| First Author | de Sousa DMB | Year | 2023 |
| Journal | Aging (Albany NY) | Volume | 15 |
| Issue | 3 | Pages | 630-649 |
| PubMed ID | 36734880 | Mgi Jnum | J:338578 |
| Mgi Id | MGI:7440182 | Doi | 10.18632/aging.204502 |
| Citation | de Sousa DMB, et al. (2023) Immune-mediated platelet depletion augments Alzheimer's disease neuropathological hallmarks in APP-PS1 mice. Aging (Albany NY) 15(3):630-649 |
| abstractText | In Alzheimer's disease (AD), platelets become dysfunctional and might contribute to amyloid beta deposition. Here, we depleted platelets in one-year-old APP Swedish PS1 dE9 (APP-PS1) transgenic mice for five days, using intraperitoneal injections of an anti-CD42b antibody, and assessed changes in cerebral amyloidosis, plaque-associated neuritic dystrophy and gliosis. In APP-PS1 female mice, platelet depletion shifted amyloid plaque size distribution towards bigger plaques and increased neuritic dystrophy in the hippocampus. In platelet-depleted females, plaque-associated Iba1+ microglia had lower amounts of fibrillar amyloid beta cargo and GFAP+ astrocytic processes showed a higher overlap with thioflavin S+ amyloid plaques. In contrast to the popular hypothesis that platelets foster plaque pathology, our data suggest that platelets might limit plaque growth and attenuate plaque-related neuritic dystrophy at advanced stages of amyloid plaque pathology in APP-PS1 female mice. Whether the changes in amyloid plaque pathology are due to a direct effect on amyloid beta deposition or are a consequence of altered glial function needs to be further elucidated. |
