Inflammatory-Mediated Neuron-Glia Communication Modulates ALS Pathophysiology

Juliani discusses how inflammatory-mediated neuron-glia communication modulates amyotrophic lateral sclerosis (ALS) pathophysiology. ALS is the most common adult-onset motor neuron disease. It is characterized by the deposition of aggregated proteins and predominantly affects motor neurons and the m...

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Bibliographic Details
Published inThe Journal of neuroscience Vol. 41; no. 6; pp. 1142 - 1144
Main Authors Juliani, Juliani, Vassileff, Natasha, Spiers, Jereme G
Format Journal Article
LanguageEnglish
Published United States Society for Neuroscience 10.02.2021
Subjects
Amyotrophic Lateral Sclerosis
Cortex (motor)
DNA-binding protein
Humans
Inflammation
Journal Club
Motor neuron diseases
Mutation
Neuroglia
Neuronal-glial interactions
Neurons
NF-kappa B
Pathophysiology
Proteins
Superoxide dismutase
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Summary:Juliani discusses how inflammatory-mediated neuron-glia communication modulates amyotrophic lateral sclerosis (ALS) pathophysiology. ALS is the most common adult-onset motor neuron disease. It is characterized by the deposition of aggregated proteins and predominantly affects motor neurons and the motor cortex. Although ALS is a genetically heteterogeneous disease, mutations in superoxide dismutase 1 (SOD-1) and transactive response DNA-binding protein 43 (TDP-43), encoded by TARDBP, are the most prevalent. SOD-1 mutations are frequent in familial ALS, whereas TDP-43 is linked to sporadic ALS, with 97% of all sporadic cases exhibiting TDP-43 protein aggregates.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
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ObjectType-Commentary-1
ISSN:0270-6474
1529-2401
DOI:10.1523/JNEUROSCI.1970-20.2020