ArticleAging and disease2022
Dietary Salt Disrupts Tricarboxylic Acid Cycle and Induces Tau Hyperphosphorylation and Synapse Dysfunction during Aging.
Article in Aging and disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Plasma and Urinary Metabolomic Profiles Associated with the Salt Sensitivity of Blood Pressure in the Dietary Approaches to Stop Hypertension-Sodium Trial.The Journal of nutrition · 2026Trial
- Impact of High Dietary Salt on Neurovascular and Cognitive Functions.Hypertension (Dallas, Tex. : 1979) · 2026Review
- The Relationship Between Dietary Sodium Intake and Cognitive Function: A Narrative Review.Current nutrition reports · 2026Review
- Neuronal Metabolism of Branched-Chain Amino Acids Alleviates Lifespan Reduction Caused by High-Salt Diet in Drosophila.Journal of molecular neuroscience : MN · 2026Article
- Association of dietary sodium intake with late-life cognitive decline and postmortem neuropathology in community-dwelling older adults.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Dual Challenges in the Context of Healthy Aging: A Comprehensive Exploration of the Association between Malnutrition and Cognitive Decline in Disabled Elderly.Aging and disease · 2025Review
- Dietary salt promotes cognitive impairment through repression of SIRT3/PINK1-mediated mitophagy and fission.Molecular and cellular biochemistry · 2025Article
- Tau Pathology Drives Disease-Associated Astrocyte Reactivity in Salt-Induced Neurodegeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Analysis of the association between dietary sodium intake and cognitive function: a NHANES-based machine learning study and animal experimental validation.Frontiers in nutrition · 2025Article
- The impact of salt consumption on cardiometabolic and cognitive health in aged female rats.Scientific reports · 2024Article
- High salt diet induces cognitive impairment and is linked to the activation of IGF1R/mTOR/p70S6K signaling.Metabolic brain disease · 2024Article
- Dietary salt promotes cognition impairment through GLP-1R/mTOR/p70S6K signaling pathway.Scientific reports · 2024Article
- The causal effects of dietary component intake and blood metabolites on risk of delirium: a Mendelian randomization study.Frontiers in nutrition · 2024Article
- Dietary sodium/potassium intake and cognitive impairment in older patients with hypertension: Data from NHANES 2011-2014.Journal of clinical hypertension (Greenwich, Conn.) · 2023Article
- Dietary High-Fat Promotes Cognitive Impairment by Suppressing Mitophagy.Oxidative medicine and cellular longevity · 2023Article
- Alterations to Cerebral Perfusion, Metabolite Profiles, and Neuronal Morphology in the Hippocampus and Cortex of Male and Female Mice during Chronic Exposure to a High-Salt Diet.International journal of molecular sciences · 2022Article
- Sex-specific effects of dietary salt intake on circulating Alzheimer's disease-related biomarkers in aged rats.Journal of Alzheimer's disease reportsArticle
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8 authors.
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Abstract
Dietary salt causes synaptic deficits and tau hyperphosphorylation, which are detrimental to cognitive function. However, the specific effects of a high-salt diet on synapse and tau protein remain poorly understood. In this study, aged (15-month-old) C57BL/6 mice received a normal (0.5% NaCl) or high-salt (8% NaCl) diet for 3 months, and N2a cells were treated with normal culture medium or a NaCl medium (40 mM). Spatial learning and memory abilities were tested using the Morris water maze. The levels of metabolites and related enzymes in the tricarboxylic acid (TCA) cycle were confirmed using liquid chromatography-tandem mass spectrometry, western blotting, and immunofluorescence. We also investigated synapse morphology and the phosphorylation of tau protein. Under the high-salt diet, mice displayed impaired learning and memory compared to mice fed the normal diet. Furthermore, excessive salt intake disturbed the TCA cycle in both animals and cells compared to the respective normal controls. High dietary salt reduced postsynaptic density protein 95 (PSD95) and brain-derived neurotrophic factor (BDNF) expression, impaired neurons, and caused synaptic loss in the mice. We also detected tau hyperphosphorylation at different sites (Thr205, Thr231, and Thr181) without increasing total tau levels in response to high salt treatment, both in vivo and in vitro. We concluded that elevated salt intake impairs the TCA cycle and induces tau hyperphosphorylation and synapse dysfunction during aging, which ultimately results in cognitive impairment.
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