Demyelination and axonal preservation in a transgenic mouse model of Pelizaeus‐Merzbacher disease-Reference-Cited by-同舟云学术

Demyelination and axonal preservation in a transgenic mouse model of Pelizaeus‐Merzbacher disease

Published:2010-02 Issue:2 Volume:2 Page:42-50
ISSN:1757-4676
Container-title:EMBO Molecular Medicine
language:en
Short-container-title:EMBO Mol Med

Author:

Edgar Julia M.¹,McCulloch Mailis C.¹,Montague Paul¹,Brown Angus M.²,Thilemann Sebastian¹,Pratola Laura¹,Gruenenfelder Fredrik I.¹,Griffiths Ian R.¹,Nave Klaus‐Armin³

Affiliation:

1. Applied Neurobiology Group, Institute of Comparative Medicine, University of Glasgow, Glasgow, Scotland, UK

2. School of Biomedical Sciences, Queens Medical Centre, University of Nottingham, Nottingham, England, UK

3. Department of Neurogenetics, Max Planck Institute of Experimental Medicine, Goettingen, Germany

Publisher

EMBO

Subject

Molecular Medicine

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/emmm.200900057

Reference39 articles.

1. Transient Axonal Injury in the Absence of Demyelination: A Correlate of Clinical Disease in Acute Experimental Autoimmune Encephalomyelitis

2. Severely dystrophic axons at amyloid plaques remain continuous and connected to viable cell bodies

3. Genetic background determines phenotypic severity of thePlp rumpshaker mutation

4. Fructose Supports Energy Metabolism of Some, But Not All, Axons in Adult Mouse Optic Nerve

5. Distinct Phenotypes Associated with Increasing Dosage of the PLP Gene: Implications for CMT1A Due toPMP22Gene Duplication

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