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El nocaut del receptor P2Y12 facilita el envolvimiento neuronal por la microglía reactiva y acelera la enfermedad

Natallia Makarava¹, Tarek Safadi¹, Olga Bocharova¹

¹Department of Neurobiology, University of Maryland School of Medicine, 111 Penn St, Baltimore, MD, 21201, USA.

Journal of neuroinflammation

|August 31, 2025

Resumen

El receptor P2Y12 regula las interacciones microgliales con las neuronas. Su pérdida interrumpe la comunicación normal y acelera la neurodegeneración al promover una envoltura microglial excesiva de las neuronas.

Área de la Ciencia:

La neurociencia
Inmunología
Biología celular

Sus antecedentes:

La microglia controla la salud neuronal a través de uniones purinérgicas, con el receptor P2Y12 crucial para la comunicación homeostática.
Durante la neurodegeneración, la microglía altera las interacciones, pasando de la vigilancia del proceso a la envoltura neuronal del soma.
El papel de P2Y12 en las enfermedades neurodegenerativas crónicas es en gran medida desconocido.

Objetivo del estudio:

Investigar el papel de P2Y12 en la morfología microglial y las interacciones neuronales en modelos sanos y de enfermedades priónicas.
Evaluar el impacto de la deleción de P2Y12 en la progresión de la enfermedad priónica y la neuropatología.

Principales métodos:

Eliminación genética de P2Y12 en ratones adultos (sanos y infectados con priones).
Análisis de la morfología microglial y las interacciones microglia-neurona.
Evaluación de la progresión de la enfermedad priónica y de los cambios neuropatológicos.

Principales resultados:

La deleción de P2Y12 interrumpió los contactos normales del proceso microglial-soma, promoviendo las interacciones cuerpo a cuerpo en ratones sanos.
En ratones infectados con priones, la pérdida de P2Y12 aumentó el envolvimiento neuronal por la microglía y aceleró la enfermedad.
La aceleración de la enfermedad se produjo independientemente de la carga de priones o la pérdida neuronal, lo que sugiere que las interacciones alteradas microglia-neuronas impulsan la exacerbación.

Conclusiones:

P2Y12 es un regulador activo de la dinámica neuroinmune, no sólo un marcador homeostático.
P2Y12 mantiene la comunicación microglia-neurona equilibrada y restringe el comportamiento microglial perjudicial en la neurodegeneración.
P2Y12 representa un objetivo terapéutico potencial para los trastornos neurodegenerativos.

Palabras clave:

Interacciones entre la microglía y las neuronas; movilidad de la microglía Enfermedades neurodegenerativas El receptor P2Y12 Enfermedades del prión Los priones La microglía reactiva

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