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Ciencia básica y patogénesis

Arash Salahinejad1,2,3, Amr Eed1,2,3, Mohammad H Alipour1

  • 1University of Western Ontario, London, ON, Canada.

Alzheimer's & dementia : the journal of the Alzheimer's Association
|December 28, 2025
PubMed
Resumen
Este resumen es generado por máquina.

El tratamiento temprano con lecanemab redujo la patología de Alzheimer en ratones APOE4 pero no previno los déficits cognitivos y puede aumentar las microhemorragias. Este estudio destaca los riesgos para los portadores de APOE4 que reciben terapias dirigidas a amiloide.

Palabras clave:
ratones APOE4lecanemabpatología de Alzheimerdéficits cognitivosmicrohemorragiasterapias dirigidas a amiloide

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Área de la Ciencia:

  • Neurociencia; Genética; Farmacología

Sus antecedentes:

  • La enfermedad de Alzheimer (AD) es una causa principal de demencia, que afecta de manera desproporcionada a los portadores de APOE4.; Los portadores de APOE4 presentan una acumulación acelerada de beta-amiloide (Aβ) y un mayor riesgo de anomalías de imagen relacionadas con amiloide (ARIA) con tratamientos con anticuerpos monoclonales (mAb).; Lecanemab, un mAb dirigido a protofibrillas de Aβ, reduce las placas amiloides pero conlleva un mayor riesgo para los portadores de APOE4.

Objetivo del estudio:

  • Investigar si el tratamiento temprano con lecanemab (mAb158) puede mitigar las microhemorragias y el declive cognitivo en modelos de ratón de la enfermedad de Alzheimer humanizados para APOE4.; Evaluar el impacto de mAb158 en la patología amiloide y la atrofia cerebral en el contexto del riesgo genético asociado con APOE4.; Establecer una plataforma preclínica para evaluar la seguridad y eficacia de las terapias con mAb en la AD.

Principales métodos:

  • Se utilizaron modelos avanzados de ratón de la enfermedad de Alzheimer con genes humanizados de APP, Tau y APOE3/APOE4.; Se administró lecanemab murino (mAb158) o vehículo semanalmente durante 26 semanas a ratones hAppNL-F-hMAPT-APOE4 y hAppNL-F-hMAPT-APOE3 a partir de los 3 meses de edad.; Se evaluó el rendimiento cognitivo utilizando una Prueba de Rendimiento Continuo (CPT) y se analizaron tejidos cerebrales para detectar patología amiloide, microhemorragias y niveles de Aβ mediante microscopía y ensayos bioquímicos.

Principales resultados:

  • Se observó una acumulación significativa de amiloide en ratones hAppNL-F-hMAPT-APOE4 en comparación con ratones hAppNL-F-hMAPT-APOE3.; El tratamiento con mAb158 redujo significativamente la acumulación de Aβ insoluble en ratones hAppNL-F-hMAPT-APOE4 a los 15 meses de edad.; Los ratones APOE4 exhibieron déficits cognitivos (CPT) a partir de los 6 meses, independientemente del tratamiento con mAb158, y datos preliminares sugieren que mAb158 puede causar microhemorragias.

Conclusiones:

  • El tratamiento temprano con mAb158 reduce eficazmente la patología de la enfermedad de Alzheimer en ratones humanizados para APOE4 pero no previene los déficits de atención.; El tratamiento puede aumentar el riesgo de microhemorragias en el genotipo vulnerable APOE4.; Este estudio demuestra una valiosa plataforma preclínica para predecir la seguridad y eficacia de los tratamientos con anticuerpos monoclonales para la enfermedad de Alzheimer.