Affiliations 

  • 1 Department of Neurosciences, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Malaysia
  • 2 Department of Family Medicine, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Malaysia
  • 3 Department of Internal Medicine, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Malaysia
  • 4 Neurobiology of Aging and Disease Laboratory, Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore
  • 5 Anatomy Unit, International Medical School (IMS), Management and Science University (MSU), Shah Alam, Malaysia
  • 6 Department of Psychology and Counselling, Faculty of Arts and Social Science, Universiti Tunku Abdul Rahman (UTAR), Kampar, Malaysia
  • 7 Translational Neuroscience Lab, University of Queensland (UQ), Centre for Clinical Research, The University of Queensland, Herston, QLD, Australia
  • 8 Center for Functional Connectomics, Brain Science Institute, Korea Institute of Science and Technology (KIST), Seoul, South Korea
  • 9 School of Pharmacy, Monash University Malaysia, Bandar Sunway, Malaysia
  • 10 Department of Human Anatomy, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang, Malaysia
  • 11 Crescent School of Pharmacy, B.S. Abdur Rahman Crescent Institute of Science and Technology, Chennai, India
Front Cardiovasc Med, 2021;8:632131.
PMID: 33718454 DOI: 10.3389/fcvm.2021.632131

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.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.