Alteraciones histológicas y neuroquímicas inducidas en el cuerpo estriado por la exposición a sulfonato de perfluoroctano (PFOS) / Morphological and neurochemical alterations induced in the corpus striatum by perfluorooctane sulphonate (PFOS) exposure

El sulfonato de perfluoroctano (PFOS) es un compuesto organofluorado y está considerado como un contaminante orgánico persistente. Atraviesa la barrera hematoencefálica y es capaz de incrementar su propio transporte a través de la misma, alcanzando así el sistema nervioso central, donde ejerce su toxicidad. El objetivo de este trabajo es evaluar la neurotoxicidad del PFOS en cuerpo estriado a nivel neuroquímico e histológico. Para ello, este xenobiótico se ha administrado oralmente durante 28 días a las dosis de 0, 0,5, 1; 3 y 6 mg/Kg/día en rata macho adulta, y tras el tratamiento, se ha determinado la concentración de los principales aminoácidos neurotransmisores en el cuerpo estriado y se ha hecho un estudio histológico de dicha región cerebral. Los animales tratados con PFOS muestran un incremento de la concentración de glutamina y un descenso del contenido de glutamato y aspartato. La concentración de ácido gamma-aminobutírico (GABA) y de taurina disminuye con la dosis de 1 mg/Kg/día, aumentando con la de 3 mg/Kg/día. PFOS induce también una degeneración celular dosis-dependiente, evidenciada por un aumento de la basofilia. Tras la exposición a dosis elevadas de PFOS (3 y 6 mg/Kg/día) se observa también satelitosis o acúmulo de los oligodendrocitos en este mismo tejido. Las alteraciones neuroquímicas e histológicas observadas en los animales tratados con PFOS podrían estar relacionadas con disfunciones a nivel cognitivo y emocional, así como con diversas patologías neurodegenerativas como la enfermedad de Parkinson (AU)

Perfluorooctane sulfonate (PFOS) is a fluorinated compound considered such as a persistent organic pollutant, which presents neurotoxicity. This chemical crosses the blood brain barrier and it is able to increase their own transportation through this structure, reaching the central nervous system, where it can induce toxicity. This work was undertaken to evaluate the possible effects of PFOS exposure in the corpus striatum at both neurochemical and histological levels. Adult male rats were orally treated with 0.5, 1, 3 and 6 mg of PFOS/Kg/day for 28 days. At the end of this treatment, the concentration of the main neurotransmitters amino acids has been determined in striatum and the possible morphological alterations have been studied in this same brain region. Animals treated with PFOS show an increase of glutamine concentration and a decrease of glutamate and aspartate content. Gamma-aminobutyric acid (GABA) and taurine concentration decreases with the dose of 1 mg/Kg/day, increasing with the dose of 3 mg/Kg/day. PFOS also induces a cellular dose-dependent degeneration. Furthermore, PFOS exposure at high doses (3 and 6 mg/kg/day) induces satellitosis in striatatal cells. These neurochemical and morphological alterations observed in adult male rat trated with PFOS could be related to cognitive and emotional dysfunctions as well as to several neurodegenerative pathologies such as Parkinson's disease (AU)

Neurochemical dementia diagnostics for Alzheimer's disease and other dementias: an ISO 15189 perspective.

Dementia is one of the most common causes of health problems in the elderly populations of Western industrialized countries. A combined analysis of cerebrospinal fluid-based neurochemical dementia diagnostics biomarkers (amyloid-ß peptides, total tau and phosphorylated forms of tau) provides sensitivity and specificity in the range of 85% for the diagnosis of Alzheimer's disease, the most common cause of dementia. The alterations occur very early in the course of neurodegeneration, enabling medical follow-up of persons with increased risk of developing dementia. With a growing number of laboratories performing neurochemical dementia diagnostics routinely, it is important to standardize protocols and laboratory performance to enable comparisons of results and their interpretations. Together with the recently published expert guidelines for sample handling and preparation, as well as the interpretation (post-analytical) algorithms developed by experienced centers, ISO 15189 norm provides an extremely useful tool for standardization of neurochemical dementia diagnostics.

Aspectos neuropsicológicos del craving por la nicotina / Neuropsychological aspects of nicotine craving

El craving se ha definido como la motivación de autoadministrarse una sustancia que previamente ha sido consumida. Se considera que el craving es responsable del consumo compulsivo de una sustancia, así como del alto nivel de recaídas después de periodos de abstinencia. Los estudios neuropsicológicos y de imagen cerebral han identificado numerosas regiones cerebrales implicadas en el craving. En este artículo se revisan los mecanismos neuropsicológicos implicados en el craving por la nicotina, centrándose en los tres sistemas involucrados en el craving. Primero, el sistema de recompensa, responsable del desarrollo de la dependencia y del craving. Segundo, el sistema emocional y asociativo que se relaciona con el craving condicionado. Tercero, el sistema implicado en la toma de decisiones y procesos cognitivos. Además, se revisa los modelos teóricos más influyentes, como los Modelos basados en el Condicionamiento, Modelos Cognitivo-Conductuales, Modelos Cognitivos y Modelo Neurobiológico. También se discuten otros aspectos relacionados con la evaluación y tratamiento del craving, haciendo énfasis en los aspectos clínicos. Como conclusión, se acentúa la importancia de un enfoque multidisciplinar para lograr un modelo común del craving, así como para mejorar las herramientas diagnósticas y las estrategias de tratamiento (AU)

Craving has been defined as the motivation to self-administer a substance previously consumed. It has been hypothesized that craving contributes significantly to compulsive drug use and relapse after a period of abstinence in humans. Neuropsychological and brain-imaging studies have identified numerous brain regions that may be involved in craving. In this paper, the neuropsychological mechanisms of craving for nicotine are reviewed, focusing on three systems that appear to be involved in craving states. First of all, the reward system, responsible for the development of dependence and craving. Secondly, the emotional and associative system, which is related to conditioned craving. And third, the system involved in the neural basis of cognitive and decision making processes. The most influential theoretical models on craving are also reviewed, including those based on conditioning mechanisms, on cognitive mechanisms and on cognitive-behavioral mechanisms, as well as the neurobiological model. Factors related to the evaluation and treatment of craving are also discussed, with particular emphasis on clinical aspects. Finally, we stress the importance of a multidisciplinary approach for achieving a common model on craving and improving the diagnostic tools and treatment strategies (AU)