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The Journal of Neuroscience, November 1, 2006, 26(44):11397-11402; doi:10.1523/JNEUROSCI.0602-06.2006

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Neurobiology of Disease
Absence of Tumor Necrosis Factor- Does Not Affect Motor Neuron Disease Caused by Superoxide Dismutase 1 Mutations

Geneviève Gowing, Florence Dequen, Geneviève Soucy, and Jean-Pierre Julien

Laboratory of Molecular Endocrinology, Centre de Recherche du Centre Hospitalier de l'Université Laval Research Center, and Department of Anatomy and Physiology, Laval University 2705, Québec, Canada G1V 4G2

Correspondence should be addressed to Jean-Pierre Julien at the above address. E-mail: Email: jean-pierre.julien{at}crchul.ulaval.ca

An increase in the expression of the proinflammatory cytokine tumor necrosis factor (TNF-) has been observed in patients with amyotrophic lateral sclerosis (ALS) and in the mice models of the disease. TNF- is a potent activator of macrophages and microglia and, under certain conditions, can induce or exacerbate neuronal cell death. Here, we assessed the contribution of TNF- in motor neuron disease in mice overexpressing mutant superoxide dismutase 1 (SOD1) genes linked to familial ALS. This was accomplished by the generation of mice expressing SOD1^G37R or SOD1^G93A mutants in the context of TNF- gene knock out. Surprisingly, the absence of TNF- did not affect the lifespan or the extent of motor neuron loss in SOD1 transgenic mice. These results provide compelling evidence indicating that TNF- does not directly contribute to motor neuron degeneration caused by SOD1 mutations.

Key words: ALS; amyotrophic lateral sclerosis; degeneration; microglia; motoneuron; motor neuron; neuroinflammation; TNF-

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Received Feb. 10, 2006; revised Sept. 22, 2006; accepted Sept. 25, 2006.

Correspondence should be addressed to Jean-Pierre Julien at the above address. E-mail: Email: jean-pierre.julien{at}crchul.ulaval.ca

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