ReviewIntegrative and comparative biology2011
Links between electrophysiological and molecular pathology of amyotrophic lateral sclerosis.
Review in Integrative and comparative biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 28 citations in OpenAlex.
- ENGRAILED-1 transcription factor has a paracrine neurotrophic activity on adult spinal α-motoneurons.EMBO reports · 2023Article
- Chronic electromyograms in treadmill running SOD1 mice reveal early changes in muscle activation.The Journal of physiology · 2017Article
- Axonal Excitability in Amyotrophic Lateral Sclerosis : Axonal Excitability in ALS.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2017Review
- Pathophysiological and diagnostic implications of cortical dysfunction in ALS.Nature reviews. Neurology · 2016Review
- Comparison of dendritic calcium transients in juvenile wild type and SOD1(G93A) mouse lumbar motoneurons.Frontiers in cellular neuroscience · 2015Article
- Dysregulated expression of death, stress and mitochondrion related genes in the sciatic nerve of presymptomatic SOD1(G93A) mouse model of Amyotrophic Lateral Sclerosis.Frontiers in cellular neuroscience · 2015Article
- Motor cortical function and the precision grip.Physiological reports · 2014Article
- Soma size and Cav1.3 channel expression in vulnerable and resistant motoneuron populations of the SOD1G93A mouse model of ALS.Physiological reports · 2014Article
- Parkin reverses TDP-43-induced cell death and failure of amino acid homeostasis.Journal of neurochemistry · 2014Article
- Selective mitochondrial Ca2+ uptake deficit in disease endstage vulnerable motoneurons of the SOD1G93A mouse model of amyotrophic lateral sclerosis.The Journal of physiology · 2013Article
- Alterations in the motor neuron-renshaw cell circuit in the Sod1(G93A) mouse model.The Journal of comparative neurology · 2013Article
- Calcium channel agonists protect against neuromuscular dysfunction in a genetic model of TDP-43 mutation in ALS.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Early pathogenesis in the adult-onset neurodegenerative disease amyotrophic lateral sclerosis.Journal of cellular biochemistry · 2012Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Multiple deficits have been described in amyotrophic lateral sclerosis (ALS), from the first changes in normal functioning of the motoneurons and glia to the eventual loss of spinal and cortical motoneurons. In this review, current results, including changes in size, and electrical properties of motoneurons, glutamate excitotoxicity, calcium buffering, deficits in mitochondrial and cellular transport, impediments to proteostasis which lead to stress of the endoplasmic reticulum (ER), and glial contributions to motoneuronal vulnerability are recapitulated. Results are mainly drawn from the mutant SOD1 mouse model of ALS, and emphasis is placed on early changes that precede the onset of symptoms and the interplay between molecular and electrical processes.
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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.