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Desarrollo de Fármacos

Suelyn Koerich1, Santiago Ramirez1, Natalia Astudillo1

  • 1The University of Texas Health Science Center at Houston, Houston, TX, USA.

Alzheimer's & dementia : the journal of the Alzheimer's Association
|December 25, 2025
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Resumen

El intercambio de plasma (PE) redujo las placas amiloides y la inflamación cerebral en ratones con enfermedad de Alzheimer avanzada (EA). Esto sugiere que el PE puede ayudar a eliminar la beta-amiloide (Aβ) del cerebro, lo que justifica una mayor investigación para el tratamiento de la EA.

Palabras clave:
intercambio de plasmaenfermedad de Alzheimerplacas amiloidesneuroinflamaciónratonesdesarrollo de fármacos

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Área de la Ciencia:

  • Neurociencia
  • Inmunología
  • Bioquímica

Sus antecedentes:

  • La enfermedad de Alzheimer (EA) es la principal causa de demencia, caracterizada por placas amiloides, ovillos neurofibrilares y neuroinflamación.
  • Las terapias actuales para la EA dirigidas a las placas amiloides tienen limitaciones en cuanto a elegibilidad y perfiles de riesgo-beneficio.
  • Se están explorando estrategias periféricas por su potencial para impactar la patología de Aβ y tau en el cerebro, y la neuroinflamación.

Objetivo del estudio:

  • Investigar la eficacia del intercambio de plasma (PE) en la reducción de la patología amiloide y la neuroinflamación en un modelo de ratón de EA.
  • Evaluar el impacto del PE en la deposición de beta-amiloide (Aβ) y los marcadores inflamatorios en el cerebro y el plasma.

Principales métodos:

  • Se administraron procedimientos mensuales de PE a ratones APP/PS1 a partir de los 11 meses de edad.
  • Los análisis histológicos cuantificaron los depósitos amiloides (Tioflavina-S, 4G8) y los marcadores de neuroinflamación (Iba-1, GFAP).
  • Los ensayos ELISA y Luminex midieron los niveles de Aβ y las concentraciones de citoquinas en homogenados cerebrales y plasma.

Principales resultados:

  • El PE redujo significativamente el número y el área de las placas amiloides en la corteza de los ratones tratados.
  • El PE disminuyó la activación de la microglía (Iba-1) y los astrocitos (GFAP) en el cerebro.
  • Los análisis bioquímicos revelaron niveles más bajos de Aβ1-40 y Aβ1-42 insolubles en los cerebros de ratones tratados con PE, junto con perfiles modulados de citoquinas inflamatorias.

Conclusiones:

  • El intercambio de plasma demuestra potencial en la reducción de la carga de amiloide cerebral y la modulación de la neuroinflamación en un modelo de EA avanzado.
  • El aumento de los niveles de Aβ en plasma post-PE sugiere un mecanismo de eliminación de Aβ del cerebro a la periferia.
  • Se necesita más investigación para dilucidar completamente los mecanismos de eliminación de Aβ y los efectos antiinflamatorios del PE.