期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
卷 1852, 期 12, 页码 2630-2644出版社
ELSEVIER
DOI: 10.1016/j.bbadis.2015.09.009
关键词
Alzheimer's disease; Potassium intake; Hypertension; Synaptic dysfunction
资金
- Basal Center of Excellence in Aging and Regeneration [CONICYT-PFB 12/2007]
- FONDECYT [1120156, 11130529, 1130747, 3150475]
- Sociedad Quimica y Minera de Chile (SQM)
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by hallmarks that include an accumulation of amyloid-beta peptide (A beta), inflammation, oxidative stress and synaptic dysfunction, which lead to a decrease in cognitive function. To date, the onset and progression of AD have been associated with pathologies such as hypertension and diabetes. Hypertension, a disease with a high incidence worldwide, is characterized by a chronic increase in blood pressure. Interestingly, this disease has a close relationship to the eating behavior of patients because high Na+ intake is a significant risk factor for hypertension. In fact, a decrease in Na+ consumption, along with an increase in K+ intake, is a primary non-pharmacological approach to preventing hypertension. In the present work, we examined whether an increase in K+ intake affects the expression of certain neuropathological markers or the cognitive performance of a murine model of AD. We observed that an increase in K+ intake leads to a change in the aggregation pattern of the A beta peptide, a partial decrease in some epitopes of tau phosphorylation and improvement in the cognitive performance. The recovery in cognitive performance was correlated with a significant improvement in the generation of long-term potentiation. We also observed a decrease in markers related to inflammation and oxidative stress such as glial fibrillary acidic protein (GFAP), interleukin 6 (IL-6) and 4-hydroxynonenal (4-HNE). Together, our data support the idea that changes in diet, such as an increase in K+ intake, may be important in the prevention of AD onset as a non-pharmacological therapy. (C) 2015 Elsevier B.V. All rights reserved.
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