| Literature DB >> 29608993 |
Kamiyu Ogyu1, Kaoruhiko Kubo1, Yoshihiro Noda1, Yusuke Iwata2, Sakiko Tsugawa3, Yuki Omura3, Masataka Wada1, Ryosuke Tarumi1, Eric Plitman2, Sho Moriguchi2, Takahiro Miyazaki1, Hiroyuki Uchida1, Ariel Graff-Guerrero2, Masaru Mimura1, Shinichiro Nakajima4.
Abstract
Abnormalities of the kynurenine (KYN) pathway may be implicated in the pathophysiology of depression. However, the relationships between depression and each metabolite of the KYN pathway remain uncertain. Therefore, we conducted a meta-analysis about the levels of the metabolites of KYN pathway between patients with depression and controls. Out of 899 initial records, we identified 22 articles to form the empirical basis. Seventeen, 10, and 18 studies examined levels of kynurenic acid (KYNA), quinolinic acid (QUIN), and KYN, respectively. KYNA and KYN levels were lower in patients with depression in comparison to controls, while QUIN levels did not differ between the two groups. Antidepressant-free patients showed decreased KYNA levels and increased QUIN levels compared with controls. Male ratios of the samples were negatively associated with study SMDs for KYNA. In conclusion, this meta-analysis revealed that patients with depression had decreased level of KYNA and KYN, whereas antidepressant-free patients showed increased level of QUIN. Nevertheless, given the heterogeneity among their sample characteristics, further research is clearly needed.Entities:
Keywords: Depression; Glutamate; Kynurenic acid; N-methyl-d-aspartate receptor; Neuroinflammation; Quinolinic acid
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Year: 2018 PMID： 29608993 DOI： 10.1016/j.neubiorev.2018.03.023
Source DB: PubMed Journal: Neurosci Biobehav Rev ISSN： 0149-7634 Impact factor: 8.989