La esquizofrenia es una enfermedad mental crónica grave caracterizada por un conjunto de síntomas que afectan al funcionamiento psicológico de la persona y a su contacto con la realidad. Afecta al 1% de la población y aunque tiene una base biológica, las causas no son totalmente conocidas.
Ahora un equipo de científicos del Hospital de Investigación St. Jude Children ha relacionado por primera vez, un circuito específico del cerebro con las alucinaciones auditivas, delirios y otros síntomas psicóticos de la esquizofrenia.
El equipo dirigido por Stanislav Zakharenko, ha vinculado estos síntomas a la delación (pérdida) de un gen, el DGCR8. Esto lleva a cambios en la química del cerebro que reducen el flujo de información entre las dos estructuras cerebrales implicadas en el procesamiento de la información auditiva. La falta de conexión entre estas estructuras, genera un estrés cerebral que desencadena en las «voces» de la esquizofrenia.
El ADN humano está organizado en 23 pares de cromosomas que se encuentran en casi todas las células. La pérdida del gen DGCR8 está vinculada a un síndrome genético llamado «síndrome de delación 22q11», que consiste en la pérdida de una copia de 25 genes pertenecientes al cromosoma 22, entre ellos el gen DGCR8.
El síndrome de delación 22q11 es uno de los mayores factores de riesgo relacionados con la esquizofrenia, ya que alrededor del 30% de las personas que padecen este síndrome padecen también esquizofrenia.
Trabajos anteriores del laboratorio de Zakharenko vincularon, en ratones con el síndrome de delación, la peŕdida del gen DGCR8 a los cambios cerebrales asociados a la pérdida de una parte importante del aprendizaje y la memoria. El gen DGCR8 codifica para pequeñas moléculas llamadas microARN, que regulan la expresión de proteínas. La pérdida de este gen y la consecuente alteración en la expresión de proteínas afecta a las conexiones sinápticas d zonas del cerebro implicadas en el aprendizaje y la memoria Ahora, además, los investigadores han encontrado, evidencias de que la pérdida de este gen se da en pacientes con esquizofrenia y conlleva cambios que afectan a otra estructura cerebral: el tálamo auditivo.
El circuito interrumpido identificado en el estudio también resuelve el misterio de cómo los fármacos antipsicóticos actuales alivian las alucinaciones auditivas de la esquizofrenia, y ofrece un nuevo enfoque a los esfuerzos por desarrollar medicamentos con menos efectos secundarios que frenen las «voces».
Los fármacos antipsicóticos impiden la unión del neurotransmisor «dopamina» a su proteína receptora «receptor de dopamina D2» (Drd2). Bloqueando así la actividad de la dopamina. Durante décadas los médicos han administrado estos fármacos a sus pacientes esquizofrénicos por ser efectivos atenuando los delirios auditivos de esta enfermedad. Pero hasta ahora, no se sabía con seguridad el mecanismo por el que calman las «voces».
Midiendo la actividad eléctrica en ratones mutantes con el síndrome de la delación 22q11 (sin el gen DGCR8) y ratones normales sin el síndrome, los investigadores hallaron que el flujo neuronal del tálamo auditivo era menor en ratones con el síndrome de delación, en comparación con los ratones normales. La actividad eléctrica en otras regiones del cerebro no presentó diferencias entre ratones con el gen DGCR8 y los ratones con el síndrome de delación.
Además asociaron la disminución del flujo neuronal con un aumento de receptores de dopamina Drd2, ya que, después de examinar los niveles de estos receptores en ratones con y sin delación del gen DGCR8, comprobaron que los niveles de los receptores de dopamina, en el tálamo auditivo, fueron significativamente mayores en ratones con el síndrome de delación y iguales en otras regiones del cerebro.
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