Amyloid load and translocator protein 18 kDa in APPswePS1-dE9 mice: a longitudinal study

NEUROBIOLOGY OF AGING

卷:36

Article

Serriere, Sophie¹  Tauber, Clovis¹  Vercouillie, Johnny¹  Mothes, Celine²  Pruckner, Christelle¹  Guilloteau, Denis^1,3  Kassiou, Michael^4,5  Domene, Aurelie¹  Garreau, Lucette¹  Page, Guylene⁶  Chalon, Sylvie¹ 

[1] Univ Tours, UMR Inserm U930, Tours, France

[2] Labs Cyclopharma, Tours, France

[3] CHRU Tours, Tours, France

[4] Univ Sydney, Sch Chem, Sydney, NSW 2006, Australia

[5] Univ Sydney, Fac Hlth Sci, Sydney, NSW 2006, Australia

[6] Univ Poitiers, EA CiMoTheMA 3808, Poitiers, France

关键词: Alzheimer's disease;    Amyloid load;    Neuroinflammation;    PET;   

DOI  :  10.1016/j.neurobiolaging.2014.11.023

来源: Elsevier

【 摘 要 】

We studied concomitantly the level of neuroinflammation and beta-amyloid (A beta) load in the APPswePS1dE9 transgenic mouse model of Alzheimer's disease using positron emission tomography. The translocator protein 18 kDa (TSPO) tracer [F-18]DPA-714 was used to measure neuroinflammation and [F-18]AV-45 for A beta load in mice at 6, 9, 12, 15, and 19 months of age. At 19 months, we also analyzed the neuroinflammatory and neuroanatomic status of mice brains. The main affected brain areas were the cortex and hippocampus, with a concomitant progression of neuroinflammation with increased amyloid burden. At 19 months, no increase in TSPO binding was observed in the cerebellum; immunostaining revealed W0-2-positive plaques, indicating that the amyloid deposits seemed not stimulate inflammation. This finding was in agreement with the observed level of microglia and astrocytes staining. Our findings provide a better understanding of the relationships between neuroinflammation and plaque accumulation in the course of the disease in this mouse model. The monitoring of both processes should be of value to validate potential therapeutic approaches. (C) 2015 Elsevier Inc. All rights reserved.

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