Intra‐gastrointestinal amyloid‐β1–42 oligomers perturb enteric function and induce Alzheimer's disease pathology

Sun, Yayi; Sommerville, Nerina R.; Liu, Julia Y.H.; Ngan, Man P.; Poon, Daniel; Ponomarev, Eugene D.; Lu, Zhonghua; Kung, Jeng S. C.; Rudd, John A.

doi:10.1113/jp279919

Cited by 92 publications

(90 citation statements)

References 45 publications

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“…Changes altering the gut microbiota can activate proinflammatory cytokines and increase intestinal permeability, which lead to the development of insulin resistance that is associated with AD [ 117 ] ( Figure 2 ). Interestingly, recent work has shown that AD development could start even in the gut and then spread to the brain [ 118 ]. In this study, the gastric wall of mice was injected with Aβ 1–42 oligomers.…”

Section: Gut Microbiota In Admentioning

confidence: 99%

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The Microbiota–Gut–Brain Axis and Alzheimer’s Disease: Neuroinflammation Is to Blame?

et al. 2020

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For years, it has been reported that Alzheimer’s disease (AD) is the most common cause of dementia. Various external and internal factors may contribute to the early onset of AD. This review highlights a contribution of the disturbances in the microbiota–gut–brain (MGB) axis to the development of AD. Alteration in the gut microbiota composition is determined by increase in the permeability of the gut barrier and immune cell activation, leading to impairment in the blood–brain barrier function that promotes neuroinflammation, neuronal loss, neural injury, and ultimately AD. Numerous studies have shown that the gut microbiota plays a crucial role in brain function and changes in the behavior of individuals and the formation of bacterial amyloids. Lipopolysaccharides and bacterial amyloids synthesized by the gut microbiota can trigger the immune cells residing in the brain and can activate the immune response leading to neuroinflammation. Growing experimental and clinical data indicate the prominent role of gut dysbiosis and microbiota–host interactions in AD. Modulation of the gut microbiota with antibiotics or probiotic supplementation may create new preventive and therapeutic options in AD. Accumulating evidences affirm that research on MGB involvement in AD is necessary for new treatment targets and therapies for AD.

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Section: Gut Microbiota In Admentioning

confidence: 99%

“…Over 1 year, it was observed that the amyloid migrated from the intestine to the brain. Consequently, the translocation of Aβ oligomers from the gut to the brain can have a major contribution in causing AD and neuroinflammation [ 118 ].…”

Section: Gut Microbiota In Admentioning

confidence: 99%

The Microbiota–Gut–Brain Axis and Alzheimer’s Disease: Neuroinflammation Is to Blame?

et al. 2020

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“…Amyloid deposition in the vagus nerve and celiac ganglions has been reported in patients with systemic amyloidosis [ 171 ]. Recently, Sun et al showed that intra-GI injection of Aβ oligomers induced vagal and cerebral amyloidosis after 12 months [ 172 ], suggesting that neural transport may be considered as a potential route of spread of Aβ pathology towards the CNS.…”

Section: Roles Of Diet and Microbiota In Neurodegenerative Diseasementioning

confidence: 99%

Diet, Microbiota and Brain Health: Unraveling the Network Intersecting Metabolism and Neurodegeneration

Gentile

Doneddu

Riva

et al. 2020

IJMS

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Increasing evidence gives support for the idea that extra-neuronal factors may affect brain physiology and its predisposition to neurodegenerative diseases. Epidemiological and experimental studies show that nutrition and metabolic disorders such as obesity and type 2 diabetes increase the risk of Alzheimer’s and Parkinson’s diseases after midlife, while the relationship with amyotrophic lateral sclerosis is uncertain, but suggests a protective effect of features of metabolic syndrome. The microbiota has recently emerged as a novel factor engaging strong interactions with neurons and glia, deeply affecting their function and behavior in these diseases. In particular, recent evidence suggested that gut microbes are involved in the seeding of prion-like proteins and their spreading to the central nervous system. Here, we present a comprehensive review of the impact of metabolism, diet and microbiota in neurodegeneration, by affecting simultaneously several aspects of health regarding energy metabolism, immune system and neuronal function. Advancing technologies may allow researchers in the future to improve investigations in these fields, allowing the buildup of population-based preventive interventions and development of targeted therapeutics to halt progressive neurologic disability.

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“…In a recent issue of The Journal of Physiology , Sun et al . (2020) used a novel dementia mouse model to study the influence of gut Aβ on CNS histopathology and function. The model consisted of injecting Aβ oligomers (labelled or unlabelled) into the gut serosa of male Institute of Cancer Research mice, a strain widely used for disease modelling studies.…”

mentioning

confidence: 99%

Gut amyloid‐β induces cognitive deficits and Alzheimer's disease‐related histopathology in a mouse model

Vonderwalde

Finlayson-Trick

2020

The Journal of Physiology

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Intra‐gastrointestinal amyloid‐β1–42 oligomers perturb enteric function and induce Alzheimer's disease pathology

Cited by 92 publications

References 45 publications

The Microbiota–Gut–Brain Axis and Alzheimer’s Disease: Neuroinflammation Is to Blame?

The Microbiota–Gut–Brain Axis and Alzheimer’s Disease: Neuroinflammation Is to Blame?

Diet, Microbiota and Brain Health: Unraveling the Network Intersecting Metabolism and Neurodegeneration

Gut amyloid‐β induces cognitive deficits and Alzheimer's disease‐related histopathology in a mouse model

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