| First Author | Rodriguez-Lopez A | Year | 2023 |
| Journal | J Neuroimmunol | Volume | 382 |
| Pages | 578150 | PubMed ID | 37467699 |
| Mgi Jnum | J:354042 | Mgi Id | MGI:7719056 |
| Doi | 10.1016/j.jneuroim.2023.578150 | Citation | Rodriguez-Lopez A, et al. (2023) Increased TSPO expression, pyroglutamate-modified amyloid beta (AbetaN3(pE)) accumulation and transient clustering of microglia in the thalamus of Tg-SwDI mice. J Neuroimmunol 382:578150 |
| abstractText | Epidemiological studies showed that Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA) frequently co-occur; however, the precise mechanism is not well understood. A unique animal model (Tg-SwDI mice) was developed to investigate the early-onset and robust accumulation of both parenchymal and vascular Abeta in the brain. Tg-SwDI mice have been extensively used to study the mechanisms of cerebrovascular dysfunction, neuroinflammation, neurodegeneration, and cognitive decline observed in AD/CAA patients and to design biomarkers and therapeutic strategies. In the present study, we documented interesting new features in the thalamus of Tg-SwDI mice: 1) a sharp increase in the expression of ionized calcium-binding adapter molecule 1 (Iba-1) in microglia in 6-month-old animals; 2) microglia clustering at six months that disappeared in old animals; 3) N-truncated/modified AbetaN3(pE) peptide in 9-month-old female and 12-month-old male mice; 4) an age-dependent increase in translocator protein (TSPO) expression. These findings reinforce the versatility of this model for studying multiple pathological issues involved in AD and CAA. |
