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Ciencia básica y patogénesis

Chetan Aware1, Maalavika Govindarajan1, Kira Ivanich1

  • 1University of Missouri, Columbia, MO, USA.

Alzheimer's & dementia : the journal of the Alzheimer's Association
|December 24, 2025
PubMed
Resumen
Este resumen es generado por máquina.

El trasplante de microbiota fecal de pacientes con accidente cerebrovascular empeoró la patología de la enfermedad de Alzheimer (EA) y la neuroinflamación en ratones. La focalización de la disbiosis intestinal presenta una estrategia terapéutica potencial para la EA relacionada con el accidente cerebrovascular.

Palabras clave:
eje intestino-cerebrodisbiosis intestinalaccidente cerebrovascularenfermedad de Alzheimerneuroinflamacióntrasplante de microbiota fecal

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Área de la Ciencia:

  • Neurociencia; Microbiología; Gastroenterología

Sus antecedentes:

  • El accidente cerebrovascular es un factor de riesgo conocido para la enfermedad de Alzheimer (EA), pero los mecanismos subyacentes no se comprenden completamente.
  • La disbiosis intestinal, un desequilibrio en la microbiota intestinal, se está implicando cada vez más en diversas afecciones neurológicas.

Objetivo del estudio:

  • Investigar si la disbiosis intestinal inducida por accidente cerebrovascular isquémico agudo exacerba la patología de la EA.
  • Explorar el papel del eje intestino-cerebro en el vínculo entre el accidente cerebrovascular y la progresión de la EA.

Principales métodos:

  • Trasplante de microbiota fecal (TMF) de pacientes con accidente cerebrovascular y controles sanos en ratones 3xTg-AD.
  • Evaluación de la neuroinflamación y los marcadores de EA (Tau Total, GFAP, IBA1) mediante inmunohistoquímica (IHQ).
  • Imagen molecular espacial de célula única (CosMx SMI) para analizar la expresión génica específica del tipo celular y la patología cerebral.

Principales resultados:

  • Los ratones con ACV-TMF mostraron un aumento significativo de la neuroinflamación y la patología de la EA, incluidos niveles elevados de Tau Total, GFAP e IBA1.
  • Se observó un aumento de la densidad de astrocitos y microglía en los ratones con ACV-TMF, lo que indica activación glial.
  • Expresión desregulada de genes clave relacionados con la EA (ApoE, GFAP, APP, PSEN1, BIN1, SORL1) en diversas células cerebrales, lo que sugiere una neuroinflamación intensificada y un deterioro sináptico.

Conclusiones:

  • La disbiosis intestinal inducida por accidente cerebrovascular exacerba la patología de la EA, lo que pone de relieve el papel del eje intestino-cerebro.
  • La focalización de la disbiosis intestinal puede representar un nuevo enfoque terapéutico para el manejo de la EA relacionada con el accidente cerebrovascular.