Astrocytes expressing ALS-linked mutated SOD1 release factors selectively toxic to motor neurons

By M. Nagai, D. Re, T. Nagata, A. Chalazonitis, T. Jessell, Hynek Wichterle, S. Przedborski. Nature Neuroscience, 2007

1,239 citations recorded by the source corpus.

Subfields: Genetics, Neurology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/1f5cfb33f67e62572d71747ace6f5e745a1ba165

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Genetics

1. Berislav Zlokovic
2. D. Cleveland
3. A. Kriegstein
4. M. Pekna
5. M. Pekny
6. M. Polymenidou

In Neurology

1. Berislav Zlokovic
2. M. Pekny
3. M. Pekna
4. R. Daneman
5. B. Barres
6. P. Shaw
7. A. Kriegstein
8. S. A. Liddelow

In Pathology and Forensic Medicine

1. Berislav Zlokovic
2. Jonathan P. Godbout

Citations in the corpus

• Non–cell autonomous effect of glia on motor neurons in an embryonic stem cell–based ALS model (2007, result): “Consistent with the results reported here, another study described in this issue has shown that primary astrocyte cultures expressing ALS-associated mutant SOD1 proteins contain diffusible factor(s) that are toxic to primary and ESC-derived motor neuron”
• The mystery and magic of glia: a perspective on their roles in health and disease. (2008, background): “As Nobel Laureate Richard Axel has put it: ‘‘Before you know, you must imagine.’’”
• Oxidative Stress in Neurodegenerative Diseases: From Molecular Mechanisms to Clinical Applications (2017, background): “These cocultured motor neurons, as well as motor neurons treated with conditioned cell culture medium from astrocytes expressing mutant SOD1, experienced increased cell damage [127].”
• Oxidative stress in ALS: key role in motor neuron injury and therapeutic target. (2010, background): “Although expression of mutant SOD1 restricted to either astrocytes [183] or microglia [77] was not sufficient to cause disease, several studies have shown reduced survival of motor neurons when cultured with mutant SOD1- expressing glial cells [184] [185] [186].”
• Neurovascular pathways to neurodegeneration in Alzheimer’s disease and other disorders (2011, background): “According to an emerging hypothesis of ALS that is based on studies in SOD1 mutant mice, the toxicity that is derived from non-neuronal neighbouring cells, particularly microglia and astrocytes, contributes to disease progression and motor neuron degeneratio”
• Normal aging induces A1-like astrocyte reactivity (2018, background): “In particular, astrocyte dysfunction has been linked to age-related neurodegenerative diseases, including Alzheimer’s disease (8–10), dementia (11), and amyotrophic lateral sclerosis (ALS) (12, 13).”
• The blood-brain barrier in health and chronic neurodegenerative disorders. (2008, positive): “Neurovascular Unit The current model of ALS disease suggests that toxicity derived from microglia and astrocytes contributes to disease progression and motor neuron degeneration (Boillée et al., 2006a, 2006b; Beers et al., 2006; Di Giorgio et al., 2007; Nagai et al., 2007).”
• Microglia induce motor neuron death via the classical NF-κB pathway in amyotrophic lateral sclerosis (2014, positive): “We utilized an embryonic stem cell line containing an Hb9-GFP reporter, which we and others have shown recapitulate aspects of MN pathology and cell death when cocultured with ALS glia (Di Giorgio et al., 2007; Haidet-Phillips et al., 2011; Nagai et al., 2007; Wichterle et al., 2002).”
• Reactive Astrocytes: Production, Function, and Therapeutic Potential. (2017, background): “Astrocytes cultured from the Sod1G93A mutant mouse release a factor that can kill motor neurons (Di Giorgio et al., 2007; Nagai et al., 2007; Lobsiger et al., 2007).”
• Converging mechanisms in ALS and FTD: Disrupted RNA and protein homeostasis (2013, positive): “SOD1 mutant-expressing astrocytes are toxic to cocultured normal motor neurons (Di Giorgio et al., 2007, 2008; Haidet- Phillips et al., 2011; Marchetto et al., 2008; Nagai et al., 2007).”