Diabetes, Vascular Aging and Stroke: Old Dogs, New Tricks?

Abstract

Background: Stroke remains a leading cause of death and disability throughout the world. It is well established that Diabetes Mellitus (DM) is a risk factor for stroke, while other risk factors include dyslipidaemia and hypertension. Given that the global prevalence of diabetes steadily increases, the need for adequate glycaemic control and prevention of DM-related cardiovascular events remains a challenge for the medical community. Therefore, a re-examination of the latest data related to this issue is of particular importance. Objective: This review aims to summarise the latest data on the relationship between DM and stroke, including epidemiology, risk factors, pathogenesis, prevention and biomarkers. Methods: For this purpose, comprehensive research was performed on the platforms PubMed, Google Scholar and EMBASE with a combination of the following keywords: diabetes mellitus, stroke, macrovascular complications, diabetic stroke, cardiovascular disease. Conclusions: Much progress has been made in stroke in people with DM in terms of prevention and early diagnosis. In the field of prevention, the adaptation of the daily habits and the regulation of co-morbidity of individuals play a particularly important role. Simultaneously, the most significant revolution has been brought by the relatively new treatment options that offer protection to the cardiovascular system. Moreover, many prognostic and diagnostic biomarkers have been identified, paving the way for early and accurate diagnoses. However, to date, there are crucial points that remain controversial and need further clarification.

Increased Prevalence of Neuropsychiatric Disorders during COVID-19 Pandemic in People Needing a Non-Deferrable Neurological Evaluation

“…Demographics, clinical status, and comorbidities are essential aspects to be considered in work exploring epidemiological aspects during the pandemic [ 38 ]. Since comorbidities may worsen or provoke neurological disorders [ 39 , 40 , 41 ], we investigated the prevalence of comorbidities in patients accessing the non-deferrable neurology outpatient clinic. The three most prevalent comorbidities were hypertension, hypercholesterolemia, and diabetes in both groups, without significant differences between the pre-COVID era and during the lockdown.…”

Inflammation as A Precursor of Atherothrombosis, Diabetes and Early Vascular Aging

“…There is an older-age-dependent redistribution of adiposity toward the abdominal viscera that occurs unrelated to the total fat tissue mass and creates immune-metabolic disturbances, leading to the hypothesis that abdominal fat is associated with early aging features [12]. Furthermore, both IL-1 and IL-18 mediate obesity and also age-induced metabolic disturbances [92].…”

“…Cytokine-induced endothelial cell apoptosis; endothelium-dependent vasodilation dysfunction [127]; accelerated atherosclerosis; local tissue renin-angiotensin-aldosterone system (RAAS) in the vascular tissue [12]; free-radical-caused abnormalities in prostacyclin (prostaglandin I 2 ) secretion [129] Chronic inflammation (general and perivascular) NLPR3 activation, Il 1 beta, Il 18, Il 6 production; production of acute-phase proteins in the hepatocyte (fibrinogen, PAI-1, SAA, CRP); increased fibrinogen, TNF α, increased oxidative stress and adhesion molecules (ICAM1, VCAM1) [31,38,112,114,130] Insulin resistance…”

“…Neuropathy and autonomous nerve dysfunction Increased sympathetic activity; glycosylation end products; impaired circulation (enhanced vasoconstriction) [139] High levels of uric acid Increased vasoconstriction-cell anoxia; stimulation of renin-angiotensin-aldosterone system; perturbated dilation of the vessels due to inhibition of nitric oxide [140,141] Oxidative stress Increased expression of angiotensin II type-1 (AT1) receptor [12] AGE-advanced glycation end products; AT1-angiotensin II type-1; CRP-C-reactive protein; eNOS-endothelial nitric oxide synthase; ER-endoplasmic reticulum; FGF23-fibroblast growth factor 23; ICAM1-intercellular adhesion molecule 1; Il 1 beta-interleukin 1 beta; Il 18-interleukin 18; Il 6-interleukin 6; LDL-low-density lipoprotein; NLRP3(Nucleotide-binding oligomerization domain, Leucine rich Repeat and Pyrin domain containing 3; NO-nitric oxide; PAI-1-plasminogen activator inhibitor 1; RAAS-renin-angiotensin-aldosterone system; ROS-reactive oxygen species; SAA-serum amyloid A; TNF α-tumor necrosis factor; VCAM1-vascular cell adhesion molecule 1.…”

“…Aging is a complex biological process characterized by a progressive decline of multiorgan structure and function, with vascular remodeling, endothelial disfunction and loss of vascular compliance as common features [11]. Along with other multiple molecular changes, a relevant feature of aging is chronic low-grade inflammation [12]. This is now termed "Inflammaging".…”