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Ciencia Básica y Patogénesis
Usman Sabir1, Takhar Kasumov1, Bovinari Alistair Csubak1
1Neomed University rootstown, Rootstown, OH, USA.
Alzheimer's & dementia : the journal of the Alzheimer's Association
|December 24, 2025
Resumen
El consumo de alcohol puede acelerar la progresión de la enfermedad de Alzheimer al alterar la acetilación cerebral y perjudicar el recambio de la proteína tau. Las ratonas mostraron una mayor susceptibilidad a la acetilación de tau inducida por el alcohol, lo que sugiere un mayor riesgo de un rápido deterioro cognitivo.
Área de la Ciencia:
- Neurociencia
- Bioquímica
- Gerontología
Sus antecedentes:
- La enfermedad de Alzheimer (EA) es una preocupación creciente para las poblaciones que envejecen.
- La ingesta de alcohol se asocia con un envejecimiento cerebral acelerado y un mayor riesgo de EA.
- El envejecimiento normal y la EA implican alteraciones en la proteostasis y el deterioro cognitivo, regulados por la acetilación; se desconoce el impacto específico del alcohol en la tauopatía dependiente de la acetilación.
Objetivo del estudio:
- Investigar el papel de la acetilación en la tauopatía dependiente de la edad.
- Examinar los efectos de la exposición aguda al alcohol en los marcadores de tauopatía y la acetilación.
- Determinar el impacto del alcohol en las vías de recambio y acetilación de tau.
Principales métodos:
- Se utilizaron inmunoensayos para analizar la acetilación en ratones htau en diferentes etapas de la enfermedad.
- Se evaluaron los marcadores de tauopatía tras la exposición aguda al alcohol (dependiente del tiempo y la dosis).
- Se utilizó espectrometría de masas con trazadores de EtOH-d6 y ²H₂O para investigar la acetilación cortical y el recambio de tau.
Principales resultados:
- En ratonas htau, la tau acetilada cortical (TauK174ac) aumentó con la edad y la enfermedad, correlacionándose con la tau total.
- La exposición al alcohol elevó TauK174ac, TauS202p y la tau total, y aumentó la acetilación de histonas (H4K16, H3K9).
- El acetato derivado del alcohol contribuyó a la acetilación de histonas; la acetilación de tau no se vio afectada directamente, pero el recambio de tau se redujo, especialmente para las formas acetiladas.
Conclusiones:
- Las alteraciones en la acetilación cerebral inducidas por el alcohol pueden acelerar el deterioro cognitivo a través de cambios epigenéticos y el deterioro del recambio de tau.
- Las hembras pueden ser más vulnerables a la tauopatía acelerada por el alcohol debido a una mayor acetilación de tau y un posible deterioro de la degradación de proteínas.
- Se necesita más investigación para explorar los efectos del consumo crónico de alcohol y el papel del alcohol en las vías de degradación de tau.
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