Platelet and Plasma Phosphatidylcholines as Biomarkers to Diagnose Cerebral Amyloid Angiopathy.

Bettina M Foidl,Herbert Oberacher,Josef Marksteiner,Christian Humpel

doi:10.3389/fneur.2020.00359

Abstract

Alzheimer's disease is a severe neurodegenerative brain disorder and characterized by deposition of extracellular toxic β-amyloid (42) plaques and the formation of intracellular tau neurofibrillary tangles. In addition, β-amyloid peptide deposits are found in the walls of small to medium blood vessels termed cerebral amyloid angiopathy (CAA). However, the pathogenesis of CAA appears to differ from that of senile plaques in several aspects. The aim of the present study was to analyze different lipids [phosphatidylcholines (PCs) and lysoPCs] in platelets and plasma of a novel mouse model of sporadic CAA (1). Our data show that lipids are significantly altered in plasma of the CAA mice. Levels of eight diacyl PCs, two acyl-alkyl PCs, and five lysoPCs were significantly increased. In extracts of mouse blood platelets, four diacyl and two acyl-alkyl PCs (but not lysoPCs) were significantly altered. Our data show that lipids are changed in CAA with a specific pattern, and we provide for the first time evidence that selected platelet and plasma PCs may help to characterize CAA.

Highlights

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder in the brain
100 lipids were determined in the plasma of wellcharacterized cerebral amyloid angiopathy (CAA) mice and compared to control mice (Table 1)
100 lipids were determined in the platelets of well-characterized CAA mice and compared to control mice (Table 2)

Summary

Introduction

The major hallmarks are extracellular β-amyloid (Aβ) plaques, intracellular tau neurofibrillary tangles, cholinergic neurodegeneration, and cerebrovascular damage [2]. A comorbid cerebral amyloid angiopathy (CAA) is found, which is characterized by the accumulation of Aβ40 in the vessels. CAA is present as an independent pathology without AD and can be characterized as a subform of vascular dementia (vaD) [3]. The origin of AD, vaD, and CAA is still not fully understood. 95% of all CAA cases are sporadic, and only 5% are explained by a genetic background [2]. More and more research suggests that vascular risk factors may play a role in the development of both sporadic CAA and AD [3,4,5,6]

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