Degeneration of axons in spinal white matter in G93A mSOD1 mouse characterized by NFL and alpha-internexin immunoreactivity-Reference-Cited by-同舟云学术

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Degeneration of axons in spinal white matter in G93A mSOD1 mouse characterized by NFL and alpha-internexin immunoreactivity

Published:2012-07 Issue: Volume:1465 Page:90-100
ISSN:0006-8993
Container-title:Brain Research
language:en
Short-container-title:Brain Research

Author:

King Anna E.,Blizzard Catherine A.,Southam Katherine A.,Vickers James C.,Dickson Tracey C.

Funder

Motor Neuron Disease Research Institute of Australia

Wicking Dementia Research and Education Centre

Alzheimer's Australia Research

University of Tasmania

Tasmanian Masonic Centenary Research Foundation

National Health and Medical Research Council Australia

Publisher

Elsevier BV

Subject

Developmental Biology,Neurology (clinical),Molecular Biology,General Neuroscience

Reference47 articles.

1. Neurofilament light chain polypeptide gene mutations in Charcot-Marie-Tooth disease: nonsense mutation probably causes a recessive phenotype;Abe;J. Hum. Genet.,2009

2. Transgenic labeling of the corticospinal tract for monitoring axonal responses to spinal cord injury;Bareyre;Nat. Med.,2005

3. Bioenergetic abnormalities in discrete cerebral motor pathways presage spinal cord pathology in the G93A SOD1 mouse model of ALS;Browne;Neurobiol. Dis.,2006

4. alpha-Internexin aggregates are abundant in neuronal intermediate filament inclusion disease (NIFID) but rare in other neurodegenerative diseases;Cairns;Acta Neuropathol. (Berl),2004

5. The significance of the “dying back” process in experimental and human neurological disease;Cavanagh;Int. Rev. Exp. Pathol.,1964

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2. Sarm1 knockout modifies biomarkers of neurodegeneration and spinal cord circuitry but not disease progression in the mSOD1 mouse model of ALS;Neurobiology of Disease;2022-10

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4. Inhibition of ER stress improves progressive motor deficits in a REEP1-null mouse model of hereditary spastic paraplegia;Biology Open;2020-01-01

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