Journal of affective disorders · 2022
Clinical course and serum amyloid β levels in elderly patients with major depressive disorder.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Natsume Shuntaro, Baba Hajime, Maeshima Hitoshi, Saida Takao, Yoshinari Naoto, Shimizu Kentaro, Suzuki Toshihito
Аннотация
BACKGROUND: Depression is known to be a risk factor for Alzheimer's disease (AD). Changes in amyloid β protein (Aβ) metabolism have been speculated as a factor contributing to the transition from depression to AD. The aim of this study is to reveal the time course and state-dependency of Aβ metabolism.
METHODS: Serum Aβ levels in 277 elderly (≥60 years) patients with depression (both early- and late-onset) were measured at admission, immediately after remission, and 1 year after remission, and compared them with 178 healthy subjects.
RESULTS: The analysis revealed decreased Aβ42 levels and increased Aβ42/40 ratios in elderly patients with depression at admission compared with healthy subjects. These changes in the acute phase of depression were not normalized immediately after remission; however, they recovered to healthy levels 1 year after remission.
LIMITATIONS: There is a possibility that the results may be influenced by antidepressants.
CONCLUSIONS: These results suggest that altered Aβ metabolism caused by depression may ameliorate, although after a lengthy period of time after remission. Our findings also suggest that the AD-related pathological changes caused or increased by depression can be reduced by maintaining remission for an extended period of time.
METHODS: Serum Aβ levels in 277 elderly (≥60 years) patients with depression (both early- and late-onset) were measured at admission, immediately after remission, and 1 year after remission, and compared them with 178 healthy subjects.
RESULTS: The analysis revealed decreased Aβ42 levels and increased Aβ42/40 ratios in elderly patients with depression at admission compared with healthy subjects. These changes in the acute phase of depression were not normalized immediately after remission; however, they recovered to healthy levels 1 year after remission.
LIMITATIONS: There is a possibility that the results may be influenced by antidepressants.
CONCLUSIONS: These results suggest that altered Aβ metabolism caused by depression may ameliorate, although after a lengthy period of time after remission. Our findings also suggest that the AD-related pathological changes caused or increased by depression can be reduced by maintaining remission for an extended period of time.