ReviewFrontiers in cellular neuroscience2015
Calcium dysregulation links ALS defective proteins and motor neuron selective vulnerability.
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 48 papers, 3 of them syntheses that pooled it.
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Who cites it
48 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Environmental risk factors, protective factors, and biomarkers for amyotrophic lateral sclerosis: an umbrella review.Frontiers in aging neuroscience · 2025Pooled it
- Medications on hypertension, hyperlipidemia, diabetes, and risk of amyotrophic lateral sclerosis: a systematic review and meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022 · on this mapPooled it
- A Systematic and Comprehensive Review on Disease-Causing Genes in Amyotrophic Lateral Sclerosis.Journal of molecular neuroscience : MN · 2020Pooled it
- Review
- The Molecular Architecture of Neurodegeneration: An Integrative Overview of Convergent Mechanisms.NeuroSci · 2026Review
- Single-nucleus RNA sequencing reveals GABAergic vulnerability and reactive gliosis driven by loss of TDP-43.iScience · 2025Article
- Machine Learning Approach for Predicting Drug-Like Molecules Targeting Calmodulin Pathway Proteins.Journal of chemical information and modeling · 2025Article
- Iron and Ferritin Dyshomeostasis Intersect with Sex, Age, and Disease Severity in Amyotrophic Lateral Sclerosis.Journal of molecular neuroscience : MN · 2025Article
- Trimetazidine stimulates intracellular CaScientific reports · 2025Article
- Circular RNA expression in ALS is progressively deregulated and tissue-dependent.BMC genomics · 2025Article
- Multi-Omic Analysis of Glutamate Excitotoxicity in Primary Neuronal Cultures.Journal of neurochemistry · 2025Article
- Primary visual cortex pathology in ALS patients with C9ORF72 expansion.Brain pathology (Zurich, Switzerland) · 2024Article
- Selective vulnerability of motor neuron types and functional groups to degeneration in amyotrophic lateral sclerosis: review of the neurobiological mechanisms and functional correlates.Brain structure & function · 2024Review
- Article
- Regulation of cortical hyperexcitability in amyotrophic lateral sclerosis: focusing on glial mechanisms.Molecular neurodegeneration · 2023Review
- CDNF rescues motor neurons in models of amyotrophic lateral sclerosis by targeting endoplasmic reticulum stress.Brain : a journal of neurology · 2023Article
- ERK MAPK signaling pathway inhibition as a potential target to prevent autophagy alterations in Spinal Muscular Atrophy motoneurons.Cell death discovery · 2023Article
- Brain expression quantitative trait locus and network analyses reveal downstream effects and putative drivers for brain-related diseases.Nature genetics · 2023Article
- The Common Cellular Events in the Neurodegenerative Diseases and the Associated Role of Endoplasmic Reticulum Stress.International journal of molecular sciences · 2022Review
- Hyperexcitability in young iPSC-derived C9ORF72 mutant motor neurons is associated with increased intracellular calcium release.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
More than 20 distinct gene loci have so far been implicated in amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disorder characterized by progressive neurodegeneration of motor neurons (MN) and death. Most of this distinct set of ALS-related proteins undergoes toxic deposition specifically in MN for reasons which remain unclear. Here we overview a recent body of evidence indicative that mutations in ALS-related proteins can disrupt fundamental Ca(2+) signalling pathways in MN, and that Ca(2+) itself impacts both directly or indirectly in many ALS critical proteins and cellular processes that result in MN neurodegeneration. We argue that the inherent vulnerability of MN to dysregulation of intracellular Ca(2+) is deeply associated with discriminating pathogenicity and aberrant crosstalk of most of the critical proteins involved in ALS. Overall, Ca(2+) deregulation in MN is at the cornerstone of different ALS processes and is likely one of the factors contributing to the selective susceptibility of these cells to this particular neurodegenerative disease.
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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.