AGING, 2023 · DOI: null · Published: February 1, 2023
Alzheimer's disease (AD) is characterized by the presence of amyloid beta plaques and neurofibrillary tau tangles, leading to memory loss and cognitive decline. Platelets, which are blood cells, can produce amyloid beta peptides, which may contribute to the formation of amyloid plaques in the brain. This study investigates how reducing platelet numbers affects AD pathology in mice. The researchers found that short-term platelet depletion in female APP-PS1 mice actually worsened AD hallmarks, such as increased amyloid plaque growth and neuritic dystrophy, suggesting that platelets might have a protective role at advanced stages of amyloid plaque pathology.
The study challenges the hypothesis that reducing platelet numbers might ameliorate AD pathology. It suggests that platelets might have a protective role at advanced stages of amyloid plaque pathology.
Platelet depletion affected AD pathology differentially in female and male APP-PS1 mice. Suggesting sex-specific differences in the systemic milieu that favor amyloid plaque formation in females.
Platelet depletion impacts microglial phagocytosis and astrocyte-plaque interaction, indicating the need to investigate the molecular mechanisms underlying the effects of platelet depletion on glial function and its biological implications for AD pathology.