Abstract
Cerebral small vessel disease (CSVD) represents a spectrum of pathological processes of various etiologies affecting the brain microcirculation that can trigger neuroinflammation and the subsequent neurodegenerative cascade. Prevalent with aging, CSVD is a recognized risk factor for stroke, vascular dementia, Alzheimer disease, and Parkinson disease. Despite being the most common neurodegenerative condition with cerebrocardiovascular axis, understanding about it remains poor. Interestingly, modifiable risk factors such as unhealthy diet including high intake of processed food, high-fat foods, and animal by-products are known to influence the non-neural peripheral events, such as in the gastrointestinal tract and cardiovascular stress through cellular inflammation and oxidation. One key outcome from such events, among others, includes the cellular activations that lead to elevated levels of endogenous cellular-derived circulating microparticles (MPs). MPs can be produced from various cellular origins including leukocytes, platelets, endothelial cells, microbiota, and microglia. MPs could act as microthrombogenic procoagulant that served as a plausible culprit for the vulnerable end-artery microcirculation in the brain as the end-organ leading to CSVD manifestations. However, little attention has been paid on the potential role of MPs in the onset and progression of CSVD spectrum. Corroboratively, the formation of MPs is known to be influenced by diet-induced cellular stress. Thus, this review aims to appraise the body of evidence on the dietary-related impacts on circulating MPs from non-neural peripheral origins that could serve as a plausible microthrombosis in CSVD manifestation as a precursor of neurodegeneration. Here, we elaborate on the pathomechanical features of MPs in health and disease states; relevance of dietary patterns on MP release; preclinical studies pertaining to diet-based MPs contribution to disease; MP level as putative surrogates for early disease biomarkers; and lastly, the potential of MPs manipulation with diet-based approach as a novel preventive measure for CSVD in an aging society worldwide.
Highlights
An acute cerebrovascular event due to an occlusion of small blood vessels deep within the brain is a known manifestation of small vessel disease (SVD) involving the brain small end arteries, capillaries, venules, and arterioles [1,2,3]
In relation to cerebral SVD (CSVD) clinical manifestations, numerous reports linking MP subpopulations as CSVD correlates may well reflect the fact that PS-bearing MPs and clotting factors aided the aggregation of platelet and synthesis of fibrin, which lead to the plausible microthrombus involvement in CSVD pathomechanism
A previous study reported the reduced level of EC-derived MPs (EDMPs) (E-selectin), thrombomodulin, Creactive protein (CRP), and plateletderived MPs (PDMPs) (P-selectin) in individuals who practiced low-carbohydrate diet (LCD) [275], i.e., likely to reduce the risk toward type 2 diabetes mellitus (T2DM) and metabolic syndrome, two major risk factors for CSVD
Summary
An acute cerebrovascular event due to an occlusion (or ischemia) of small blood vessels deep within the brain is a known manifestation of small vessel disease (SVD) involving the brain small end arteries, capillaries, venules, and arterioles [1,2,3]. Among the known modifiable risk factors for stroke, dietary patterns are recognized to modulate the non-neural peripheral events such as in the gastrointestinal tract (GIT) (i.e., GIT dysbiosis) and cardiovascular stress through cellular inflammations and oxidation. Unhealthy dietary habits have been reported to contribute to higher risk of developing metabolic disease, coronary heart disease, and stroke [11] and likely to modulate systemic peripheral events that can influence the development and progression of NDD such as CSVD. MPs could act as microthrombogenic procoagulant that could be detrimental to the vulnerable microcirculation, the penetrating, poorly collateralized end-arteries in the brain parenchyma, leading to CSVD manifestations. This review aims to appraise the body of evidence on the dietary-related impacts on circulating MPs from nonneural peripheral origins that could serve as a plausible microthrombogenic role in CSVD manifestation and a precursor of NDD. We elaborate on the pathomechanical features of MPs in health and disease states; relevance of dietary patterns on MP release; preclinical studies pertaining to diet-based MPs contribution to disease; MP level as putative surrogates for early disease biomarkers; and lastly, the potential of MPs manipulation with diet-based approach as a novel preventive measure for CSVD
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