Abstract
Metabolic syndrome increases the risk of vascular dementia and other neurodegenerative disorders. Recent studies underline that platelets play an important role in linking peripheral with central metabolic and inflammatory mechanisms. In this narrative review, we address the activation of platelets in metabolic syndrome, their effects on neuronal processes and the role of the mediators (e.g., serotonin, platelet-derived growth factor). Emerging evidence shows that nutritional compounds and their metabolites modulate these interactions—specifically, long chain fatty acids, endocannabinoids and phenolic compounds. We reviewed the role of activated platelets in neurovascular processes and nutritional compounds in platelet activation.
Highlights
Platelets, the smallest anucleate cells in our blood, can rapidly respond to environmental changes and are best known for their essential contribution in hemostasis, thrombosis and wound healing [1,2]
Metabolic syndrome has been associated with both increased levels of activated platelets and with dementia, in particular vascular dementia and Alzheimer’s disease (AD) [5,6]
Partly overlapping processes involved in metabolic syndrome (MetS) can activate platelets mainly via intracellular changes in osmolality, calcium concentration, membrane charge and oxidation and glycosylation of low-density lipoprotein (LDL) (Figure 2)
Summary
The smallest anucleate cells in our blood, can rapidly respond to environmental changes and are best known for their essential contribution in hemostasis, thrombosis and wound healing [1,2]. On the other hand, emerging data underline that platelets may play possibly crucial roles in neurovascular signaling and blood–brain interactions and thereby neurodegenerative disorders such as AD, as was recently reviewed by Leiter et al [7,8] This raises the question of which role platelets could play in the interactions between peripheral metabolic dysregulation, inflammation and neurodegenerative processes, and whether dietary active compounds could affect these processes. This is underlined by recent insights demonstrating that platelets can take up, transport and secrete various mediators that are of relevance for both MetS and brain neuronal and immunological functions, including the functionality of the blood-brain-barrier [7,8]. We aim to contribute to the understanding of platelets and their effects in brain function in MetS and to provide possible new directions for diet-based therapeutic interventions
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