Amyotrophic lateral sclerosis is a distal axonopathy: evidence in mice and man

The SOD1 mutant mouse is the most widely used model of human amyotrophic lateral sclerosis (ALS). To determine where and when the pathological changes of motor neuron disease begins, we performed a comprehensive spatiotemporal analysis of disease progression in SOD1 G93A mice. Quantitative pathologi...

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Bibliographic Details
Published in	Experimental neurology Vol. 185; no. 2; pp. 232 - 240
Main Authors	Fischer, Lindsey R., Culver, Deborah G., Tennant, Philip, Davis, Albert A., Wang, Minsheng, Castellano-Sanchez, Amilcar, Khan, Jaffar, Polak, Meraida A., Glass, Jonathan D.
Format	Journal Article
Language	English
Published	Amsterdam Elsevier Inc 01.02.2004 Elsevier
Subjects	Amyotrophic Lateral Sclerosis - enzymology Amyotrophic Lateral Sclerosis - genetics Amyotrophic Lateral Sclerosis - pathology Animals Axonopathy Axons - enzymology Axons - pathology Biological and medical sciences Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Denervation Humans Male Medical sciences Mice Mice, Mutant Strains Mice, Transgenic Neurology Sclerosis Superoxide Dismutase - biosynthesis Superoxide Dismutase - genetics Superoxide Dismutase-1 Time Factors Axonopathy Sclerosis Denervation Animal model Sporadic Motor neuron disease Motor neuron Neuromuscular junction Spinal root Autopsy Degenerative disease Degeneration Quantitative analysis Human Nervous system diseases Rodentia Axon Amyotrophic lateral sclerosis Vertebrata Anatomic pathology Mammalia Mouse Cell death Animal Central nervous system disease Reinnervation Spinal cord disease
Online Access	Get full text
ISSN	0014-4886 1090-2430
DOI	10.1016/j.expneurol.2003.10.004

