Encuentran una vía molecular responsable de la muerte de células nerviosas cuya pérdida provoca Parkinson

LA MUTACIÓN PROVOCA UNA DISCAPACIDAD EN LA ACTIVIDAD DE LOS MICROARN

Científicos de la Universidad de Stanford, en California, han identificado una vía molecular responsable de la muerte de células nerviosas claves cuya pérdida provoca enfermedad de Parkinson. Este descubrimiento podría no sólo explicar cómo una mutación genética ligada al Parkinson causa la muerte celular, sino que también abriría la puerta a una nueva aproximación terapéutica para la malaria.

En el estudio, que se publica hoy en Nature, los investigadores, coordinados por Bingwei Lu, profesor de Patología en la citada universidad, han mostrado que la mutación provoca una discapacidad en la actividad de los microARN. Esta discapacidad conduce a la muerte prematura de las células nerviosas específicamente implicadas en la secreción de la dopamina cerebral. La degeneración de esas células nerviosas en el cerebro es una característica del Parkinson.

Según Lu, “el microARN ha sido relacionado con el cáncer, la disfunción cardiaca y la alteración de la respuesta inmune. Pero esta es la primera vez que ha sido identificado como un jugador crucial en una enfermedad neurodegenerativa”.

Los nuevos hallazgos han demostrado que la mutación LRRK2 interfiere en la actividad normal de los microARN dando lugar la sobreproducción de al menos dos proteínas que pueden causar la muerte a ciertas células, como las del cerebro.

Dos proteínas claves
Los investigadores del laboratorio de Lu han realizado experimentos en Drosophila, observando que ciertas proteínas eran producidas en niveles altos en el modelo de mosca de la fruta LRRK2 de enfermedad de Parkinson. Lo que les llamó la atención especialmente fueron dos proteínas importantes en la regulación de la división celular. Las células nerviosas maduras no deberían tener niveles altos de estas proteínas; y cuando lo hacen son propensas a la muerte celular temprana.

Los investigadores han observado el microARN que contiene la fórmula genética para las dos proteínas sobreproducidas y han predicho que podrían ser ligadas mediante dos microARN específicos: let-7 y miR-184. Cuando manipularon las funciones de aquellos dos microARN en los cerebros de las moscas, tuvieron resultados consecuentes con el daño asociado a la enfermedad de Parkinson.

El equipo de Lu ha añadido que reducir la actividad de let-7 en las células nerviosas dopaminérgicas provocó la producción excesiva de una de las proteínas sospechosas y la degeneración de las células.

Fuente: www.diariomedico.com

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