| First Author | Osse AML | Year | 2023 |
| Journal | Brain Behav Immun | Volume | 110 |
| Pages | 260-275 | PubMed ID | 36906075 |
| Mgi Jnum | J:335782 | Mgi Id | MGI:7463615 |
| Doi | 10.1016/j.bbi.2023.03.002 | Citation | Osse AML, et al. (2023) Reduction in GABAB on glia induce Alzheimer's disease related changes. Brain Behav Immun 110:260-275 |
| abstractText | Alzheimer's Disease (AD) is a neurodegenerative disorder characterized by beta-amyloid plaques (Abeta), neurofibrillary tangles (NFT), and neuroinflammation. Data have demonstrated that neuroinflammation contributes to Abeta and NFT onset and progression, indicating inflammation and glial signaling is vital to understanding AD. A previous investigation demonstrated a significant decrease of the GABA(B) receptor (GABA(B)R) in APP/PS1 mice (Salazar et al., 2021). To determine if changes in GABA(B)R restricted to glia serve a role in AD, we developed a mouse model with a reduction of GABA(B)R restricted to macrophages, GAB/CX3ert. This model exhibits changes in gene expression and electrophysiological alterations similar to amyloid mouse models of AD. Crossing the GAB/CX3ert mouse with APP/PS1 resulted in significant increases in Abeta pathology. Our data demonstrates that decreased GABA(B)R on macrophages leads to several changes observed in AD mouse models, as well as exacerbation of AD pathology when crossed with existing models. These data suggest a novel mechanism in AD pathogenesis. |
