Astrocytes as determinants of disease progression in inherited amyotrophic lateral sclerosis

By Koji Yamanaka, S. Chun, S. Boillée, Noriko Fujimori-Tonou, H. Yamashita, D. Gutmann, R. Takahashi, H. Misawa, D. Cleveland. Nature Neuroscience, 2008

1,128 citations recorded by the source corpus.

Subfields: Genetics, Neurology

View Paper: https://www.semanticscholar.org/paper/ae706faa17699c28be544ab8623fd406ec325c54

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. D. Cleveland
2. M. Pekna
3. M. Pekny
4. M. Polymenidou

In Neurology

1. M. Pekna
2. M. Pekny
3. M. Polymenidou
4. D. Cleveland
5. Shuo-Chien Ling
6. M. Sofroniew

Citations in the corpus

• Microglia induce motor neuron death via the classical NF-κB pathway in amyotrophic lateral sclerosis (2014, neutral): “We observed robust RFP expression in GFAP+ and EAAT2+ cells (Figure S2D); RFP expression was absent in Iba-1+ microglia as well as in ChAT+ neurons in the spinal cord as previously reported (Figure S2C) (Yamanaka et al., 2008; Zhuo et al., 2001).”
• Converging mechanisms in ALS and FTD: Disrupted RNA and protein homeostasis (2013, positive): “…et al., 2009; Yamanaka et al., 2008) and NG2+ oligodendrocyte precursors (Kang et al., 2013), while mutant SOD1 synthesized within two additional glial cell types (astrocytes; Yamanaka et al., 2008; and microglia; Boillé e et al., 2006) are primary determinants of accelerated disease progression.”
• Astrocyte reactivity and reactive astrogliosis: costs and benefits. (2014, background): “More recent data suggest that at least in some forms of ALS, the neuronal damage is mediated by oligodendrocytes (111), microglia (25, 253), and astrocytes (57, 88, 155, 268), which thus emerge as a novel therapeutic target for this devastating disease.”
• Reactive gliosis and the multicellular response to CNS damage and disease (2014, neutral): “For example, in ALS, glial cell dysfunction is causally implicated in mediating neuronal degeneration (Yamanaka et al., 2008), and ongoing reactive gliosis and inflammation are also thought to contribute to disease progression (Maragakis and Rothstein, 2006).”
• Rethinking ALS: the FUS about TDP-43. (2009, background): “…emerged as to how SOD1 mutations lead to selective premature death of motor neurons, except that damage within motor neurons expressing mutant SOD1 drives disease onset, whereas damage within their glial cell neighbors expressing mutant SOD1 accelerates disease progression (Yamanaka et al., 2008).”