{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T14:18:08Z","timestamp":1791296288619,"version":"4.1.0"},"reference-count":43,"publisher":"Society for Neuroscience","issue":"44","license":[{"start":{"date-parts":[[2007,5,1]],"date-time":"2007-05-01T00:00:00Z","timestamp":1177977600000},"content-version":"vor","delay-in-days":181,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. Neurosci."],"published-print":{"date-parts":[[2006,11,1]]},"abstract":"<jats:p>An increase in the expression of the proinflammatory cytokine tumor necrosis factor \u03b1 (TNF-\u03b1) has been observed in patients with amyotrophic lateral sclerosis (ALS) and in the mice models of the disease. TNF-\u03b1 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-\u03b1 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<jats:sup>G37R<\/jats:sup>or SOD1<jats:sup>G93A<\/jats:sup>mutants in the context of TNF-\u03b1 gene knock out. Surprisingly, the absence of TNF-\u03b1 did not affect the lifespan or the extent of motor neuron loss in SOD1 transgenic mice. These results provide compelling evidence indicating that TNF-\u03b1 does not directly contribute to motor neuron degeneration caused by SOD1 mutations.<\/jats:p>","DOI":"10.1523\/jneurosci.0602-06.2006","type":"journal-article","created":{"date-parts":[[2006,11,2]],"date-time":"2006-11-02T18:08:27Z","timestamp":1162490907000},"page":"11397-11402","source":"Crossref","is-referenced-by-count":93,"title":["Absence of Tumor Necrosis Factor-\u03b1 Does Not Affect Motor Neuron Disease Caused by Superoxide Dismutase 1 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