| First Author | Hemonnot-Girard AL | Year | 2021 |
| Journal | Brain Behav Immun | Volume | 91 |
| Pages | 404-417 | PubMed ID | 33190798 |
| Mgi Jnum | J:322016 | Mgi Id | MGI:6741563 |
| Doi | 10.1016/j.bbi.2020.10.021 | Citation | Hemonnot-Girard AL, et al. (2021) Analysis of CX3CR1 haplodeficiency in male and female APP(swe)/PSEN1(dE9) mice along Alzheimer disease progression. Brain Behav Immun 91:404-417 |
| abstractText | Microglia, the resident immune cells of the brain, have recently emerged as key players in Alzheimer Disease (AD) pathogenesis, but their roles in AD remain largely elusive and require further investigation. Microglia functions are readily altered when isolated from their brain environment, and microglia reporter mice thus represent valuable tools to study the contribution of these cells to neurodegenerative diseases such as AD. The CX3CR1(+/eGFP) mice is one of the most popular microglia reporter mice, and has been used in numerous studies to investigate in vivo microglial functions, including in the context of AD research. However, until now, the impact of CX3CR1 haplodeficiency on the typical features of Alzheimer Disease has not been studied in depth. To fill this gap, we generated APP(swe)/PSEN1(dE9):CX3CR1(+/eGFP) mice and analyzed these mice for Alzheimer's like pathology and neuroinflammation hallmarks. More specifically, using robust multifactorial statistical and multivariate analyses, we investigated the impact of CX3CR1 deficiency in both males and females, at three typical stages of the pathology progression: at early stage when Amyloid-beta (Abeta) deposition just starts, at intermediate stage during Abeta accumulation phase and at more advanced stages when Abeta plaque number stabilizes. We found that CX3CR1 haplodeficiency had little impact on the progression of the pathology in the APP(swe)/PSEN1(dE9) model and demonstrated that the APP(swe)/PSEN1(dE9):CX3CR1(+/eGFP) line is a relevant and useful model to study the role of microglia in Alzheimer Disease. In addition, although Abeta plaques density is higher in females compared to age-matched males, we show that their glial reaction, inflammation status and memory deficits are not different. |
