ORIGINAL ARTICLE Plasma microparticles in Alzheimer’s disease: The role of vascular dysfunction Soheila Hosseinzadeh 1,2 & Maryam Noroozian 3 & Esmaeil Mortaz 4 & Kazem Mousavizadeh 5 Received: 15 July 2017 /Accepted: 14 November 2017 # Springer Science+Business Media, LLC, part of Springer Nature 2017 Abstract Cerebrovascular lesions, a potent stimulus for endothelial cell activation, trigger cognitive and degenerative changes and contribute to pathology of Alzheimer’s disease (AD). Circulating microparticles (MPs) are actively involved in the patho- genesis of AD and cerebrovascular diseases, which share common vascular risk factors. We examined the plasma changes of endothelial MPs (EMPs) and platelet MPs (PMPs) in AD patients with vascular risk factors. The plasma Annexin V + CD 41a - CD144 + EMPs and Annexin V + CD41a + CD144 - PMPs of 37 patients with AD, with or without vascular risk factors (hyper- tension, diabetes, dyslipidemia, stroke, coronary artery disease, and smoking), and 10 age-matched controls were quantified by flow cytometry. Pearson correlation analysis used to evaluate the linear relationship between variables. Significantly higher plasma levels of EMPs were observed in AD patients with vascular risk factors as compared to the patients without vascular risk factors [Mean Difference (MD): 2587.80, 95% confidence interval (CI) 770.30-4404.80], and control subjects (MD: 4990.60, 95% CI, 3054.40-6926.79). Significant correlations were found between circulating EMPs, total MPs, and PMPs. There were no significant correlations between plasma levels of EMPs/ PMPs, and cognitive decline indices. Circulating EMP levels are influenced by AD disease status, and plasma levels of MPs and PMPs are associated with vascular risk factors in patients with AD. EMP phenotyping, as cellular biomarkers of vascular injury/dysfunction, and their effects on cerebral perfusion, and cognitive decline should be further investigated. Keywords Alzheimer’s disease . Blood platelets . Cell-derived microparticles . Cognitive dysfunction . Dementia . Vascular risk factors Introduction Cerebrovascular dysfunction is an important factor in biological basis of Alzheimer ’s disease (AD) (Zamolodchikov and Strickland 2016). Whether vascular pathology is a cause, or consequence of AD has not yet been established (Tractenberg and Aisen 2009). Vascular endothelial cell activation results in release of a large number of inflammatory proteins, procoagulant, and anticoagulant moieties (e. g. microparticles (MPs), pro-inflammatory cytokines, and others), that can injure neural cells (Felmeden et al. 2003). Both prothrombotic state and chronic inflammation are implicated in AD pathogenesis. MPs/microvesicles, less than 1.1 μm in diameter, are mem- brane vesicles released in response to various stimuli; such as activation or apoptosis (Porro et al. 2015). MPs of endothelial, platelet, and leukocyte origin are consistently detectable in plasma of healthy individuals. Their levels are increased under conditions of vascular injury/dysfunction, and appear to re- flect vascular health (Burger et al. 2012). Shedding of cellular MPs in the neurovascular network may be linked to the onset and progression of a variety of central nervous system dis- eases; including stroke, vascular dementia, inflammatory, and age-related neurodegenerative disorders (Doeuvre et al. 2009). The role of MPs derived from platelets, endothelial * Maryam Noroozian maryam.noroozian.mn@gmail.com 1 Neuroscience Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran 2 Department of Physiology, School of Medicine, Babol University of Medical Sciences, Babol, Iran 3 Memory and Behavioral Neurology Division, Department of Psychiatry, Roozbeh Hospital, Tehran University of Medical Sciences, Tehran 1333795914, Iran 4 Department of Immunology, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran 5 Cellular and Molecular Research Center and Department of Molecular Medicine, Faculty of Advanced Technologies in Medicine, Iran University of Medical Sciences, Tehran, Iran Metabolic Brain Disease https://doi.org/10.1007/s11011-017-0149-3