Abnormal platelet amyloid‐β precursor protein metabolism in SAMP8 mice: Evidence for peripheral marker in Alzheimer's disease

Abstract Senescence‐accelerated mouse strains have proved to be an accelerated‐aging model, which mimics numerous features with Alzheimer's disease (AD). Three, six, and nine‐month senescence‐accelerated resistant 1 and senescence‐accelerated prone 8 (SAMP8) mice were used in the current study, to unravel potential mechanisms for dementia and explore new diagnostic approaches for AD. The amyloid‐β (Aβ40) and Aβ42 levels were elevated in hippocampi and platelets from SAMP8, along with a reduced α‐secretase expression and an enhanced β‐secretase expression extent with age, compared to control mice. Furthermore, hippocampal Aβ40 and Aβ42 of SAMP8 were positively correlated with platelet of these mice with aging progression. In addition, β‐γ‐secretase‐modulated proteolytic proceeding of amyloid precursor protein in platelet might work through the PI3K/Akt/GSK3β pathway. These results indicate that platelet could be a potential early marker in the periphery to study the age‐correlative aggregation of the amyloid‐β peptide in patients with AD, while still requiring the considerable study.