The increased potassium intake improves cognitive performance and attenuates histopathological markers in a model of Alzheimer's disease.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by hallmarks that include an accumulation of amyloid-β peptide (Aβ), 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 Aβ 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.