ReviewNeural regeneration research2019
Amyotrophic lateral sclerosis as a synaptopathy.
Review in Neural regeneration research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 64 citations in OpenAlex.
- Written in the Stars: Astrocyte Biology From Evolution to Disease.Acta physiologica (Oxford, England) · 2026Review
- A mutation in the nuclear speckle and splicing factor SRRM2 is associated with multisystem proteinopathy and causes dysregulation of synapse-associated genes.RNA (New York, N.Y.) · 2026Article
- Hypoglossal and lumbar motor neuron death in old Sprague-Dawley rats.Physiological reports · 2026Article
- Spinal circuit mechanisms constrain therapeutic windows for ALS intervention: A computational modeling study.Neurobiology of disease · 2026Article
- Synaptopathy in the TDP-43ΔNLS Mouse Model of Sporadic Amyotrophic Lateral Sclerosis.The European journal of neuroscience · 2025Article
- Synaptic loss in motor neurons precipitates age-related dysphagia: Middle agers gotta keep in touch!The Journal of physiology · 2025Article
- Dendritic alterations precede age-related dysphagia and nucleus ambiguus motor neuron death.The Journal of physiology · 2025Article
- An Effective DNA Methylation Biomarker Screening Mechanism for Amyotrophic Lateral Sclerosis (ALS) Based on Comorbidities and Gene Function Analysis.Bioengineering (Basel, Switzerland) · 2024Article
- A Review of Biomarkers of Amyotrophic Lateral Sclerosis: A Pathophysiologic Approach.International journal of molecular sciences · 2024Review
- Genome-wide DNA methylation analysis related to ALS patient progression and survival.Journal of neurology · 2024Article
- Cognitive synaptopathy: synaptic and dendritic spine dysfunction in age-related cognitive disorders.Frontiers in aging neuroscience · 2024Review
- Pathomechanistic Networks of Motor System Injury in Amyotrophic Lateral Sclerosis.Current neuropharmacology · 2024Review
- Sodium butyrate does not protect spinal motor neurons from AMPA-induced excitotoxic degeneration in vivo.Disease models & mechanisms · 2023Article
- Medium-Chain Fatty Acids Rescue Motor Function and Neuromuscular Junction Degeneration in aCells · 2023Article
- An impaired splicing program underlies differentiation defects in hSOD1Cellular and molecular life sciences : CMLS · 2023Article
- Synaptic expression of TAR-DNA-binding protein 43 in the mouse spinal cord determined using super-resolution microscopy.Frontiers in molecular neuroscience · 2023Article
- Neuronal models of TDP-43 proteinopathy display reduced axonal translation, increased oxidative stress, and defective exocytosis.Frontiers in cellular neuroscience · 2023Article
- Synaptic proteomics reveal distinct molecular signatures of cognitive change and C9ORF72 repeat expansion in the human ALS cortex.Acta neuropathologica communications · 2022Article
- Synaptic Effects of Palmitoylethanolamide in Neurodegenerative Disorders.Biomolecules · 2022Review
- Feasibility of imaging synaptic density in the human spinal cord using [EJNMMI physics · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The synapse is an incredibly specialized structure that allows for the coordinated communication of information from one neuron to another. When assembled into circuits, steady streams of excitatory and inhibitory synaptic activity shape neural outputs. At the organismal level, ensembles of neural networks underlie behavior, emotion and memory. Disorder or dysfunctions of synapses, a synaptopathy, may underlie a host of developmental and degenerative neurological conditions. There is a possibility that amyotrophic lateral sclerosis may be a result of a synaptopathy within the neuromotor system. To this end, particular attention has been trained on the excitatory glutamatergic synapses and their morphological proxy, the dendritic spine. The extensive detailing of these dysfunctions in vulnerable neuronal populations, including corticospinal neurons and motor neurons, has recently been the subject of original research in rodents and humans. If amyotrophic lateral sclerosis is indeed a synaptopathy, it is entirely consistent with other proposed pathogenic mechanisms - including glutamate excitotoxicity, accumulation of misfolded proteins and mitochondrial dysfunction at distal axon terminals (cortico-motor neuron and neuromuscular). Further, although the exact mechanism of disease spread from region to region is unknown, the synaptopathy hypothesis is consistent with emerging die-forward evidence and the prion-like propagation of misfolded protein aggregates to distant neuronal populations. Here in this mini-review, we focus on the timeline of synaptic observations in both cortical and spinal neurons from different rodent models, and provide a conceptual framework for assessing the synaptopathy hypothesis in amyotrophic lateral sclerosis.
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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.