Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-7-24
pubmed:abstractText
Numerous neurological diseases which include neuroinflammatory components exhibit an age-related prevalence. The aging process is characterized by an increase of inflammatory mediators both systemically and in the brain, which may prime glial cells. However, little information is available on age-related changes in the glial response of the healthy aging brain to an inflammatory challenge. This problem was here examined using a mixture of the proinflammatory cytokines interferon-gamma and tumor necrosis factor-alpha, which was injected intracerebroventricularly in young (2-3.5 months), middle-aged (10-11 months) and aged (18-21 months) mice. Vehicle (phosphate-buffered saline) was used as control. After a survival of 1 or 2 days (all age groups) or 4 days (young and middle-aged animals), immunohistochemically labeled astrocytes and microglia were investigated both qualitatively and quantitatively. In all age groups, astrocytes were markedly activated in periventricular as well as in deeper brain regions 2 days following cytokine treatment, whereas microglia activation was already evident at 24 h. Interestingly, cytokine-induced activation of both astrocytes and microglia was significantly more marked in the brain of aged animals, in which it included numerous ameboid microglia, than of younger age groups. Moderate astrocytic activation was also seen in the hippocampal CA1 field of vehicle-treated aged mice. FluoroJade B histochemistry and the terminal deoxynucleotidyl transferase-mediated UTP nick-end labeling technique, performed at 2 days after cytokine administration, did not reveal ongoing cell death phenomena in young or aged animals. This indicated that glial cell changes were not secondary to neuronal death. Altogether, the findings demonstrate for the first time enhanced activation of glial cells in the old brain, compared with young and middle-aged subjects, in response to cytokine exposure. Interestingly, the results also suggest that such enhancement does not develop gradually since youth, but appears characterized by relatively late onset.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:day
25
pubmed:volume
141
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
645-61
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16730918-Age Factors, pubmed-meshheading:16730918-Aging, pubmed-meshheading:16730918-Analysis of Variance, pubmed-meshheading:16730918-Animals, pubmed-meshheading:16730918-Antigens, CD11b, pubmed-meshheading:16730918-Antigens, Differentiation, pubmed-meshheading:16730918-Brain, pubmed-meshheading:16730918-Cell Death, pubmed-meshheading:16730918-Cytokines, pubmed-meshheading:16730918-Glial Fibrillary Acidic Protein, pubmed-meshheading:16730918-Immunohistochemistry, pubmed-meshheading:16730918-In Situ Hybridization, pubmed-meshheading:16730918-In Situ Nick-End Labeling, pubmed-meshheading:16730918-Male, pubmed-meshheading:16730918-Mice, pubmed-meshheading:16730918-Mice, Inbred C57BL, pubmed-meshheading:16730918-Neuroglia, pubmed-meshheading:16730918-Organic Chemicals, pubmed-meshheading:16730918-Time Factors
pubmed:year
2006
pubmed:articleTitle
Cytokine-induced activation of glial cells in the mouse brain is enhanced at an advanced age.
pubmed:affiliation
Department of Morphological and Biomedical Sciences, University of Verona, Faculty of Medicine, Strada Le Grazie 8, 37134 Verona, Italy.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't