Abstract
ObjectiveAlzheimer’s disease (AD) is a global health problem without effective methods to alleviate the disease progression. Amyloid β-protein (Aβ) is widely accepted as a key biomarker for AD. Metabolic syndromes, including obesity and insulin resistance, are key high risk factors for AD. Akkermansia muciniphila (Akk), the only representative human gut microbe in the genus Verrucomicrobia, can prevent the weight gain caused by a high-fat diet, repair the damaged integrity of the intestinal epithelium barrier, reduce endotoxin levels in blood and improve insulin resistance. The aim of this study is to explore the impact of Akk administration in AD model mice in different diets.MethodsAPP/PS1 mice were fed either a normal chow diet or a high-fat diet and were treated with Akk by gavage each day for 6 months. The impacts of Akk on glucose metabolism, intestinal barrier and lipid metabolism in the mouse model of AD were determined. Changes in brain pathology and neuroethology were also analyzed.ResultsAkk effectively reduced the fasting blood glucose and serum diamine oxidase levels, and alleviated the reduction of colonic mucus cells in APP/PS1 mice. After treatment with Akk, the APP/PS1 mice showed obviously reduced blood lipid levels, improved hepatic steatosis and scapular brown fat whitening. Moreover, Akk promoted the reduction of Aβ 40–42 levels in the cerebral cortex of APP/PS1 mice, shortened the study time and improved the completion rate in Y-maze tests.ConclusionAkk effectively improved glucose tolerance, intestine barrier dysfunction and dyslipidemia in AD model mice. Our study results suggested that Akk could delay the pathological changes in the brain and relieve impairment of spatial learning and memory in AD model mice, which provides a new strategy for prevention and treatment of AD.
Highlights
Alzheimer’s disease (AD) is a disease with generalized dementia, such as memory impairment, loss of visual skills, performance impairment and behavioral changes
Our study results suggested that Akkermansia muciniphila (Akk) could delay the pathological changes in the brain and relieve impairment of spatial learning and memory in AD model mice, which provides a new strategy for prevention and treatment of AD
Many studies have shown that the development of insulin resistance in the brain appears in AD patients, which may be caused by Amyloid β-protein (Aβ) protein deposition, as it is associated with multiple pathological features[19,20]
Summary
Alzheimer’s disease (AD) is a disease with generalized dementia, such as memory impairment, loss of visual skills, performance impairment and behavioral changes. AD is characterized by serious cognitive impairment and significant pathological changes in the brain. Experts speculate that the population of AD patients could reach 30 million by 20504, 71% of Nutrition and Diabetes. A large number of reports have indicated that metabolic syndromes, including obesity and insulin resistance, are key high risk factors for cognitive impairment and dementia[5]. Type 2 diabetes greatly increased the risk of AD, and Aβ protein deposition competes with insulin for insulin receptors, causing insulin resistance[10,11,12,13]. Many studies have shown that the development of insulin resistance in the brain appears in AD patients, which may be caused by Aβ protein deposition, as it is associated with multiple pathological features[19,20]. Many scholars believed that a dysfunctional cerebral insulin pathway might be a partial cause of AD21
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