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Ciencia básica y patogénesis

Julian V Pentchev1, Trever Jackson2, Thea Jacobson Rosewood3,4,5

  • 1Indiana University, Bloomington, IN, USA.

Alzheimer's & dementia : the journal of the Alzheimer's Association
|December 25, 2025
PubMed
Resumen
Este resumen es generado por máquina.

Las puntuaciones poligénicas de la enfermedad de Alzheimer de inicio tardío (PGS) predicen el riesgo de enfermedad de Alzheimer de inicio temprano (EOAD), pero no impulsan fuertemente el inicio de la EOAD. Sin embargo, estas variantes genéticas pueden influir en los déficits cognitivos en pacientes con EOAD.

Palabras clave:
enfermedad de Alzheimer de inicio tempranopuntuación poligénicaenfermedad de Alzheimer de inicio tardíovariantes genéticasfunción cognitiva

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Área de la Ciencia:

  • Genética; Neurociencia; Investigación de la enfermedad de Alzheimer

Sus antecedentes:

  • Los factores genéticos de la enfermedad de Alzheimer de inicio temprano (EOAD) siguen siendo en gran medida desconocidos.; Una hipótesis sugiere que la EOAD puede compartir factores genéticos con la enfermedad de Alzheimer de inicio tardío (LOAD), potencialmente con una mayor carga de polimorfismos de un solo nucleótido (SNP) de riesgo de LOAD.; Este estudio investiga si las puntuaciones poligénicas (PGS) más altas en pacientes con EOAD se correlacionan con una edad de inicio (AoO) más temprana.

Objetivo del estudio:

  • Comparar la capacidad predictiva de una PGS basada en LOAD para EOAD y LOAD.; Analizar la relación entre la PGS y la edad de inicio (AoO) en cohortes de EOAD y LOAD.; Explorar la correlación entre la PGS y la función cognitiva en pacientes con EOAD.

Principales métodos:

  • Se aplicó una PGS de LOAD desarrollada previamente a datos de estudios de asociación del genoma completo (GWAS) de la cohorte Longitudinal Early Onset Alzheimer's Disease Study (LEADS) y la Alzheimer's Disease Neuroimaging Initiative (ADNI).; Se utilizaron modelos de regresión logística binaria para predecir el estado de EOAD y LOAD, con análisis adicionales que incluían el estado de portador de APOE4 como covariable.; La regresión de Cox evaluó las diferencias en AoO entre los tertiles de PGS y, dentro de la cohorte LEADS EOAD, se correlacionaron los dominios cognitivos con la PGS.

Principales resultados:

  • La PGS de LOAD predijo significativamente el estado de caso/control en cohortes combinadas, ADNI y LEADS, con una PGS más alta asociada con un mayor riesgo de desarrollar EOAD/LOAD.; Después de tener en cuenta APOE4, la PGS siguió siendo un predictor significativo en las cohortes combinadas y ADNI, pero no en la cohorte solo LEADS.; El análisis de supervivencia reveló diferencias significativas en AoO según los grupos de PGS en las cohortes combinadas y ADNI, pero no en LEADS. En pacientes con EOAD, la PGS se correlacionó con el rendimiento visuoespacial y del lenguaje.

Conclusiones:

  • Los factores de riesgo genético para LOAD, excluyendo APOE4, no parecen ser los principales impulsores de la edad de inicio de la EOAD.; Sin embargo, estas variantes genéticas pueden desempeñar un papel en la mediación de déficits cognitivos específicos observados en la EOAD.; Se necesita más investigación para dilucidar completamente la arquitectura genética de la EOAD.