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Desarrollo de Fármacos

Leelavathi N Madhu1, Yogish Somayaji2, Sanya Kotian1

  • 1Institute for Regenerative Medicine, Department of Cell Biology and Genetics, Texas A&M University College of Medicine, Bryan/College Station, Texas, USA., College Station, TX, USA.

Alzheimer's & dementia : the journal of the Alzheimer's Association
|December 25, 2025
PubMed
Resumen
Este resumen es generado por máquina.

El tratamiento con psilocibina mejoró la función cognitiva y redujo la neuroinflamación en un modelo de ratón de la enfermedad de Alzheimer (EA). Esto sugiere que la psilocibina puede ofrecer una nueva vía terapéutica para la EA al mejorar la función cerebral y la neurogénesis.

Palabras clave:
psilocibinaenfermedad de Alzheimerneuroinflamaciónneurogénesisfunción cognitivaratones 5xFADdesarrollo de fármacos

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Área de la Ciencia:

  • Neurociencia; Farmacología; Investigación de la Enfermedad de Alzheimer.

Sus antecedentes:

  • La neuroinflamación crónica es un motor clave de la patogénesis de la enfermedad de Alzheimer (EA), que provoca deterioro cognitivo y del estado de ánimo.
  • Las terapias actuales para el Alzheimer tienen una capacidad limitada para detener la progresión de la enfermedad.
  • La psilocibina, conocida por su eficacia en el tratamiento de la depresión, demuestra potencial para reducir la neuroinflamación y promover la neurogénesis hipocampal.

Objetivo del estudio:

  • Investigar la eficacia de la psilocibina para mitigar el deterioro cognitivo en un modelo de ratón de la enfermedad de Alzheimer familiar 5x (5xFAD).
  • Evaluar el impacto de la psilocibina en la neuroinflamación, la neurogénesis y la función sináptica en el contexto de la EA.

Principales métodos:

  • Administración mensual de psilocibina (0,5 mg/Kg) o vehículo a ratones 5xFAD durante 4 meses.
  • Pruebas neuroconductuales para evaluar las funciones cognitivas y del estado de ánimo post-tratamiento.
  • Análisis de tejidos cerebrales para marcadores de neuroinflamación, neurogénesis hipocampal, pérdida sináptica y placas de beta-amiloide; también se realizó proteómica hipocampal.

Principales resultados:

  • Los ratones tratados con psilocibina mostraron una mejora de las funciones cognitivas, incluida la separación de patrones y la memoria de reconocimiento asociativa, y carecieron de anhedonia en comparación con los controles tratados con vehículo.
  • Se observaron reducciones significativas en los marcadores de neuroinflamación (inflamasoma NLRP3, p38 MAPK, señalización cGAS-STING) en los ratones tratados con psilocibina.
  • Se observó un aumento de la neurogénesis, una mejora de la señalización BDNF-ERK-CREB y una preservación de las proteínas sinápticas, junto con evidencia proteómica de proteínas reguladas al alza implicadas en la neuroinflamación, la señalización mTOR y la función sináptica.

Conclusiones:

  • El tratamiento con psilocibina mantuvo eficazmente la función cognitiva en un modelo de ratón de EA sin alterar la carga de placas de beta-amiloide.
  • Los beneficios cognitivos observados se atribuyen a la reducción inducida por la psilocibina de la neuroinflamación, la mejora de la neurogénesis hipocampal y la preservación sináptica.