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Ensayo controlado aleatorizado2016

Effects of Creatine Monohydrate Augmentation on Brain Metabolic and Network Outcome Measures in Women With Major Depressive Disorder

Yoon S, Kim JE, Hwang J, Kim TS, Kang HJ, Namgung E, Ban S, Oh S, Yang J, Renshaw PF, Lyoo IK

Biological psychiatry · 40 citas

Cómo se estudió

Diseño
Ensayo controlado aleatorizado (indexado por PubMed)
Estudiado en
Personas
Resultado principal
Marcadores de salud y funcionamiento

Quién lo pagó

Financiación
Financiación independiente
Gobierno
National Research Foundation of Korea
Gobierno
Ministry of Science, ICT and Future Planning/Institute for Information and Communications Technology Promotion
Subvenciones
National Research Foundation of Korea (2015M3C7A1028373)

Según 2 financiadores declarados.

Publicación

Publicado
2015-12-18 · Biol Psychiatry · vol. 80 · número 6 · págs. 439–447
Editorial
Elsevier BV
Citado
71 citas · más que el 91% de estudios similares · 3.2× el promedio de su campo
Impacto
Entre el 10 % más citado de su campo
Referencias
55 trabajos
Acceso
De pago
Áreas de investigación
Treatment of Major Depression · Tryptophan and brain disorders · Neurotransmitter Receptor Influence on Behavior
Palabras clave
creatine monohydrate, major depressive disorder, women, escitalopram, selective serotonin reuptake inhibitors, brain energy metabolism, N-acetylaspartate, prefrontal cortex, structural brain networks, antidepressant augmentation, 1H NMR, diffusion tensor imaging
MeSH
brain, prefrontal cortex, neural pathways, humans, creatine, citalopram, aspartic acid, drug therapy, combination, case-control studies, double-blind method, adult, aged, middle aged, female, young adult, diffusion tensor imaging, proton magnetic resonance spectroscopy, major depressive disorder

11 autores

  • Sujung J. Yoon
  • Jieun E. Kim
  • Jaeuk Hwang🇰🇷Soonchunhyang University
  • Tae Suk Kim🇰🇷Catholic University of Korea
  • Hee Jin Kang
  • Eun Namgung
  • Soonhyun Ban
  • Subin Oh
  • Jeongwon Yang
  • Perry Franklin Renshaw🇺🇸University of Utah
  • In Kyoon Lyoo🇺🇸 · autor de correspondenciaUniversity of Utah

Resumen

El texto original del estudio, en el idioma en que se publicó.

Background

Creatine monohydrate (creatine) augmentation has the potential to accelerate the clinical responses to and enhance the overall efficacy of selective serotonin reuptake inhibitor treatment in women with major depressive disorder (MDD). Although it has been suggested that creatine augmentation may involve the restoration of brain energy metabolism, the mechanisms underlying its antidepressant efficacy are unknown.

Methods

In a randomized, double-blind, placebo-controlled trial, 52 women with MDD were assigned to receive either creatine augmentation or placebo augmentation of escitalopram; 34 subjects participated in multimodal neuroimaging assessments at baseline and week 8. Age-matched healthy women (n = 39) were also assessed twice at the same intervals. Metabolic and network outcomes were measured for changes in prefrontal N-acetylaspartate and changes in rich club hub connections of the structural brain network using proton magnetic resonance spectroscopy and diffusion tensor imaging, respectively.

Results

We found MDD-related metabolic and network dysfunction at baseline. Improvement in depressive symptoms was greater in patients receiving creatine augmentation relative to placebo augmentation. After 8 weeks of treatment, prefrontal N-acetylaspartate levels increased significantly in the creatine augmentation group compared with the placebo augmentation group. Increment in rich club hub connections was also greater in the creatine augmentation group than in the placebo augmentation group.

Conclusions

N-acetylaspartate levels and rich club connections increased after creatine augmentation of selective serotonin reuptake inhibitor treatment. Effects of creatine administration on brain energy metabolism and network organization may partly underlie its efficacy in treating women with MDD.

Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial.

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