ReviewFrontiers in neuroscience2020
Cortical Circuit Dysfunction as a Potential Driver of Amyotrophic Lateral Sclerosis.
Review in Frontiers in neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 66 citations in OpenAlex.
- Large-scale mapping of the MCH network in ALS mice reveals the vulnerability of dopaminergic and GABAergic neurons in zona incerta.Acta neuropathologica communications · 2026Article
- Imaging biomarkers in neurodegenerative diseases: advances and challenges.Frontiers in aging neuroscience · 2026Review
- Dynamic changes in excitability and viability of sporadic andFrontiers in cell and developmental biology · 2026Article
- Targeted antisense oligonucleotide treatment rescues developmental alterations in spinal muscular atrophy organoids.Nature communications · 2025Article
- Glycerophospholipids in ALS: insights into disease mechanisms and clinical implication.Molecular neurodegeneration · 2025Review
- Kv3 channel agonist ameliorates the phenotype of a mouse model of amyotrophic lateral sclerosis.Acta neuropathologica communications · 2025Article
- Trimetazidine stimulates intracellular CaScientific reports · 2025Article
- Longitudinal assessment of cortical motor function in amyotrophic lateral sclerosis.Scientific reports · 2025Article
- Autonomic dysfunction in neurodegenerative disease.Nature reviews. Neuroscience · 2025Review
- High-density multielectrode arrays bring cellular resolution to neuronal activity and network analyses of corticospinal motor neurons.Scientific reports · 2025Article
- Excitatory/Inhibitory balance in autism spectrum disorders: Integrating genetic, neurotransmitter and computational perspectives.AIMS neuroscience · 2025Review
- Neuroprotective actions of norepinephrine in neurological diseases.Pflugers Archiv : European journal of physiology · 2024Review
- A patient-derived amyotrophic lateral sclerosis blood-brain barrier model for focused ultrasound-mediated anti-TDP-43 antibody delivery.Fluids and barriers of the CNS · 2024Article
- Insulin restores retinal ganglion cell functional connectivity and promotes visual recovery in glaucoma.Science advances · 2024Article
- Advances in Brain Stimulation, Nanomedicine and the Use of Magnetoelectric Nanoparticles: Dopaminergic Alterations and Their Role in Neurodegeneration and Drug Addiction.Molecules (Basel, Switzerland) · 2024Review
- RNA editing regulates glutamatergic synapses in the frontal cortex of a molecular subtype of Amyotrophic Lateral Sclerosis.Molecular medicine (Cambridge, Mass.) · 2024Article
- Article
- Cell type specification and diversity in subpallial organoids.Frontiers in genetics · 2024Review
- Unsupervised machine learning identifies distinct ALS molecular subtypes in post-mortem motor cortex and blood expression data.Acta neuropathologica communications · 2023Article
- Intranasal neuropeptide Y1 receptor antagonism improves motor deficits in symptomatic SOD1 ALS mice.Annals of clinical and translational neurology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease that affects selected cortical and spinal neuronal populations, leading to progressive paralysis and death. A growing body of evidences suggests that the disease may originate in the cerebral cortex and propagate in a corticofugal manner. In particular, transcranial magnetic stimulation studies revealed that ALS patients present with early cortical hyperexcitability arising from a combination of increased excitability and decreased inhibition. Here, we discuss the possibility that initial cortical circuit dysfunction might act as the main driver of ALS onset and progression, and review recent functional, imaging and transcriptomic studies conducted on ALS patients, along with electrophysiological, pathological and transcriptomic studies on animal and cellular models of the disease, in order to evaluate the potential cellular and molecular origins of cortical hyperexcitability in ALS.
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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.