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Ciencia básica y patogénesis

Sally A Frautschy1,2, Kapil Manglani2,3, Xiaohong Zuo1,4

  • 1Veterans Greater Los Angeles Healthcare System, Los Angeles, CA, USA.

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

La proteína espiga del SARS-CoV-2 exacerba la patología de la enfermedad de Alzheimer (EA) y la activación del complemento en ratas, particularmente cuando hay hipertensión o ApoE4 presente. Esto resalta los mecanismos potenciales para los síntomas neurológicos del Covid persistente en poblaciones de riesgo.

Palabras clave:
proteína espigaSARS-CoV-2enfermedad de AlzheimerhipertensiónApoE4Covid persistenteneuroinflamaciónactivación del complemento

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Área de la Ciencia:

  • Neurociencia
  • Inmunología
  • Patología

Sus antecedentes:

  • Los síntomas persistentes (Covid persistente) afectan al 7% de los supervivientes de COVID-19.
  • La proteína espiga del SARS-CoV-2 se une a los receptores ACE2, activando las vías del complemento.
  • Los pacientes con Covid persistente presentan biomarcadores elevados de EA y neuroinflamación.

Objetivo del estudio:

  • Investigar los efectos moduladores de la hipertensión y ApoE4 en la respuesta de la proteína espiga S1 en modelos de ratas con enfermedad de Alzheimer (EA).
  • Explorar el vínculo entre la exposición a la proteína espiga y la patología de la EA, el daño de la sustancia blanca y la activación del complemento.

Principales métodos:

  • Se utilizaron modelos de ratas con EA y EA mixta (EA con enfermedad de pequeños vasos cerebrales), con y sin ApoE4.
  • Se administró proteína espiga S1 recombinante y se evaluó la función ejecutiva, la patología de la EA, el daño de la sustancia blanca y la activación del complemento.
  • Se desarrollaron ensayos plasmáticos de alto rendimiento para la activación del complemento vascular y del SNC en modelos de ratas y pacientes humanos con Neuro-Covid.

Principales resultados:

  • La proteína S1 aumentó la patología amiloide, ptau217 y la activación del complemento (C3, C5b-9) independientemente de ApoE o la hipertensión.
  • La hipertensión y ApoE4 sinergizaron para empeorar la patología vascular inducida por la espiga y la adhesión de leucocitos.
  • La proteína espiga indujo disfunción ejecutiva, daño de la sustancia blanca y activación del complemento, potenciados por la hipertensión preexistente.

Conclusiones:

  • La proteína espiga aumenta de manera robusta la patología de la EA y la activación del complemento, causando pérdida sináptica y daño de la barrera hematoencefálica en ratas con condiciones vasculares y de EA preexistentes.
  • Estos hallazgos son relevantes para una parte significativa de la población que envejece con comorbilidades.
  • El desarrollo de ensayos escalables para la activación del complemento en Neuro-Covid podría ayudar en las estrategias de tratamiento.