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Neurobiol Aging. 2015 Apr;36(4):1639-1652. doi: 10.1016/j.neurobiolaging.2014.11.023. Epub 2015 Jan 16.

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

Author information

1
UMR Inserm U930, Université François-Rabelais de Tours, Tours, France.
2
Laboratoires Cyclopharma, Tours, France.
3
UMR Inserm U930, Université François-Rabelais de Tours, Tours, France; CHRU de Tours, Tours, France.
4
School of Chemistry and Faculty of Health Sciences, University of Sydney, Sydney, Australia.
5
EA 3808 CiMoTheMA, Université de Poitiers, Poitiers, France.
6
UMR Inserm U930, Université François-Rabelais de Tours, Tours, France. Electronic address: sylvie.chalon@univ-tours.fr.

Abstract

We studied concomitantly the level of neuroinflammation and β-amyloid (Aβ) load in the APPswePS1dE9 transgenic mouse model of Alzheimer's disease using positron emission tomography. The translocator protein 18 kDa (TSPO) tracer [(18)F]DPA-714 was used to measure neuroinflammation and [(18)F]AV-45 for Aβ 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.

KEYWORDS:

Alzheimer's disease; Amyloid load; Neuroinflammation; PET

[Indexed for MEDLINE]

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