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Ciencia básica y patogénesis
Jessica Fisher1, Sama Jaberi1, Erika Kropf1
1McMaster University, Hamilton, ON, Canada.
Alzheimer's & dementia : the journal of the Alzheimer's Association
|December 24, 2025
Resumen
El estrés nitrativo activa JNK, perjudicando el transporte del factor neurotrófico derivado del cerebro (BDNF) en las neuronas colinérgicas del prosencéfalo basal (BFCN). La inhibición de JNK previene este déficit, sugiriendo un objetivo para el deterioro cognitivo relacionado con la edad y la enfermedad de Alzheimer.
Área de la Ciencia:
- Neurociencia; Biología celular; Investigación sobre el envejecimiento
Sus antecedentes:
- Las neuronas colinérgicas del prosencéfalo basal (BFCN) son cruciales para el aprendizaje y la memoria.; La degeneración de las BFCN y el transporte alterado del factor neurotrófico derivado del cerebro (BDNF) contribuyen al deterioro cognitivo en el envejecimiento y la enfermedad de Alzheimer (EA).; El estrés nitrativo en el cerebro envejecido puede alterar el transporte de BDNF, pero los mecanismos subyacentes no se comprenden completamente.
Objetivo del estudio:
- Investigar si la activación de la c-Jun N-terminal quinasa (JNK) inducida por estrés nitrativo contribuye a los déficits en el transporte axonal retrógrado de BDNF en las BFCN.; Determinar si la inhibición de JNK puede prevenir el deterioro del transporte de BDNF inducido por estrés nitrativo.
Principales métodos:
- Se cultivaron BFCN de rata primarias en cámaras de microfluidos para el aislamiento axonal.; Las neuronas se trataron con un donante de peroxinitrito (SIN-1) para inducir estrés nitrativo.; Se midió la activación de JNK mediante inmunocitoquímica y se evaluó el transporte de BDNF utilizando BDNF marcado con puntos cuánticos y microscopía de fluorescencia de células vivas.
Principales resultados:
- El tratamiento con SIN-1 aumentó significativamente la activación de JNK y disminuyó el transporte axonal de BDNF.; La coadministración de un inhibidor de JNK (CC401) con SIN-1 previno la reducción del transporte de BDNF causada por SIN-1.; Estos hallazgos indican que la activación de JNK media los efectos inhibitorios del estrés nitrativo sobre el transporte de BDNF.
Conclusiones:
- La activación de JNK por peroxinitrito es un mecanismo clave que vincula el estrés nitrativo con el transporte de BDNF alterado en las BFCN.; Este estudio destaca una vía potencial a través de la cual el estrés nitrativo relacionado con la edad contribuye a la degeneración de las BFCN y al deterioro cognitivo en la EA.; Dirigirse a la señalización de JNK puede ofrecer una estrategia terapéutica para preservar el transporte de BDNF y mitigar los déficits cognitivos.
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