期刊
NEURODEGENERATIVE DISEASES
卷 2, 期 3-4, 页码 128-134出版社
KARGER
DOI: 10.1159/000089617
关键词
Amyotrophic lateral sclerosis; SOD1 mutants; Tumor necrosis factor-alpha; Cytokines; Neuroinflammation; Reactive oxygen species; Nitric oxide; p38 mitogen-activated protein kinase
资金
- Telethon, Italy [GP0222Y01, RBNEO1B5WW-004]
The pathogenetic processes underlying the selective motor neuron degeneration in amyotrophic lateral sclerosis (ALS) are complex and still not completely understood even in the cases of inherited disease caused by mutations in the Cu/Zn superoxide dismutase-dependent (SOD1) gene. Recent evidence supports the view that ALS is not a cell-autonomous disease and that glialneuron cross-talk, throughout cytokines and other toxic factors like the nitric oxide and superoxide, is a crucial determinant for the induction of motor neuron death. This cell-cell interaction may determine the progression of the disease through processes that are likely independent of the initial trigger and that may converge on the activation of intracellular death pathways in the motor neurons. In this review we provide support to the hypothesis that aberrant expression and activity of p38 mitogen protein-activated kinases cascade (p38MAPK) in motor neurons and glial cells may play a role in the development and progression of ALS. Increased activation of p38MAPK may phosphorylate neuron-specifi c substrates altering their physiological properties and it may turn on responsive genes leading to neurotoxicity. Copyright (C) 2005 S. Karger AG, Basel
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