ABSTRACT
Alzheimer's disease (AD) is the most common form of dementia. It affects approximately 6% of people over the age of 65 years. It is a clinicopathological, degenerative, chronical and progressive disease that exhibits a deterioration of memory, orientation, speech and other functions. Factors contributing to the pathogenesis of the disease are the presence of extracellular amyloid deposits, called neuritic senile plaques, and fibrillary protein deposits inside neurons, known as neurofibrillary bundles, that appear mainly in the frontal and temporal lobes. AD has a long preclinical latency and is difficult to diagnose and prevent at early stages. Despite the advent of novel high-throughput technologies, it is a great challenge to identify precise biomarkers to understand the progression of the disease and the development of new treatments. In this sense, important knowledge is emerging regarding novel molecular and biological candidates with diagnostic potential, including microRNAs that have a key role in gene repression. On the other hand, proteomic approaches offer a platform for the comprehensive analysis of the whole proteome in a certain physiological time. Proteomic technology investigates protein expression directly and reveals post-translational modifications known to be determinant for many human diseases. Clinically, there is growing evidence for the role of proteomic and metabolomic technologies in AD biomarker discovery. This review discusses the role of several miRNAs identified using genomic technologies, and the importance of novel proteomic and metabolomic approaches to identify new proteins and metabolites that may be useful as biomarkers for monitoring the progression and treatment of AD.
Subject(s)
Alzheimer Disease , MicroRNAs , Aged , Alzheimer Disease/diagnosis , Biomarkers , Humans , Metabolomics , ProteomicsABSTRACT
Se presenta el caso de un varón caucásico de 40 años de edad valorado en el servicio de urgencias por paraparesia de 1 h de evolución con hipopotasemia concomitante. Tras una progresión clínica brusca en las primeras 5 h de evolución, el cuadro se resolvió en relación con la normalización de la potasemia. La determinación analítica reveló un hipertiroidismo primario, y se estableció el diagnóstico de parálisis periódica tirotóxica. El abordaje terapéutico se centró en la administración de cloruro potásico, propranolol y metimazol. Pese a la aceptación generalizada del aporte potásico como primera medida terapéutica, la revisión de trabajos previos revela la necesidad de esclarecer la efectividad y el lugar del propranolol en el tratamiento de la crisis de parálisis periódica tirotóxica (AU)
A 40-year-old Caucasian man presented to the emergency room of our hospital with bilateral lower extremity weakness with onset 1 hour previously and concurrent hypokalemia. After dramatic clinical progression for the first 5 hours, the episode resolved once serum potassium levels were normalized. Laboratory data revealed primary hyperthyroidism, indicating a diagnosis of thyrotoxic periodic paralysis (TPP). Treatment consisted of potassium, propranolol and methimazole administration. Although the mainstay of therapy is potassium replacement, the role of propranolol in improving the acute clinical manifestations of TPP has yet to be adequately clarified (AU)
