated with hyperhomocysteinemia.Frontiers in cellular neuroscience · 2015Article
- Ultrastructural studies of ALS mitochondria connect altered function and permeability with defects of mitophagy and mitochondriogenesis.Frontiers in cellular neuroscience · 2015Review
- Oxidative stress and mitochondrial damage: importance in non-SOD1 ALS.Frontiers in cellular neuroscience · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Abundant evidence indicates that mitochondrial dysfunction and Ca(2+) dysregulation contribute to the muscle denervation and motor neuron death that occur in mouse models of familial amyotrophic lateral sclerosis (fALS). This perspective considers measurements of mitochondrial function and Ca(2+) handling made in both motor neuron somata and motor nerve terminals of SOD1-G93A mice at different disease stages. These complementary studies are integrated into a model of how mitochondrial dysfunction disrupts handling of stimulation-induced Ca(2+) loads in presymptomatic and end-stages of this disease. Also considered are possible mechanisms underlying the findings that some treatments that preserve motor neuron somata fail to postpone degeneration of motor axons and terminals.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.