| pubmed-article:17287338 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17287338 | lifeskim:mentions | umls-concept:C0000098 | lld:lifeskim |
| pubmed-article:17287338 | lifeskim:mentions | umls-concept:C0010656 | lld:lifeskim |
| pubmed-article:17287338 | lifeskim:mentions | umls-concept:C0033634 | lld:lifeskim |
| pubmed-article:17287338 | lifeskim:mentions | umls-concept:C0001721 | lld:lifeskim |
| pubmed-article:17287338 | lifeskim:mentions | umls-concept:C0598954 | lld:lifeskim |
| pubmed-article:17287338 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:17287338 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:17287338 | pubmed:dateCreated | 2007-2-14 | lld:pubmed |
| pubmed-article:17287338 | pubmed:abstractText | Parkinson's disease (PD), a late-onset condition characterized by dysfunction and loss of dopaminergic neurons in the substantia nigra, has both sporadic and neurotoxic forms. Neurotoxins such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and its metabolite 1-methyl-4-phenylpyridinium (MPP+) induce PD symptoms and recapitulate major pathological hallmarks of PD in human and animal models. Both sporadic and MPP+-induced forms of PD proceed through a "dying-back" pattern of neuronal degeneration in affected neurons, characterized by early loss of synaptic terminals and axonopathy. However, axonal and synaptic-specific effects of MPP+ are poorly understood. Using isolated squid axoplasm, we show that MPP+ produces significant alterations in fast axonal transport (FAT) through activation of a caspase and a previously undescribed protein kinase C (PKCdelta) isoform. Specifically, MPP+ increased cytoplasmic dynein-dependent retrograde FAT and reduced kinesin-1-mediated anterograde FAT. Significantly, MPP+ effects were independent of both nuclear activities and ATP production. Consistent with its effects on FAT, MPP+ injection in presynaptic domains led to a dramatic reduction in the number of membranous profiles. Changes in availability of synaptic and neurotrophin-signaling components represent axonal and synaptic-specific effects of MPP+ that would produce a dying-back pathology. Our results identify a critical neuronal process affected by MPP+ and suggest that alterations in vesicle trafficking represent a primary event in PD pathogenesis. We propose that PD and other neurodegenerative diseases exhibiting dying-back neuropathology represent a previously undescribed category of neurological diseases characterized by dysfunction of vesicle transport and associated with the loss of synaptic function. | lld:pubmed |
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| pubmed-article:17287338 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17287338 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17287338 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17287338 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17287338 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17287338 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:17287338 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:17287338 | pubmed:author | pubmed-author:LlinásR RRR | lld:pubmed |
| pubmed-article:17287338 | pubmed:author | pubmed-author:SugimoriMM | lld:pubmed |
| pubmed-article:17287338 | pubmed:author | pubmed-author:MoreiraJ EJE | lld:pubmed |
| pubmed-article:17287338 | pubmed:author | pubmed-author:PiginiMM | lld:pubmed |
| pubmed-article:17287338 | pubmed:author | pubmed-author:BradyS TST | lld:pubmed |
| pubmed-article:17287338 | pubmed:author | pubmed-author:MorfiniGG | lld:pubmed |
| pubmed-article:17287338 | pubmed:author | pubmed-author:SerulleYY | lld:pubmed |
| pubmed-article:17287338 | pubmed:author | pubmed-author:OpalachKK | lld:pubmed |
| pubmed-article:17287338 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17287338 | pubmed:day | 13 | lld:pubmed |
| pubmed-article:17287338 | pubmed:volume | 104 | lld:pubmed |
