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Desarrollo de Fármacos

Apostolos Manolopoulos1, Konstantinos Avgerinos2, Qinghua Chen1

  • 1National Institute on Aging, Baltimore, MD, USA.

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Resumen

La suplementación con éster de cetona (KE) aumentó los niveles de cetona en el cerebro y redujo el glutamato cerebral en personas con síndrome metabólico. Esto sugiere una posible neuroprotección y beneficios cognitivos para el Alzheimer

Palabras clave:
síndrome metabólicoenfermedad de Alzheimeréster de cetonaneuroprotecciónmetabolismo cerebralfunción cognitiva

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Área de la Ciencia:

  • Neurociencia; Trastornos Metabólicos; Investigación de la Enfermedad de Alzheimer

Sus antecedentes:

  • Los cuerpos cetónicos ofrecen energía y señalización alternativas para la salud cerebral, lo que podría beneficiar la enfermedad de Alzheimer (AD).
  • La administración exógena de éster de cetona (KE) muestra resultados prometedores en modelos animales para mejorar la cognición y reducir la patología de la AD.
  • El síndrome metabólico aumenta el riesgo de AD, lo que hace que esta población sea relevante para las estrategias preventivas.

Objetivo del estudio:

  • Proporcionar una prueba de concepto para la participación del objetivo de éster de cetona (KE) en humanos.
  • Evaluar los efectos pro-cognitivos de KE en individuos con mayor riesgo de AD.
  • Investigar el impacto de KE en el metabolismo cerebral y la función cognitiva.

Principales métodos:

  • Un ensayo controlado aleatorizado, doble ciego, que involucró a 50 participantes con síndrome metabólico.
  • Los participantes recibieron 25 g de KE oral o placebo tres veces al día durante cuatro semanas.
  • Resultado primario: concentración de β-hidroxibutirato (βHB) en el cerebro mediante espectroscopia de resonancia magnética (MRS); Resultados secundarios: rendimiento cognitivo (PACC, NIH Toolbox).

Principales resultados:

  • KE aumentó significativamente los niveles de βHB en el cerebro, confirmando la participación del objetivo y la penetración cerebral.
  • La administración de KE redujo los niveles de glutamato en el cerebro, lo que indica una disminución de la excitotoxicidad.
  • Las tendencias favorecieron a KE para las mejoras de la memoria, y se observaron algunas ganancias cognitivas solo en el grupo KE.

Conclusiones:

  • La suplementación oral con KE indujo eficazmente la cetosis cerebral y se dirigió al objetivo.
  • La reducción del glutamato cerebral sugiere que KE puede ofrecer neuroprotección al modular la hiperexcitabilidad neuronal.
  • KE demuestra potencial para la prevención de la AD a través de mejoras metabólicas y cognitivas.