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1.
J Affect Disord ; 345: 394-403, 2024 01 15.
Artigo em Inglês | MEDLINE | ID: mdl-38190276

RESUMO

BACKGROUND: Depressive disorder in adolescents is a major health problem with inadequate treatment. Omega-3 (ω3) polyunsaturated fatty acids are a promising adjuvant therapy in adult depression. The primary objective of this study was to investigate the efficacy of adjuvant ω3 treatment on depressive symptoms in adolescent depression. Secondarily, we explored the effects of ω3 on cognitive function and memory and niacin skin flushing response (NSFR), as their robust associations with adolescent depression. METHODS: A total of 71 adolescents with depression (aged 13-24; 59.2 % female) were randomly assigned to receive ω3 plus Paxil (n = 34) or Paxil alone (n = 37) for 12 weeks. Primary outcome was depression severity according to scores on Montgomery-Asberg Depression Rating Scale (MADRS). Secondary outcomes were cognitive function and memory, and NSFR. RESULTS: Significant improvements in depressive symptoms over time (p = 0.00027 at week 12) were observed in the ω3 + Paxil group compared with Paxil group. Additionally, in the ω3 + Paxil group, significant improvements in memory over time, and greater cognitive function and NSFR were also observed compared with the Paxil group; the NSFR was negatively correlated with MADRS scores at baseline. LIMITATIONS: The trial was open label; thus, the outcome measures should be viewed as preliminary since inherent bias in outcomes due to the potential of a placebo effect. CONCLUSIONS: Our results demonstrate that adjuvant ω3 treatment is effective for reducing depressive symptoms as well as improving cognitive function, memory and the NSFR; these results suggest ω3 is a promising adjuvant treatment for adolescent depression.


Assuntos
Niacina , Adulto , Adolescente , Feminino , Humanos , Masculino , Depressão/tratamento farmacológico , Paroxetina , Cognição , Suplementos Nutricionais
2.
Neurosci Bull ; 31(1): 61-74, 2015 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-25575479

RESUMO

Major depressive disorder (MDD) is a common and devastating psychiatric disorder characterized by persistent low mood, cognitive disorder, and impaired social function. Despite its complex mechanisms, increasing evidence has identified the involvement of neurotrophic factors, inflammatory cytokines, the hypothalamus-pituitary-adrenal axis, and glutamate receptors in the pathophysiology of this illness. The present review synthesizes recent research achievements to define the network between different hypotheses of MDD and to understand which part is most pivotal for its pathogenesis. By integrating MDD-related signal pathways, we highlight brain-derived neurotrophic factor (BDNF) dysfunction and increased apoptosis as the final common cascades, and new therapeutic strategies aiming to enhance BDNF function have been shown to exert a rapid and effective antidepressant action.


Assuntos
Transtorno Depressivo Maior/tratamento farmacológico , Transtorno Depressivo Maior/metabolismo , Transtorno Depressivo Maior/fisiopatologia , Antidepressivos/uso terapêutico , Encéfalo/metabolismo , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Ritmo Circadiano , Citocinas/metabolismo , Transtorno Depressivo Maior/etiologia , Humanos , Hipotálamo/metabolismo , Inflamação/metabolismo , Fatores de Crescimento Neural/metabolismo , Sistema Hipófise-Suprarrenal/metabolismo , Receptores de Glutamato/metabolismo , Transdução de Sinais
3.
Neurosci Lett ; 580: 125-9, 2014 Sep 19.
Artigo em Inglês | MEDLINE | ID: mdl-25123439

RESUMO

Several studies have reported the ketamine-induced cognitive impairment. Docosahexaenoic acid (DHA) supplementation improves cognitive function in human infants and protects against learning impairment in patients with Alzheimer's disease (AD). In this study, we investigated the effect of DHA on ketamine-induced impairment of spatial cognition and learning ability in Institute of Cancer Research (ICR) mice. Morris water maze (MWM) was used to assess spatial learning and memory. Gamma-aminobutyric acid (GABA) levels in the hippocampus and prefrontal cortex were measured using high-performance liquid chromatography (HPLC). The results showed that intraperitoneal injection of ketamine (30mg/kg, twice per day) for 4 weeks led to the decline of spatial cognitive ability in mice, and 420mg/(kgd) DHA supplementation for 6 weeks improved ketamine-induced spatial cognitive impairment to a certain extent. The up-regulation of GABA levels in the hippocampus and prefrontal cortex was related to the improvement in spatial learning. Our results suggested that DHA supplementation would be a promising intervention to improve ketamine-induced spatial memory and cognitive dysfunction, and this effect of DHA might be correlated with the up-regulation of GABA levels.


Assuntos
Transtornos Cognitivos/tratamento farmacológico , Cognição/efeitos dos fármacos , Ácidos Docosa-Hexaenoicos/farmacologia , Drogas Ilícitas/toxicidade , Ketamina/toxicidade , Deficiências da Aprendizagem/tratamento farmacológico , Aprendizagem Espacial/efeitos dos fármacos , Animais , Transtornos Cognitivos/induzido quimicamente , Transtornos Cognitivos/psicologia , Ácidos Docosa-Hexaenoicos/uso terapêutico , Hipocampo/efeitos dos fármacos , Hipocampo/metabolismo , Deficiências da Aprendizagem/induzido quimicamente , Deficiências da Aprendizagem/psicologia , Masculino , Aprendizagem em Labirinto/efeitos dos fármacos , Camundongos Endogâmicos ICR , Córtex Pré-Frontal/efeitos dos fármacos , Córtex Pré-Frontal/metabolismo , Ácido gama-Aminobutírico/metabolismo
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