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Manifestaciones Clínicas

Yi Jin Leow1, Justin Jit Hong Ong2, Jia Dong James Wang3

  • 1Lee Kong Chian School of Medicine, Singapore, Singapore, Singapore.

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

La proteína glía fibrilar ácida (GFAP) y las microhemorragias cerebrales (CMBs) afectan el sueño de manera diferente en las etapas cognitivas. La elevación de GFAP altera el sueño en personas sanas, mientras que las CMBs empeoran el sueño en personas con deterioro cognitivo.

Palabras clave:
proteína glía fibrilar ácidamicrohemorragias cerebralesalteraciones del sueñodeterioro cognitivoenfermedad de Alzheimerenfermedad de pequeño vaso cerebralmedicina del sueñoneurocienciagerontología

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Área de la Ciencia:

  • Neurociencia
  • Medicina del Sueño
  • Gerontología

Sus antecedentes:

  • Las alteraciones crónicas del sueño impulsan la neuroinflamación, la disfunción astrocítica y la neurodegeneración.
  • La proteína glía fibrilar ácida (GFAP) es un marcador de activación astrocítica relacionado con las alteraciones del sueño-vigilia en la enfermedad de Alzheimer (EA).
  • Las microhemorragias cerebrales (CMBs), indicativas de enfermedad de pequeño vaso cerebral (CSVD), también contribuyen a las alteraciones del sueño, pero su interrelación con la GFAP y el sueño en las distintas etapas cognitivas no está clara.

Objetivo del estudio:

  • Investigar las asociaciones entre la GFAP plasmática, las CMBs y las alteraciones del sueño en individuos cognitivamente sanos (CU) y cognitivamente deteriorados (CI).
  • Explorar cómo estos factores difieren en las distintas etapas de la función cognitiva.

Principales métodos:

  • Estudio transversal de 1.801 participantes que viven en la comunidad (edad media 58,7 años).
  • Los participantes se clasificaron como CU o CI (incluyendo deterioro cognitivo leve y EA leve).
  • Se evaluó la GFAP plasmática, el estado de APOE ε4, la calidad del sueño y la neuroimagen para detectar marcadores de CSVD (CMBs). Se analizaron las asociaciones mediante ANOVA, correlación y regresión.

Principales resultados:

  • En individuos CU, una mayor GFAP se correlacionó con un aumento de las probabilidades de mal sueño y una mayor latencia del sueño.
  • En individuos CI, una mayor GFAP se asoció con una disminución de las probabilidades de mal sueño y una mayor eficiencia del sueño.
  • Las CMBs se asociaron con una mayor latencia del sueño y un mayor uso de medicamentos para dormir en el grupo CI.

Conclusiones:

  • La GFAP y las CMBs tienen roles distintos en las alteraciones del sueño en las trayectorias cognitivas.
  • En individuos CU, la elevación de GFAP puede alterar la homeostasis del sueño a través de la activación astrocítica.
  • En individuos CI, las CMBs exacerban problemas específicos del sueño, lo que subraya las contribuciones vasculares; las intervenciones para las alteraciones del sueño pueden mitigar la neurodegeneración.