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Altan Rentsendorj1, Dieu-Trang Fuchs2, Jean-Philippe Vit1

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

La patología de la enfermedad de Alzheimer (EA) afecta la retina, causando pérdida sináptica y niveles reducidos de UCH-L1. Estos cambios se correlacionan con el deterioro cognitivo y la patología cerebral, lo que sugiere el potencial de UCH-L1 como biomarcador de la EA.

Palabras clave:
Enfermedad de AlzheimerRetinaUCH-L1Pérdida sinápticaBiomarcadorDeterioro cognitivo

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Área de la Ciencia:

  • Neurociencia; Oftalmología; Bioquímica

Sus antecedentes:

  • La patología de la enfermedad de Alzheimer (EA) se extiende a la retina, afectando la función neurosensorial.; La ubiquitina carboxil-terminal hidrolasa L1 (UCH-L1) está implicada en la patología cerebral de la EA, pero se desconoce su papel retiniano.

Objetivo del estudio:

  • Investigar la expresión de UCH-L1 en la retina y su relación con la integridad sináptica y la función cognitiva en la enfermedad de Alzheimer.; Explorar la retina como un sitio potencial para biomarcadores de la EA.

Principales métodos:

  • Se utilizaron inmunohistoquímica y espectrometría de masas para analizar retinas post mortem de individuos con EA, deterioro cognitivo leve (MCI) y controles.; Se cuantificaron los marcadores retinianos de integridad sináptica y los niveles de UCH-L1 y se correlacionaron con la patología cerebral (puntuaciones Braak, ABC) y la función cognitiva (puntuaciones MMSE, CDR).; El análisis de Random Forest basado en IA identificó predictores clave del estado de la enfermedad.

Principales resultados:

  • Se observó una pérdida sináptica significativa (marcadores presinápticos y postsinápticos) en las capas interna y externa de la plexiforme de las retinas de MCI y EA.; Los niveles de UCH-L1 asociada a membrana (UCH-L1M) se redujeron significativamente en las retinas de MCI y EA.; La pérdida sináptica retiniana y la disminución de UCH-L1M se correlacionaron fuertemente con la patología cerebral de amiloide-beta (Aβ), tau fosforilada, el deterioro cognitivo y la patología cerebral de la EA.

Conclusiones:

  • Ocurren pérdida sináptica temprana y sustancial y disminución de UCH-L1M en las retinas de individuos con MCI y EA.; UCH-L1M es un predictor significativo de la progresión de la taupatía y el deterioro cognitivo, lo que sugiere su potencial como biomarcador para la detección de la EA.; UCH-L1M también puede representar un objetivo terapéutico para la EA.