Introduction: Over the years the prevalence of metabolic syndrome (MetS) has drastically increased in developing countries as a major byproduct of industrialization. Many factors, such as the consumption of high-calorie diets and a sedentary lifestyle, bolster the spread of this disorder. Undoubtedly, the massive and still increasing incidence of MetS places this epidemic as an important public health issue. Hereon we revisit another outlook of MetS beyond its classical association with cardiovascular disease (CVD) and Diabetes Mellitus Type 2 (DM2), for MetS also poses a risk factor for the nervous tissue and threatens neuronal function. First, we revise a few essential concepts of MetS pathophysiology. Second, we explore some neuroprotective approaches in MetS pertaining brain hypoxia. The articles chosen for this review range from the years 1989 until 2017; the selection criteria was based on those providing data and exploratory information on MetS as well as those that studied innovative therapeutic approaches.Pathophysiology: The characteristically impaired metabolic pathways of MetS lead to hyperglycemia, insulin resistance (IR), inflammation, and hypoxia, all closely associated with an overall pro-oxidative status. Oxidative stress is well-known to cause the wreckage of cellular structures and tissue architecture. Alteration of the redox homeostasis and oxidative stress alter the macromolecular array of DNA, lipids, and proteins, in turn disrupting the biochemical pathways necessary for normal cell function.Neuroprotection: Different neuroprotective strategies are discussed involving lifestyle changes, medication aimed to mitigate MetS cardinal symptoms, and treatments targeted toward reducing oxidative stress. It is well-known that the routine practice of physical exercise, aerobic activity in particular, and a complete and well-balanced nutrition are key factors to prevent MetS. Nevertheless, pharmacological control of MetS as a whole and pertaining hypertension, dyslipidemia, and endothelial injury contribute to neuronal health improvement.Conclusion: The development of MetS has risen as a risk factor for neurological disorders. The therapeutic strategies include multidisciplinary approaches directed to address different pathological pathways all in concert.

In 1934, J. C. Fasciolo had to submit a thesis and Dr. Houssay suggested he investigate about nephrogenic hypertension. E. Braun-Menéndez showed interest in helping and Drs. L.F. Leloir and J.M. Muñoz from the Institute of Physiology joined them in their attempt to isolate and purify the pressor substance. In 1939, they extracted the substance "hypertension" from the venous blood from the ischemic kidneys. They proposed an enzymesubstrate reaction. They named hypertensinogen the substrate and hypertensinases the enzymes that break down the hypertension. Two months following the Argentine publication, the team in the United States, formed by I.H. Page and O.M. Helmer, published their findings, which were in agreement with those reported by the Argentine team. By 1940, they isolated angiotonin, the equivalent of hypertension, and called the renin substrate hypertensinogen. In 1957, in the conference held in Ann Arbor, Braun-Menéndez and Page agreed on a new nomenclature. As a result, the words angiotensinogen and angiotensin were born from the combination of the names originally set by both teams. The discovery of the renin-angiotensin system is an example that science should follow: Value the progress made by colleagues, collaborate side by side, and pursue the ultimate truth.

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