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Un viejo fármaco corrige los síntomas de autismo
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Un viejo fármaco corrige los síntomas de autismo

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Un viejo fármaco corrige los síntomas de autismo

Investigadores de la Escuela de Medicina San Diego de la Universidad de California (UC San Diego), en Estados Unidos, han utilizado una función recién descubierta de un antiguo medicamento para restablecer las comunicaciones móviles en un modelo de ratón con autismo, revirtiendo los síntomas de este trastorno, según las conclusiones del estudio, publicadas en la revista Plos One (doi:10.1371/journal.pone.0057380).

"Nuestra teoría sugiere que el autismo se debe a que las células se atascan en un modo defensivo metabólico y no hablan entre sí con normalidad, lo que puede interferir con el desarrollo y la función del cerebro", dijo Robert Naviaux, profesor de Medicina y codirector del Centro de la Enfermedad Mitocondrial y del Metabolismo de la UC San Diego. "Utilizamos una clase de drogas que ha existido durante casi un siglo para tratar otras enfermedades con el fin de bloquear el peligro de la señal en un modelo de ratón, permitiendo que las células vuelvan al metabolismo normal y restaurar la comunicación celular", concreta.


No obstante, Naviaux reconoce que la corrección de las anomalías en el ratón está muy lejos de una cura para los humanos, pero señala que los investigadores se sienten lo suficiente alentados para poner a prueba este método en un pequeño ensayo clínico de niños con trastorno del espectro autista en el próximo año. "Este proceso se encuentra todavía en las primeras etapas de desarrollo. Creemos que este enfoque, llamado terapia antipurinergic o APT, ofrece un camino nuevo, fresco y emocionante que podría conducir al desarrollo de una nueva clase de medicamentos para tratar el autismo", agrega.

Trastornos del espectro autista (TEA) son trastornos complejos definidos por anormalidades en el desarrollo del lenguaje, comportamientos sociales y repetitivos, a los cuales confieren un riesgo cientos de diferentes factores genéticos y el medio ambiente. En este estudio, casi una docena de científicos de diferentes disciplinas de la Universidad de California en San Diego colaboraron para encontrar un mecanismo unificador que explique el autismo.

Al describir una teoría completamente nueva para el origen y el tratamiento del autismo utilizando APT, Naviaux y sus colegas introdujeron el concepto de que una gran mayoría de causas genéticas y ambientales para el autismo actúan mediante la producción de una respuesta de células al peligro constante, el estado metabólico subyacente en la inmunidad innata y la inflamación.

"Cuando las células se exponen a formas clásicas de peligro, tales como un virus, una infección o una sustancia tóxica ambiental, un mecanismo de defensa se activa --explicó Naviaux--. Esto se traduce en cambios en el metabolismo y la expresión génica, y reduce la comunicación entre las células vecinas. En pocas palabras, cuando las células dejan de relacionarse unas con otras, los niños dejan de hablar".

Dado que las mitocondrias, las llamados "plantas de energía" de la célula,  juegan un papel central tanto en estrés celular infeccioso y no infeccioso, la inmunidad innata y la inflamación, los científicos han buscado un sistema de señalización en el cuerpo vinculado a mitocondrias y crítico para la inmunidad innata. Lo encontraron en los nucleótidos extracelulares como el trifosfato de adenosina (ATP) y otros mitokines: señalización de moléculas formadas por angustiadas mitocondrias.

Estos mitokines han separado las funciones metabólicas del exterior de la célula donde se unen y regular los receptores presentes en cada célula del cuerpo. Un total de 15 tipos de receptores purinérgicos son conocidos como estimulados por estos nucleótidos extracelulares, y los receptores son conocidos para controlar una amplia gama de características biológicas de relevancia para el autismo.

Los investigadores probaron en ratones suramina, un conocido inhibidor de la señalización de purinérgicos que se utiliza médicamente para el tratamiento de la enfermedad del sueño africana desde poco después de que se sintetizara en 1916 y hallaron que este mediador APT corrigió síntomas del autismo en el modelo animal, aun cuando el tratamiento se inició después de la aparición de los síntomas. El fármaco restauró 17 tipos de síntomas de múltiples anormalidades, incluyendo la estructura de normalización de sinapsis del cerebro, la señalización célula a célula, el comportamiento social, la coordinación motora y normalizar el metabolismo mitocondrial.

"La eficacia sorprendente mostrada en este estudio utilizando APT para reprogramar la respuesta del peligro celular y reducir la inflamación presenta una oportunidad para desarrollar una clase completamente nueva de antiinflamatorios no esteroideos para el tratamiento del autismo y otros trastornos", concluye Naviaux.

marzo 18/2013 (Diario Salud);

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