The Committee for Treatment Guidelines of Mood Disorders, Japanese Society of Mood Disorders, published a Japanese guideline for the treatment of late‐life depression in 2020. Based on that guideline, the present guideline was developed and revised to incorporate the suggestions of global experts and the latest published evidence. In the diagnosis of late‐life depression, it is important to carefully differentiate it from bipolar disorders, depressive states caused by physical and organic brain disease, drug effects, and dementia, and to determine the comorbidity between late‐life depression and dementia. It is necessary to fully understand the clinical characteristics and psychosocial background of late‐life depression, evaluate the patient's condition, and provide basic interventions based on these factors. Problem‐solving therapy, reminiscence therapy/life review therapy, and behavioral activation therapy, and other forms of psychotherapy can reduce depressive symptoms. In terms of pharmacotherapy, newer antidepressants or non‐tricyclic antidepressants are recommended for late‐life depression, and it is recommended that the efficacy of least the minimal effective dosage should first be determined. Switching antidepressants and aripiprazole augmentation can be used to treatment‐resistant therapy. Electroconvulsive therapy and repetitive transcranial magnetic stimulation have demonstrated usefulness for late‐life depression. Exercise therapy, high‐intensity light therapy, and diet therapy also show some effectiveness and are useful for late‐life depression. Continuation therapy should be maintained for at least 1 year after remission.

These results support a significant association between hippocampal atrophy and executive dysfunction as a non-memory cognitive impairment in patients with early AD and A-MCI.

Background: In the present study, we examined whether brain-derived neurotrophic factor (BDNF) polymorphism (Val66Met) influenced the changeable executive dysfunction of patients with two separate disease stages: amnestic mild cognitive impairment (A-MCI) or mild Alzheimer disease (AD), which are comparatively similar demented conditions. Methods: Among 200 outpatients with dementia and MCI, 146 outpatients with mild AD or A-MCI were recruited and divided into two genotypic groups, valine homozygosity (Val/Val) and methionine (Met) carriers, based on the representative BDNF functional polymorphism Val66Met. Next, we compared the Frontal Assessment Battery (FAB) total and subtest scores between the two genotypic groups according to each of two different disease stages: A-MCI (n = 42) and mild AD (n = 104). Results: Among patients with only a mild stage of AD, the FAB total and go/no-go scores were significantly lower (p < 0.05) among the subjects with the Val/Val genotype than among the Met carriers. However, no significant differences in any other demographic variables were observed between the genotypes according to each of different disease stages. A significant interaction between Val66Met and age was not observed for the FAB scores. Conclusion: These results suggested thatthe BDNF gene may significantly influence executive dysfunction, including inhibition tasks, among patients with mild-stage AD.