Linked Life Data

18457819

Source:http://linkedlifedata.com/resource/pubmed/id/18457819

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2008-6-2
pubmed:abstractText
The aim of this study is to clarify the relationship of microglia to phosphorylated tau accumulation and the characteristics of microglial activation in brain lesions of human tauopathies in comparison to mutant tau transgenic (TG) mice. We performed immunocytochemical analyses of brains from six patients with tauopathies, and 24 mice (18 TG mice expressing mutant tau P301L and six non-TG control mice, 11 to 27 months of age) using anti-tau antibodies and various microglial markers. In the tau TG, both semiquantitative severity ratings of microglial activation and an ultrastructural study were performed. In human tauopathies, Iba1- and major histocompatibility complex (MHC) class II-positive activated microglia increased in regions of phosphorylated tau (AT8) accumulation. The immunoreactivity of scavenger receptor class A (SRA) was present in some activated microglia, including phagocytic microglia in Alzheimer's disease (AD). Double-immunofluorescent analysis under a confocal microscope showed activated microglia at the vicinity of AT8-positive cells. Semiquantitative data of the TG and control mice indicated that the immunopositivity of AT8 was closely associated with the number of Iba1-positive microglia in the cortical area. Tau-associated microglia showed rare immunoreactivity for MHC class II antigen and SRA in the TG mice. Ultrastructurally, activated microglia with enlarged cytoplasm were located near neurons containing abnormal cytoskeletons. This comparative study of human tauopathies and tau TG mice indicated that microglial activation was closely related to phosphorylated tau accumulation, and that activated microglia of the TG mice may have the low expression of MHC class II and SRA compared with those of human tauopathies.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
12
pubmed:volume
1214
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
159-68
pubmed:meshHeading
pubmed-meshheading:18457819-Age Factors, pubmed-meshheading:18457819-Aged, pubmed-meshheading:18457819-Aged, 80 and over, pubmed-meshheading:18457819-Animals, pubmed-meshheading:18457819-Brain, pubmed-meshheading:18457819-DNA-Binding Proteins, pubmed-meshheading:18457819-Female, pubmed-meshheading:18457819-Histocompatibility Antigens Class II, pubmed-meshheading:18457819-Humans, pubmed-meshheading:18457819-Leucine, pubmed-meshheading:18457819-Male, pubmed-meshheading:18457819-Mice, pubmed-meshheading:18457819-Mice, Transgenic, pubmed-meshheading:18457819-Microglia, pubmed-meshheading:18457819-Microscopy, Electron, Transmission, pubmed-meshheading:18457819-Middle Aged, pubmed-meshheading:18457819-Mutation, pubmed-meshheading:18457819-Proline, pubmed-meshheading:18457819-Receptors, Scavenger, pubmed-meshheading:18457819-Tauopathies, pubmed-meshheading:18457819-tau Proteins
pubmed:year
2008
pubmed:articleTitle
Microglial activation in brain lesions with tau deposits: comparison of human tauopathies and tau transgenic mice TgTauP301L.
pubmed:affiliation
Department of Human Pathology, Gunma University Graduate School of Medicine, Gunma, Japan. achie@med.gunma-u.ac.jp
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't