A stereological study of glial activation in GFAP-IL6 mice: A model of chronic neuroimmune conditions.

Gliosis Astrocytosis Neuroglia
DOI: 10.1002/alz.053164 Publication Date: 2021-12-01
ABSTRACT
Understanding the role of chronic neuroinflammation, described by increased astro- and microglia activation, in pathogenesis Alzheimer's disease (AD) is becoming crucial due to its throughout progression (Deczkowska et al., 2018). In search a suitable mouse model glial we characterized GFAP-IL6 transgenic which pro-inflammatory cytokine interleukine-6 overexpressed under control fibrillary acidic protein (GFAP) promoter (Campbell 1993). The mice display inflammatory conditions brain, with homozygous developing an aggressive pathology tremor, ataxia, seizures 6 months age While heterozygous phenotype milder astrocytosis, microgliosis, angiogenesis, neurodegeneration. Moreover, evidences showed that progressive motor cognitive impairment correlated level microgliosis (Heyser 1997).Using immunohistochemically stained brain sections 3 old wild-type (WT) (n=4), (n=5), (n=5) mice, estimated absolute number morphology Iba1 GFAP positive cells, astrocytes respectively. We focused analysis on cortex, hippocampus, cerebellum, medial septum (MS) find possible connection loss cholinergic neurons during AD.Homozygous increase 50-80% all areas compared WT, while was 35-60%. 40% MS nearly 50% cerebellum heterozygous. are 70% more than heterozygous, similar WT. morphological different ramification microglial cell body size WT.The stronger impact neuroinflammation at suggests application evaluating early stages. results highlight high vulnerability inflammation MS. Increased cerebellar mediated emphasized chance develop deficits.
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