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Ciencia básica y patogénesis
Stefan H Sillau1, Md Mahiuddin Ahmed2, Christina M Coughlan3
1University of Colorado Department of Neurology and Alzheimer's and Cognition Center, Aurora, CO, USA.
Alzheimer's & dementia : the journal of the Alzheimer's Association
|December 25, 2025
Resumen
Las personas con síndrome de Down (SD) muestran un envejecimiento cerebral acelerado con aumento de los marcadores de daño neuronal e inflamación desde la infancia. Esto sugiere dianas terapéuticas potenciales como el GM-CSF para el SD y el envejecimiento típico.
Área de la Ciencia:
- Neurociencia
- Gerontología
- Genética
Sus antecedentes:
- El aumento de la edad es un factor de riesgo principal para la enfermedad de Alzheimer (EA) y el deterioro cognitivo.
- Las personas con síndrome de Down (SD) tienen un riesgo cercano al 100% de desarrollar neuropatología de la EA y demencia.
- Investigaciones previas mostraron que el factor estimulante de colonias de granulocitos-macrófagos (GM-CSF) mejoró la cognición y redujo la apoptosis neuronal en modelos animales y pacientes con EA.
Objetivo del estudio:
- Investigar los cambios relacionados con la edad en los biomarcadores de daño neuronal e inflamación en personas con SD.
- Comparar estos cambios con los observados en individuos normosómicos.
- Evaluar la apoptosis neuronal y la gliosis en un modelo de ratón de SD.
Principales métodos:
- Se midieron las concentraciones plasmáticas de UCH-L1, NfL y GFAP en 316 personas con SD (edades 2-60) utilizando Quanterix SIMOA.
- Estos niveles se compararon con datos de controles normosómicos sanos emparejados por edad.
- Se evaluó la apoptosis neuronal mediante tinción de Caspasa-3 en el modelo de ratón Dp16 de SD.
Principales resultados:
- Las personas con SD presentan niveles plasmáticos significativamente elevados de marcadores de daño neuronal (UCH-L1, NfL) e inflamación (GFAP) desde la infancia.
- La tasa de aumento exponencial de estos marcadores con la edad es sustancialmente más rápida en el SD en comparación con los individuos normosómicos.
- Los hallazgos preliminares indican un aumento de la apoptosis neuronal y la gliosis en los cerebros de ratones Dp16.
Conclusiones:
- El envejecimiento cerebral acelerado en el SD, evidenciado por un aumento del daño neuronal y la inflamación, es probablemente impulsado por una mayor expresión de APP y producción de Ab neurotóxica, agravado por la astrogliosis.
- Se justificarían ensayos clínicos que investiguen el GM-CSF (sargramostim) para evaluar su potencial para mitigar el daño neuronal y la inflamación y mejorar la cognición en adultos jóvenes con SD y en personas con envejecimiento normal.
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