Microbiota intestinal y modulación central del síndrome dolor - depresión. ¿Mito o realidad?
DOI:
https://doi.org/10.47924/neurotarget20215Palabras clave:
Dolor, Depresión, Neuroinflamación, Microbiota intestinalResumen
Durante mucho tiempo hemos observado tanto en la práctica médica diaria como en distintos estudios clínicos, que la comorbilidad entre procesos psiquiátricos afectivos como la depresión y los procesos dolorosos crónicos, son condiciones muy prevalentes en forma individual, pero ante la evaluación de su comorbilidad podemos observar que es alta, siendo aproximadamente de un 70%. Las teorías que explican esta comorbilidad se basan en localizaciones y neurotransmisores compartidos entre ambas patologías. Esto podría explicar por ejemplo, porqué el uso de moléculas antidepresivas es una terapéutica útil en el tratamiento de esta comorbilidad ya que regula estos neurotransmisores en las localizaciones cerebrales compartidas como así también las vías ascendentes y descendentes del dolor. Sin embargo a la luz de nuevas investigaciones se presenta la inflamación como teoría etiopatogénica válida. Inflamación primero periférica y luego central, denominándose neuroinflamación. Complejo proceso en el cual se involucra la barrera hematoencefálica (BHE) y un intrincado juego microglial astrocitario que resulta en productos tóxicos relacionados a la serotonina, glutamato y fenómenos oxidativos que determinan, desde fallas funcionales hasta fenómenos neurodegenerativos con múltiples implicancias psiconeuroinmunoendocrinológicas. Por último, la posible regulación de esta inflamación por medio de la manipulación de la microbiota intestinal, ecosistema interno, el cual se presenta como blanco posible de futuros tratamientos.
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