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Hybrid PET/MRI Imaging of Alzheimer's Disease Based on 18F-AV-1451
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Consorcio de Imagenología de Alzheimer

Marcelo Madrid de Bittencourt1, Gabriela Mantovani Baldasso1, Marco Antônio De Bastiani1

  • 1Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.

Alzheimer's & dementia : the journal of the Alzheimer's Association
|December 23, 2025
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Resumen
Este resumen es generado por máquina.

El alelo APOEε4 altera significativamente la expresión génica en sangre en personas con deterioro cognitivo, creando distintas firmas moleculares. Estos cambios influyen en biomarcadores clave de la enfermedad de Alzheimer como FDG-PET y Aβ42.

Palabras clave:
APOEε4expresión génicaenfermedad de Alzheimerbiomarcadoresdeterioro cognitivotranscriptómicaneuroimagenologíagenéticaAlzheimer's Disease Neuroimaging InitiativeADNI

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Área de la Ciencia:

  • Genética; Neurociencia; Biología Molecular

Sus antecedentes:

  • El alelo Apolipoproteína E ε4 (APOEε4) es un factor de riesgo genético principal para la enfermedad de Alzheimer esporádica (EA).
  • El impacto del alelo APOEε4 en la expresión génica de la sangre periférica, particularmente en relación con el estado cognitivo, no se comprende bien.
  • Este estudio investiga cómo el alelo APOEε4 influye en la expresión génica sanguínea en individuos cognitivamente sanos (CU) e con deterioro cognitivo (CI).

Objetivo del estudio:

  • Examinar los patrones diferenciales de expresión génica en sangre periférica asociados con el alelo APOEε4 en individuos CU y CI.
  • Identificar vías biológicas específicas afectadas por la portación del alelo APOEε4 en el contexto del estado cognitivo.
  • Explorar la relación entre la expresión génica asociada al APOEε4 y los biomarcadores de la enfermedad de Alzheimer.

Principales métodos:

  • Análisis de datos de microarrays de 423 individuos de la base de datos ADNI, estratificados por portación del alelo APOEε4 y estado cognitivo (CU/CI).
  • Identificación de genes diferencialmente expresados (DEGs) entre los grupos CU y CI dentro de portadores y no portadores utilizando el paquete Limma.
  • Análisis de enriquecimiento de vías (Gene Ontology, KEGG) y modelos de regresión lineal para asociar los DEGs con Aβ42 en LCR, pTau181, Tau total y FDG-PET.

Principales resultados:

  • Los portadores de APOEε4 exhibieron perfiles de expresión génica distintos en comparación con los no portadores, con una regulación positiva significativa de las vías de señalización de la inmunidad innata y MAPK y una regulación negativa de la biogénesis ribosomal y la función mitocondrial.
  • Los no portadores mostraron enriquecimiento en procesos relacionados con la ubiquitina y el transporte de vesículas del Golgi.
  • Los patrones de expresión génica se asociaron con biomarcadores de EA; el FDG-PET en portadores y el Aβ42 en no portadores mostraron correlaciones significativas con los DEG.

Conclusiones:

  • El alelo APOEε4 da forma significativamente a las firmas transcriptómicas de la sangre en individuos con deterioro cognitivo, destacando distintas vías fisiopatológicas.
  • Las diferencias en la expresión génica influenciadas por el estado del alelo APOEε4 contribuyen a la variabilidad en biomarcadores clave de la EA, incluido el FDG-PET y el Aβ42.
  • Estos hallazgos subrayan el papel del alelo APOEε4 en la modulación de las respuestas moleculares periféricas relevantes para la patogénesis de la enfermedad de Alzheimer.