| PMID |
10544701 ( ![]() ![]() ![]() ) |
|---|---|
| Title | [Neuro-degenerative diseases: role of reactive oxygen species and of apoptosis] |
| Abstract | NEURON DEATH: Major progress in our understanding of the pathophysiology of neurodegenerative diseases has greatly benefited from the convergence between work devoted to reactive oxygen species (including nitric oxide) and programmed cell death, or apoptosis, and exitotoxicity. LATERAL AMYOTROPHIC SCLEROSIS: The discovery of a mutation in the copper-zinc superoxide dismutase gene in patients with lateral amyotrophic sclerosis has made it possible to analyze the events leading to neuron death in transgenic mice. An overload of reactive oxygen species accelerates apoptosis and oxidative stress is implicated in excitotoxicity which is a hyperstimulation of excitatory amino acides (glutamate, aspartate) producing neuron death. OTHER CHRONIC CONDITIONS: Based on evidence from the mouse model, apoptosis, excitotoxicity and oxygenated free radicals could play a causal role in other neurodegenerative diseases including HIV-related encephalopathy, Parkinsonis disease and Alzheimeris disease. l'apoptose. |
NOTE: Color highlight is limited to the abstract and SciMiner text-mining mode. If you see much more identified targets below from "Targets by SciMiner Summary" and "Targets by SciMiner Full list", they may have been identified from the full text.
Targets by SciMiner Summary
| HUGO ID | Symbol | Target Name | #Occur | ActualStr |
|---|---|---|---|---|
| 11179 | SOD1 | superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult)) | 1 | superoxide dismutase | |
Targets by SciMiner Full list
| HUGO ID | Symbol | Name | ActualStr | Score | FlankingText |
|---|---|---|---|---|---|
| 11179 | SOD1 | superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult)) | superoxide dismutase | 1.0 | lateral amyotrophic sclerosis: the discovery of a mutation in the copper zinc superoxide dismutase gene in patients with lateral amyotrophic sclerosis has made it possible to analyze the events leading to neuron death in transgenic mice. |