В 3xTg-AD, но не в Tg-SwDI Mice.

Splenomegaly, Spleen Amyloidosis and Neutrophil Infiltration are Present in 3xTg-AD, but not Tg-SwDI Mice.

It is now widely accepted that the development of neurodegenerative diseases depends on and affects many pathological processes, both in the brain and the periphery. Inflammatory, cardiovascular, metabolic, cerebrovascular, autoimmune, and other environmental factors have been extensively studied and shown to contribute notably to the onset, pathogenesis, and clinical outcome of Alzheimer´s disease (AD), Parkinson´s disease (PD), cerebral amyloid angiopathy (CAA), multiple sclerosis, and other neurological disorders. Likewise, AD-induced changes in other tissues outside the central nervous system, such as abnormalities observed in the liver, spleen, or lungs, have been documented and extensively studied, leading to a better understanding of brain-periphery crosstalk in neurodegenerative diseases and the development of novel diagnostic and therapeutic approaches. In this study, we documented striking differences in the periphery in two frequently used, well-established APP transgenic mouse models of AD: 3xTg-AD mice, harboring three human genes (APP, tau, and Psen1), and Tg-SwDI mice, expressing human APP with the Swedish and vasculotropic Dutch/Iowa mutations in the brain. We documented splenomegaly, immunoglobulin-associated spleen amyloidosis, and an increase in the percentage of neutrophils in the spleen and macrophages in the liver in 3xTg-AD mice but not in age-matched Tg-SwDI mice, which are commonly used as an AD/CAA model. Our data suggest that the results observed in any transgenic mouse strain should be taken into account with caution. A detailed knowledge of pathological characteristics recapitulated in a particular strain can help to determine which mice are more appropriate for studying a specific mechanism or therapeutic approach.