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.

Coenzyme Q10 (CoQ10) is an important cofactor in the mitochondrial respiratory chain and a potent endogenous antioxidant. CoQ10 deficiency is currently associated with numerous diseases like mitochondrial and neurodegenerative pathologies, in which the earliest diagnosis and treatment with CoQ10 supplementation becomes paramount for patient's treatment. Consequently, the determination of CoQ10 levels in different biological matrices positions as a fundamental tool. Urine is an attractive and non-invasive alternative source to tissue, blood or other biofluids for CoQ10 analysis. However, it poses an analytical challenge, as it generally requires a complex sample preparation, with multiple steps. In this work we developed and validated a molecularly imprinted polymer solid phase extraction (MIP-SPE) followed by an HPLC-MS/MS method for the analysis of CoQ10 in urine. The MIP-SPE method developed is simple and fast compared to previously traditional reported methods, with reduced processing time, improved sample cleaning and excellent recovery values, along with its inherent high selectivity. The developed chromatographic method was validated according to FDA guidelines, and demonstrated to be suitable for the analysis of CoQ10 in urine samples with LOQ and LOD values of 0.6 ng/mL and 0.2 ng/mL of CoQ10 in urine respectively. Recovery values at three concentration levels were higher than 90.0 %.The proposed method is amenable to be applied in pediatric patients due to the low sample requirement and useful for diagnosis and post-treatment control