Psychiatry and clinical neurosciences
December 1, 2024
Yohei Ohtani, Hideaki Tani, Kie Nomoto-Takahashi et al.
13 citations
In a double-blind randomized placebo-controlled trial with 34 Japanese patients suffering from treatment-resistant depression, intravenous ketamine (0.5 mg/kg) given twice a week for two weeks did not show a statistically significant advantage over placebo in reducing depression scores when all participants were analyzed together. However, among those who completed the full treatment protocol, ketamine led to a significantly greater reduction in depressive symptoms than placebo. Higher baseline depression severity and body mass index were linked to greater symptom improvement with ketamine. Adverse events were more common with ketamine but no serious events occurred. These results suggest ketamine may be effective for treatment-resistant depression across diverse ethnic groups.
Molecular Psychiatry
March 5, 2026
Waki Nakajima, Mai Hatano, Yohei Ohtani et al.
1 citation
About 30% of people with depression have treatment-resistant depression (TRD). Ketamine can help, but how it works in the human brain was unclear. Using a PET tracer that shows AMPAR density, researchers found that AMPAR density was lower in patients with more severe TRD, and its distribution differed from healthy people. After ketamine, changes in AMPAR density in certain brain areas correlated with antidepressant effects, partially restoring normal AMPAR patterns. AMPAR dynamics underlie ketamine's antidepressant effect in TRD.
Pharmacopsychiatry
July 7, 2026
Kie Nomoto, Yohei Ohtani, Taisuke Yatomi et al.
In a double-blind, randomized, placebo-controlled trial, 34 Japanese patients with treatment-resistant depression received four intravenous doses of either ketamine (0.5 mg/kg) or saline. No significant differences emerged between the groups on objective or subjective cognitive function measures. Among ketamine-treated patients, those who responded to treatment (at least 50% reduction on the Montgomery-Åsberg Depression Rating Scale) showed greater improvement in subjective cognitive function than non-responders. Participants with weaker inhibitory control at baseline experienced larger reductions in depressive symptoms after ketamine. Repeated ketamine administration did not worsen cognitive function compared to placebo, suggesting cognitive safety, and baseline cognitive control deficits may predict better treatment response.