Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
Association of dietary sodium intake with late-life cognitive decline and postmortem neuropathology in community-dwelling older adults.
СтатьяНазвание и аннотация: Перевод в очереди
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.
Tong Han, Capuano Ana W, Agarwal Puja, Mehta Rupal I, Sood Ajay, Bennett David A, Arvanitakis Zoe
Аннотация
INTRODUCTION: Studies link sodium intake to cognition, but most were cross-sectional, and associations with neuropathology remain unclear.
METHODS: 1520 community-dwelling adults (mean age 80.7 years) had annual evaluations (mean follow-up 7.6 years), including 19 neuropsychological tests and a food frequency questionnaires (FFQ). Postmortem neuropathologies were documented in 717 deceased participants. Associations of dietary sodium intake estimated from the FFQ with cognitive decline and neuropathology were examined using adjusted regression models.
RESULTS: Compared to the middle sodium intake quintile (median 2264 mg/day), the lowest quintile (1764 mg/day), but not the highest (2800 mg/day), was associated with faster decline in global cognition, particularly episodic memory and semantic memory. Among the deceased, the lowest quintile was associated with higher immunohistochemistry-based tau tangle density, but not with amyloid burden or infarcts.
DISCUSSION: Low dietary sodium intake is associated with faster cognitive decline and more neuropathology, specifically tangles. Dietary sodium likely plays a role in brain health.
HIGHLIGHTS: The relation of dietary sodium to brain health is not well understood. In this community-based study, FFQs were used to estimate dietary sodium intake. Longitudinal neurocognitive and postmortem neuropathology evaluations were conducted. Among 1520 older adults without known dementia followed annually for 7.6 years, low sodium intake was associated with faster decline in global cognition. Among a subset who died and came to autopsy, low sodium intake was associated with higher tangle density, but not with amyloid burden or infarcts.
METHODS: 1520 community-dwelling adults (mean age 80.7 years) had annual evaluations (mean follow-up 7.6 years), including 19 neuropsychological tests and a food frequency questionnaires (FFQ). Postmortem neuropathologies were documented in 717 deceased participants. Associations of dietary sodium intake estimated from the FFQ with cognitive decline and neuropathology were examined using adjusted regression models.
RESULTS: Compared to the middle sodium intake quintile (median 2264 mg/day), the lowest quintile (1764 mg/day), but not the highest (2800 mg/day), was associated with faster decline in global cognition, particularly episodic memory and semantic memory. Among the deceased, the lowest quintile was associated with higher immunohistochemistry-based tau tangle density, but not with amyloid burden or infarcts.
DISCUSSION: Low dietary sodium intake is associated with faster cognitive decline and more neuropathology, specifically tangles. Dietary sodium likely plays a role in brain health.
HIGHLIGHTS: The relation of dietary sodium to brain health is not well understood. In this community-based study, FFQs were used to estimate dietary sodium intake. Longitudinal neurocognitive and postmortem neuropathology evaluations were conducted. Among 1520 older adults without known dementia followed annually for 7.6 years, low sodium intake was associated with faster decline in global cognition. Among a subset who died and came to autopsy, low sodium intake was associated with higher tangle density, but not with amyloid burden or infarcts.