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Abstract	The SOD1 mutant mouse is the most widely used model of human amyotrophic lateral sclerosis (ALS). To determine where and when the pathological changes of motor neuron disease begins, we performed a comprehensive spatiotemporal analysis of disease progression in SOD1 G93A mice. Quantitative pathological analysis was performed in the same mice at multiple ages at neuromuscular junctions (NMJ), ventral roots, and spinal cord. In addition, a patient with sporadic ALS who died unexpectedly was examined at autopsy. Mice became clinically weak at 80 days and died at 131 ± 5 days. At 47 days, 40% of end-plates were denervated whereas there was no evidence of ventral root or cell body loss. At 80 days, 60% of ventral root axons were lost but there was no loss of motor neurons. Motor neuron loss was well underway by 100 days. Microglial and astrocytic activation around motor neurons was not identified until after the onset of distal axon degeneration. Autopsy of the ALS patient demonstrated denervation and reinnervation changes in muscle but normal appearing motor neurons. We conclude that in this widely studied animal model of human ALS, and in this single human case, motor neuron pathology begins at the distal axon and proceeds in a “dying back” pattern.
AbstractList	The SOD1 mutant mouse is the most widely used model of human amyotrophic lateral sclerosis (ALS). To determine where and when the pathological changes of motor neuron disease begins, we performed a comprehensive spatiotemporal analysis of disease progression in SOD1(G93A) mice. Quantitative pathological analysis was performed in the same mice at multiple ages at neuromuscular junctions (NMJ), ventral roots, and spinal cord. In addition, a patient with sporadic ALS who died unexpectedly was examined at autopsy. Mice became clinically weak at 80 days and died at 131 +/- 5 days. At 47 days, 40% of end-plates were denervated whereas there was no evidence of ventral root or cell body loss. At 80 days, 60% of ventral root axons were lost but there was no loss of motor neurons. Motor neuron loss was well underway by 100 days. Microglial and astrocytic activation around motor neurons was not identified until after the onset of distal axon degeneration. Autopsy of the ALS patient demonstrated denervation and reinnervation changes in muscle but normal appearing motor neurons. We conclude that in this widely studied animal model of human ALS, and in this single human case, motor neuron pathology begins at the distal axon and proceeds in a "dying back" pattern.The SOD1 mutant mouse is the most widely used model of human amyotrophic lateral sclerosis (ALS). To determine where and when the pathological changes of motor neuron disease begins, we performed a comprehensive spatiotemporal analysis of disease progression in SOD1(G93A) mice. Quantitative pathological analysis was performed in the same mice at multiple ages at neuromuscular junctions (NMJ), ventral roots, and spinal cord. In addition, a patient with sporadic ALS who died unexpectedly was examined at autopsy. Mice became clinically weak at 80 days and died at 131 +/- 5 days. At 47 days, 40% of end-plates were denervated whereas there was no evidence of ventral root or cell body loss. At 80 days, 60% of ventral root axons were lost but there was no loss of motor neurons. Motor neuron loss was well underway by 100 days. Microglial and astrocytic activation around motor neurons was not identified until after the onset of distal axon degeneration. Autopsy of the ALS patient demonstrated denervation and reinnervation changes in muscle but normal appearing motor neurons. We conclude that in this widely studied animal model of human ALS, and in this single human case, motor neuron pathology begins at the distal axon and proceeds in a "dying back" pattern. The SOD1 mutant mouse is the most widely used model of human amyotrophic lateral sclerosis (ALS). To determine where and when the pathological changes of motor neuron disease begins, we performed a comprehensive spatiotemporal analysis of disease progression in SOD1(G93A) mice. Quantitative pathological analysis was performed in the same mice at multiple ages at neuromuscular junctions (NMJ), ventral roots, and spinal cord. In addition, a patient with sporadic ALS who died unexpectedly was examined at autopsy. Mice became clinically weak at 80 days and died at 131 +/- 5 days. At 47 days, 40% of end-plates were denervated whereas there was no evidence of ventral root or cell body loss. At 80 days, 60% of ventral root axons were lost but there was no loss of motor neurons. Motor neuron loss was well underway by 100 days. Microglial and astrocytic activation around motor neurons was not identified until after the onset of distal axon degeneration. Autopsy of the ALS patient demonstrated denervation and reinnervation changes in muscle but normal appearing motor neurons. We conclude that in this widely studied animal model of human ALS, and in this single human case, motor neuron pathology begins at the distal axon and proceeds in a "dying back" pattern. The SOD1 mutant mouse is the most widely used model of human amyotrophic lateral sclerosis (ALS). To determine where and when the pathological changes of motor neuron disease begins, we performed a comprehensive spatiotemporal analysis of disease progression in SOD1 G93A mice. Quantitative pathological analysis was performed in the same mice at multiple ages at neuromuscular junctions (NMJ), ventral roots, and spinal cord. In addition, a patient with sporadic ALS who died unexpectedly was examined at autopsy. Mice became clinically weak at 80 days and died at 131 ± 5 days. At 47 days, 40% of end-plates were denervated whereas there was no evidence of ventral root or cell body loss. At 80 days, 60% of ventral root axons were lost but there was no loss of motor neurons. Motor neuron loss was well underway by 100 days. Microglial and astrocytic activation around motor neurons was not identified until after the onset of distal axon degeneration. Autopsy of the ALS patient demonstrated denervation and reinnervation changes in muscle but normal appearing motor neurons. We conclude that in this widely studied animal model of human ALS, and in this single human case, motor neuron pathology begins at the distal axon and proceeds in a “dying back” pattern.
Author	Wang, Minsheng Glass, Jonathan D. Culver, Deborah G. Castellano-Sanchez, Amilcar Polak, Meraida A. Fischer, Lindsey R. Davis, Albert A. Khan, Jaffar Tennant, Philip
Author_xml	– sequence: 1 givenname: Lindsey R. surname: Fischer fullname: Fischer, Lindsey R. organization: Department of Neurology, Emory University School of Medicine, Atlanta, GA 30322, USA – sequence: 2 givenname: Deborah G. surname: Culver fullname: Culver, Deborah G. organization: Department of Neurology, Emory University School of Medicine, Atlanta, GA 30322, USA – sequence: 3 givenname: Philip surname: Tennant fullname: Tennant, Philip organization: Department of Neurology, Emory University School of Medicine, Atlanta, GA 30322, USA – sequence: 4 givenname: Albert A. surname: Davis fullname: Davis, Albert A. organization: Department of Neurology, Emory University School of Medicine, Atlanta, GA 30322, USA – sequence: 5 givenname: Minsheng surname: Wang fullname: Wang, Minsheng organization: Department of Neurology, Emory University School of Medicine, Atlanta, GA 30322, USA – sequence: 6 givenname: Amilcar surname: Castellano-Sanchez fullname: Castellano-Sanchez, Amilcar organization: Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA – sequence: 7 givenname: Jaffar surname: Khan fullname: Khan, Jaffar organization: Department of Neurology, Emory University School of Medicine, Atlanta, GA 30322, USA – sequence: 8 givenname: Meraida A. surname: Polak fullname: Polak, Meraida A. organization: Department of Neurology, Emory University School of Medicine, Atlanta, GA 30322, USA – sequence: 9 givenname: Jonathan D. surname: Glass fullname: Glass, Jonathan D. email: jglas03@emory.edu organization: Department of Neurology, Emory University School of Medicine, Atlanta, GA 30322, USA
BackLink	http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15483992$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/14736504$$D View this record in MEDLINE/PubMed
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Snippet	The SOD1 mutant mouse is the most widely used model of human amyotrophic lateral sclerosis (ALS). To determine where and when the pathological changes of motor...
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SubjectTerms	Amyotrophic Lateral Sclerosis - enzymology Amyotrophic Lateral Sclerosis - genetics Amyotrophic Lateral Sclerosis - pathology Animals Axonopathy Axons - enzymology Axons - pathology Biological and medical sciences Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Denervation Humans Male Medical sciences Mice Mice, Mutant Strains Mice, Transgenic Neurology Sclerosis Superoxide Dismutase - biosynthesis Superoxide Dismutase - genetics Superoxide Dismutase-1 Time Factors
Title	Amyotrophic lateral sclerosis is a distal axonopathy: evidence in mice and man
URI	https://dx.doi.org/10.1016/j.expneurol.2003.10.004 https://www.ncbi.nlm.nih.gov/pubmed/14736504 https://www.proquest.com/docview/80112962
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