Metabolic syndrome and neuroprotection

Abstract

Introduction. Over the years, the prevalence of metabolic syndrome has increased dramatically in developing countries as a major by-product of industrialization. Many factors, such as the consumption of hypercaloric diets and sedentary lifestyles, favor the spread of this disorder. Undoubtedly, the massive and still growing incidence of metabolic syndrome makes this epidemic a major public health problem. Metabolic syndrome is also a neurological and psychiatric risk factor. In this paper, an exploratory literature review on the subject will be performed. In this paper, we survey the information as to what is known about the metabolic syndrome beyond its classical association with cardiovascular disease and type 2 diabetes mellitus, since the metabolic syndrome also represents a risk factor for nervous tissue and threatens neuronal function. First, we present some essential concepts of the pathophysiology of metabolic syndrome. Second, we explore some neuroprotective approaches in metabolic syndrome related to cerebral hypoxia. Objectives. To update, review in an exploratory manner, and synthesize the literature concerning the neurological impact of metabolic syndrome, beyond its classical association with cardiovascular disease and type 2 diabetes mellitus. Define and review essential concepts of the pathophysiology of metabolic syndrome. To explore neuropreventive and neuroprotective strategies in metabolic syndrome related to therapeutic cerebral hypoxia. Material and methods. An exploratory survey of scientific literature from January 1989-November 2022 was carried out. Selection/inclusion criteria: scientific publications containing exploratory data and information on metabolic syndrome and neurological comorbidity and possible neurotherapeutic approaches. Pathophysiology. The metabolic pathways characteristically impaired in metabolic syndrome lead to hyperglycemia, insulin resistance, inflammation and hypoxia, all closely related to a generalized prooxidative state. Oxidative stress is well known to cause destruction of cellular structures and tissue architecture. Altered redox homeostasis and oxidative stress alter the macromolecular matrix of nuclear genetic material, lipids and proteins, which in turn disrupts biochemical pathways necessary for normal cellular function. Neuroprotection. Different neuroprotective strategies involving lifestyle changes, medications aimed at mitigating the cardinal symptoms of metabolic syndrome, and treatments aimed at reducing oxidative stress are discussed. It is well known that routine physical exercise, particularly aerobic activity, and a complete and balanced diet are key factors in preventing metabolic syndrome. However, pharmacological control of the metabolic syndrome as a whole and related hypertension, dyslipidemia and endothelial injury contribute to the improvement of neuronal health. Conclusion. The development of metabolic syndrome presents as a risk factor for the development and/or exacerbation of neurological alterations. Therapeutic strategies include multidisciplinary approaches aimed at addressing, in a concerted manner, different pathways involved in its pathophysiology