| pubmed-article:21437247 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21437247 | lifeskim:mentions | umls-concept:C0002736 | lld:lifeskim |
| pubmed-article:21437247 | lifeskim:mentions | umls-concept:C1522424 | lld:lifeskim |
| pubmed-article:21437247 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:21437247 | lifeskim:mentions | umls-concept:C0927232 | lld:lifeskim |
| pubmed-article:21437247 | lifeskim:mentions | umls-concept:C0206417 | lld:lifeskim |
| pubmed-article:21437247 | lifeskim:mentions | umls-concept:C0206116 | lld:lifeskim |
| pubmed-article:21437247 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
| pubmed-article:21437247 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:21437247 | lifeskim:mentions | umls-concept:C0333348 | lld:lifeskim |
| pubmed-article:21437247 | lifeskim:mentions | umls-concept:C1708481 | lld:lifeskim |
| pubmed-article:21437247 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:21437247 | pubmed:dateCreated | 2011-3-25 | lld:pubmed |
| pubmed-article:21437247 | pubmed:abstractText | Mutations in the enzyme superoxide dismutase-1 (SOD1) cause hereditary variants of the fatal motor neuronal disease Amyotrophic lateral sclerosis (ALS). Pathophysiology of the disease is non-cell-autonomous: neurotoxicity is derived not only from mutant motor neurons but also from mutant neighbouring non-neuronal cells. In vivo imaging by two-photon laser-scanning microscopy was used to compare the role of microglia/macrophage-related neuroinflammation in the CNS and PNS using ALS-linked transgenic SOD1(G93A) mice. These mice contained labeled projection neurons and labeled microglia/macrophages. In the affected lateral spinal cord (in contrast to non-affected dorsal columns), different phases of microglia-mediated inflammation were observed: highly reactive microglial cells in preclinical stages (in 60-day-old mice the reaction to axonal transection was ?180% of control) and morphologically transformed microglia that have lost their function of tissue surveillance and injury-directed response in clinical stages (reaction to axonal transection was lower than 50% of control). Furthermore, unlike CNS microglia, macrophages of the PNS lack any substantial morphological reaction while preclinical degeneration of peripheral motor axons and neuromuscular junctions was observed. We present in vivo evidence for a different inflammatory activity of microglia and macrophages: an aberrant neuroinflammatory response of microglia in the CNS and an apparently mainly neurodegenerative process in the PNS. | lld:pubmed |
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| pubmed-article:21437247 | pubmed:language | eng | lld:pubmed |
| pubmed-article:21437247 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21437247 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:21437247 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:21437247 | pubmed:issn | 1932-6203 | lld:pubmed |
| pubmed-article:21437247 | pubmed:author | pubmed-author:KirchhoffFran... | lld:pubmed |
| pubmed-article:21437247 | pubmed:author | pubmed-author:SchomburgEike... | lld:pubmed |
| pubmed-article:21437247 | pubmed:author | pubmed-author:SteffensHeinz... | lld:pubmed |
| pubmed-article:21437247 | pubmed:author | pubmed-author:NeuschClemens... | lld:pubmed |
| pubmed-article:21437247 | pubmed:author | pubmed-author:NadrignyFabie... | lld:pubmed |
| pubmed-article:21437247 | pubmed:author | pubmed-author:DibajPayamP | lld:pubmed |
| pubmed-article:21437247 | pubmed:author | pubmed-author:ZschüntzschJa... | lld:pubmed |
| pubmed-article:21437247 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:21437247 | pubmed:volume | 6 | lld:pubmed |
| pubmed-article:21437247 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:21437247 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:21437247 | pubmed:pagination | e17910 | lld:pubmed |
| pubmed-article:21437247 | pubmed:dateRevised | 2011-7-27 | lld:pubmed |
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