Association of dietary sodium intake with late-life cognitive decline and postmortem neuropathology in community-dwelling older adults

Abstract

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.

Keywords: Alzheimer's disease; arteriolosclerosis; cerebrovascular disease; cognitive decline; dietary sodium; neurodegenerative; neuropathology; tau.