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P1‐110: Microglia ablation does not alter plaque formation and maintenance in a mouse model of cerebral amyloidosis
Author(s) -
Grathwohl Stefan,
Kälin Roland,
Bolmont Tristan,
Radde Rebecca,
Kohsaka Shinichi,
Wolburg Hartwig,
Heppner Frank L.,
Jucker Mathias
Publication year - 2008
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2008.05.697
Subject(s) - microglia , genetically modified mouse , transgene , pathology , amyloidosis , amyloid (mycology) , in vivo , biology , medicine , immunology , inflammation , biochemistry , microbiology and biotechnology , gene
longitudinal designs. Results: Histological analysis revealed an age dependent increase in tau-immunoreactivity in L1 mice carrying the truncated version of the human tau protein; aggregates took the form pre-filamentous amorphous aggregates also seen in AD and were highest in cortical and hippocampal regions. In young and old mice, anxiety levels were normal. Non-associative memory tested in the open field was impaired paralleled by hyperactivity. Spatial memory was impaired in a gene-dose related manner: homozygous animals performed worse than heterozygous animals. In heterozygous mice, although muscle tone was normal, motor learning/ coordination and sensory-motor abilities were compromised. Deficits were less severe in a longitudinal relative to cross-sectional study design, but independent of gene-expression levels. Conclusions: Transgenic mice expressing a truncated form of human tau develop pre-filamentous pathology in forebrain in conjunction with subtle deficiencies in learning and motor coordination.