High‐salt diet enhances Helicobacter pylori infection and increases the prevalence of Alzheimer’s disease

Abstract

AbstractBackgroundThe American Heart Association recommends that adults consume less than 2,300 milligrams of salt (sodium chloride) daily; anything surpassing this limit is classified as a “high‐salt diet (HSD)” [1]. Research has shown that excessive salt intake stimulates the gastric mucosa, favoring Helicobacter pylori (Hp) colonization [2]. In this review, the relationship between HSD and the susceptibility to Hp infection will be discussed. It is proposed that increased salt consumption will cause neurodegeneration, i.e. Alzheimer’s disease (AD) by way of increased expression of Hp strains in the gastric mucosa.MethodsA complex and specific literature search was conducted across various scientific, international databases for English, peer‐reviewed articles and reviews published in the last decade using the following terms: Helicobacter pylori, amyloid‐β, high‐salt diet, and Alzheimer’s disease. Case reports were excluded. The main objectives were predominantly focused on animal‐based studies.ResultsExperimental data shows HSD enhances Hp growth in mice. The subsequent microglial activation containing H. pylori‐specific IgG, IL‐8 and TNF‐α in the cerebrospinal fluid, induces oxidative damage in neuronal cells. In addition, urease in Hp increases cytosolic [Ca2+] apoptosis and autophagy of neurons. Hp filtrate induces tau hyperphosphorylation at AD‐tau phosphorylation sites such as Thr231 and Ser404. Hp ‐infected mice show a significantly larger GFAP‐positive astrocyte area than non‐infected mice. Immunostaining reveals microglia and astrocytes to be found adjacent to amyloid‐β plaques in Hp‐infected AD model mice. Injection of Hp filtrate impairs the maturation of dendritic spines, increasing Aβ42 production in the hippocampus and cortex, and enhancing expression of PS‐2, resulting in delayed spatial learning and impaired memory in rats.ConclusionThis review provides comprehensive evidence of potential synergistic effects of HSD and Hp on the brain resulting in neurodegeneration and AD progression. Understanding the pathologic consequences of salt consumption on this infection may be key in the prevention of dementia and AD. Thus, further research is required for substantiation of causality, the role of antibiotics and to examine other novel therapeutics.