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Ciencia básica y patogénesis

Sunny Kumar1,2,3, Ibai Diez1,4, Ana Claudia Amaral1,2,5

  • 1Harvard Medical School, Boston, MA, USA.

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

Los individuos con cambios neuropatológicos de la enfermedad de Alzheimer (ADNC) pero sin deterioro cognitivo muestran una reducción de la neuroinflamación y una regulación a la baja de las vías TNF y NF-κB. Esto sugiere que las reacciones proinflamatorias de las células gliales influyen en los resultados cognitivos en ADNC.

Palabras clave:
resilienciaenfermedad de Alzheimerneuroinflamaciónvías TNF/NF-κBcélulas gliales

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Área de la Ciencia:

  • Neurociencia
  • Genómica
  • Patología

Sus antecedentes:

  • Algunos individuos con cambios neuropatológicos de la enfermedad de Alzheimer (ADNC) permanecen cognitivamente normales, lo que indica mecanismos de resiliencia.
  • Comprender la resiliencia a la ADNC es crucial para identificar nuevos biomarcadores y dianas terapéuticas para la enfermedad de Alzheimer (EA).

Objetivo del estudio:

  • Comparar los cambios cerebrales y los perfiles de expresión génica en individuos resilientes (cognitivamente normales con ADNC) y pacientes con EA con demencia y cargas de ADNC equivalentes.
  • Identificar los mecanismos moleculares que subyacen a la resiliencia cognitiva en presencia de patología AD.

Principales métodos:

  • Se compararon las evaluaciones neuropatológicas y los datos de RNA-seq del córtex prefrontal dorsolateral de individuos resilientes, con EA y demencia, y controles (cohorte ROSMAP).
  • Se utilizó DESeq2 para el análisis diferencial de la expresión génica, teniendo en cuenta la edad, el sexo, el lote y el intervalo post mortem.
  • Se empleó una prueba de Wald para identificar genes expresados diferencialmente (DEGs) entre los grupos con EA y demencia y los resilientes.

Principales resultados:

  • Los cerebros resilientes tenían placas amiloides y ovillos equivalentes pero menores niveles de hilos de neuropilo de tau y pTau en comparación con los cerebros de EA con demencia.
  • Los cerebros resilientes mostraron cargas reducidas de astrocitos y microglia activados, con disminución de los procesos apoptóticos, neuroinflamatorios y de fosforilación de proteínas.
  • El análisis de vías reveló una regulación a la baja de las vías de señalización TNF, JAK-STAT y NF-κB en los cerebros resilientes, incluida la regulación a la baja compartida de CXCL1 y CXCL2.

Conclusiones:

  • Las especies de tau patológicas aberrantes en neuronas y sinapsis pueden desencadenar respuestas proinflamatorias gliales que involucran las vías TNF y NF-κB.
  • Estas vías inflamatorias parecen ser críticas para determinar el destino cognitivo (demencia frente a cognición preservada) en individuos con ADNC.