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Las mutaciones de la migraña aumentan la vulnerabilidad al accidente cerebrovascular al facilitar las

Katharina Eikermann-Haerter1, Jeong Hyun Lee, Izumi Yuzawa

  • 1Stroke and Neurovascular Regulation Laboratory, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.

Circulation
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PubMed
Resumen

Las mutaciones de migraña hemipléjica familiar (FHM) aumentan el riesgo de accidente cerebrovascular al hacer que el cerebro sea más vulnerable a los eventos isquémicos. Esta mayor susceptibilidad a la despolarización cerebral conduce a accidentes cerebrovasculares más grandes y peores resultados.

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Área de la Ciencia:

  • La neurociencia es la neurociencia.
  • Genética La genética.
  • Investigación del ictus Investigación del ictus.

Sus antecedentes:

  • La migraña es un conocido factor de riesgo de accidente cerebrovascular, pero los mecanismos subyacentes siguen sin estar claros.
  • La migraña hemipléjica familiar (FHM) sirve como un modelo valioso para la migraña común debido a las características y mecanismos compartidos.
  • FHM se asocia con un mayor riesgo de accidente cerebrovascular.

Objetivo del estudio:

  • Para investigar el impacto de las mutaciones FHM tipo 1 (FHM1) en la vulnerabilidad del cerebro al ictus isquémico.
  • Para aclarar los mecanismos celulares y fisiológicos que vinculan FHM al riesgo de accidente cerebrovascular.

Principales métodos:

  • Se utilizaron dos cepas de ratón mutante FHM1 y controles de tipo salvaje.
  • Se evaluó la actividad cerebral utilizando la despolarización anóxica y las despolarizaciones periinfarto.
  • Tamaño cuantificado del infarto y resultados neurológicos utilizando resonancia magnética ponderada por difusión y fluometría de manchas láser.
  • Investigó el efecto de un antagonista del receptor de glutamato.

Principales resultados:

  • Las mutaciones de FHM1 llevaron a una despolarización anóxica más temprana y despolarizaciones periinfarto más frecuentes en ratones mutantes.
  • Los ratones mutantes exhibieron una rápida expansión del núcleo del infarto y mayores déficits de perfusión.
  • Los ratones mutantes requerían un mayor flujo sanguíneo cerebral para sobrevivir, lo que condujo a un infarto con isquemia más leve.
  • Los ratones mutantes desarrollaron infartos más grandes y peores resultados neurológicos, que se redujeron con el tratamiento con antagonistas de los receptores de glutamato.

Conclusiones:

  • La mayor susceptibilidad a las despolarizaciones isquémicas, similar a la propagación de la depresión, predispone a los migrañeros al infarto durante eventos isquémicos leves.
  • Este mecanismo contribuye al aumento del riesgo de accidente cerebrovascular observado en las migrañas.
  • Dirigirse a los mecanismos glutamatérgicos puede ofrecer un potencial terapéutico para la prevención del accidente cerebrovascular en individuos susceptibles.