Platelet-Derived Amyloid-β Protein Precursor as a Biomarker of Alzheimer's Disease

Background: Platelet proteins may be associated with Alzheimer's disease (AD) pathology. Objective: To investigate the relationship between platelet proteins and cerebrospinal fluid (CSF) biomarkers of AD and cognition in individuals with memory decline to identify effective screening methods for detecting the early stages of the disease. Methods: We classified 68 participants with subjective memory decline according to the ATN framework determined by CSF amyloid-beta (A), CSF p-tau (T), and t-tau (N). All participants underwent Mini-Mental State Examination (MMSE) and platelet-related protein content testing. Results: Eighteen participants had normal AD biomarkers (NCs), 24 subjects had non-AD pathologic changes (non-AD), and 26 subjects fell within the Alzheimer's continuum (AD). The platelet amyloid-beta protein precursor (A beta PP) ratio in the AD group was significantly lower than in the non-AD and NCs groups, and positively correlated with MMSE scores and CSF amyloid-beta 42 level, which could affect MMSE scores through CSF amyloid-beta 42. Levels of platelet phosphorylated-tau 231 and ser396/404 phosphorylated tau were elevated in both AD and non-AD compared to NCs. Additionally, the receiver operating characteristic analysis demonstrated that the platelet A beta PP ratio was a sensitive identifier for differentiating the AD from NCs (AUC= 0.846) and non-AD (AUC= 0.768). And ser396/404 phosphorylated tau could distinguish AD from NCs. Conclusion: Our study was the first to find an association between platelet A beta PP ratio and CSF biomarkers of AD, which contribute to the understanding of the peripheral changes in AD. These findings may help to discover potential feasible and effective screening tools for AD.

Automated summary

This study found an association between platelet proteins and cerebrospinal fluid (CSF) biomarkers of Alzheimer's disease (AD). The platelet AβPP ratio was found to be a sensitive identifier for differentiating AD from non-AD pathologies. Additionally, phosphorylated tau levels were elevated in both AD and non-AD groups compared to normal controls.