Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-1-17
pubmed:abstractText
It has been established that neuroinflammation is present in the substantia nigra (SN) of Parkinson disease (PD) cases but the factors responsible are as yet unknown. One contributing protein may be the intercellular adhesion molecule-1 (ICAM-1, CD54). ICAM-1 with its counter receptor, the lymphocyte function-associated antigen 1 (LFA-1) is known to play a key role in inflammatory processes and in T-cell mediated host defense mechanisms. We detected large numbers of ICAM-1-positive reactive astrocytes in the SN of a series of 14 patients with neuropathologically confirmed PD, including 3 of familial origin, compared with 11 age-matched controls. In PD SN, these ICAM-1-positive reactive astrocytes were particularly concentrated around many residual neurons in areas of heavy neuronal loss and extracellular melanin accumulation. LFA-1-positive reactive microglia gathered in areas of intense ICAM-1 expression, and LFA-1-positive leukocytes were identified infiltrating the tissue. Double immunostaining for ICAM-1 and LFA-1 revealed aggregates of reactive microglia embedded in areas of diffuse ICAM-1. Leukocyte counts were 5 fold higher in PD SN compared to controls (P < 0.001). Similar over-expression of ICAM-1 was found in monkeys that had been exposed to MPTP from 5.5 to 14 years previously compared with control monkeys. The presence of ICAM-1-positive reactive astrocytes in Parkinson disease and MPTP-treated monkeys is indicative of a sustained inflammatory process and suggests that antiinflammatory agents may have a place in PD therapy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0014-4886
pubmed:author
pubmed:issnType
Print
pubmed:volume
197
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
275-83
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16336966-1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, pubmed-meshheading:16336966-Adult, pubmed-meshheading:16336966-Aged, pubmed-meshheading:16336966-Aged, 80 and over, pubmed-meshheading:16336966-Animals, pubmed-meshheading:16336966-Astrocytes, pubmed-meshheading:16336966-Case-Control Studies, pubmed-meshheading:16336966-Cell Count, pubmed-meshheading:16336966-Disease Models, Animal, pubmed-meshheading:16336966-Female, pubmed-meshheading:16336966-Humans, pubmed-meshheading:16336966-Immunohistochemistry, pubmed-meshheading:16336966-Inflammation, pubmed-meshheading:16336966-Intercellular Adhesion Molecule-1, pubmed-meshheading:16336966-Leukocytes, pubmed-meshheading:16336966-Lymphocyte Function-Associated Antigen-1, pubmed-meshheading:16336966-MPTP Poisoning, pubmed-meshheading:16336966-Macaca mulatta, pubmed-meshheading:16336966-Male, pubmed-meshheading:16336966-Middle Aged, pubmed-meshheading:16336966-Parkinson Disease, pubmed-meshheading:16336966-Postmortem Changes, pubmed-meshheading:16336966-Substantia Nigra
pubmed:year
2006
pubmed:articleTitle
Role of ICAM-1 in persisting inflammation in Parkinson disease and MPTP monkeys.
pubmed:affiliation
Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, Canada V6T1Z3.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't