New research shows how a high-salt diet leads to excessive levels of interleukin-17 (IL-17) in multiple sclerosis (MS) patients, causing changes in endothelial cells that result in dementia.
These findings suggest that therapeutics targeting IL-17 may help halt the neurovascular damages of MS and other autoimmune diseases linked to high levels of IL-17.
The study, “Dietary salt promotes neurovascular and cognitive dysfunction through a gut-initiated TH17 response,” appeared in the journal Nature Neuroscience.
Diets rich in sodium chloride are common among Americans, 90 percent of whom exceed the recommended 2,300 mg intake of salt per day. While such diets have been linked with an increased risk for cerebrovascular diseases and dementia, exactly how high levels of salt damage the brain remained unclear.
Eager to find out, researchers at New York’s Weill Cornell University fed mice a high-salt diet, either with 4 or 8 percent of salt, corresponding to a 8- to 16-fold increase in salt content compared to a normal mouse diet.
“Although estimating salt consumption at the population level is challenging, this diet is comparable to the high end of the spectrum of human salt consumption,” researchers wrote.
Mice were fed for eight, 12 or 24 weeks. Using magnetic resonance imaging, researchers discovered that such a diet led to significant reductions in cerebral blood flow (CBF) in the brain’s cortex (by 28%) and hippocampus (by 25%) — two areas responsible for learning and memory.
Moreover, in rodents fed a high-salt diet during 12 weeks, researchers detected dysfunctions in the endothelium — the thin membrane composed of endothelial cells that line all blood vessels. The endothelial cells also reduced the production of nitric oxide, a gas that relaxes blood vessels and increases blood flow.
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