Fecal microbiota transplantation attenuates Alzheimer’s disease symptoms in APP/PS1 transgenic mice via inhibition of the TLR4-MyD88-NF-κB signaling pathway-mediated inflammation

Alzheimer’s disease (AD) is a prevalent and progressive neurodegenerative disorder that is the leading cause of dementia. The underlying mechanisms of AD have not yet been completely explored. Neuroinflammation, an inflammatory response mediated by certain mediators, has been exhibited to play a cru...

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Veröffentlicht in:	Behavioral and brain functions Jg. 21; H. 1; S. 2 - 21
Hauptverfasser:	Li, Xiang, Ding, Qingyong, Wan, Xinxin, Wu, Qilong, Ye, Shiqing, Lou, Yongliang
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	London BioMed Central 08.01.2025 Springer Nature B.V BMC
Schlagworte:	Alzheimer Disease - microbiology Alzheimer Disease - therapy Alzheimer's disease Amyloid beta-Protein Precursor - genetics Animals Behavioral Therapy Biomedical and Life Sciences Biomedicine Brain research Cognitive ability Cytokines Dementia disorders Design of experiments Disease Disease Models, Animal Dysbacteriosis Ethanol Fecal microbiota transplantation Fecal Microbiota Transplantation - methods Fecal microflora Feces Gastrointestinal Microbiome - physiology Gut-brain axis Hypotheses Inflammation Inflammation - metabolism Inflammation - therapy Intestinal microbiota Intestinal microflora Investigations Laboratory animals Male Memory Metabolites Mice Mice, Inbred C57BL Mice, Transgenic Microbiota Microbiota-gut-brain axis Mutation MyD88 protein Myeloid Differentiation Factor 88 - metabolism Neurodegenerative diseases Neurology Neurosciences NF-kappa B - metabolism NF-κB protein Pathogenesis Permeability Presenilin 1 Presenilin-1 - genetics Psychiatry Short-chain fatty acids Signal transduction Signal Transduction - physiology Software TLR4 protein Toll-Like Receptor 4 - metabolism Toll-like receptors Transgenic animals Transgenic mice Transplantation Transplants & implants Tumor necrosis factor-TNF Short-chain fatty acids Microbiota-gut-brain axis Inflammation Alzheimer’s disease Fecal microbiota transplantation Intestinal microbiota
ISSN:	1744-9081, 1744-9081
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Abstract	Alzheimer’s disease (AD) is a prevalent and progressive neurodegenerative disorder that is the leading cause of dementia. The underlying mechanisms of AD have not yet been completely explored. Neuroinflammation, an inflammatory response mediated by certain mediators, has been exhibited to play a crucial role in the pathogenesis of AD. Additionally, disruption of the gut microbiota has been found to be associated with AD, and fecal microbiota transplantation (FMT) has emerged as a potential therapeutic approach. However, the precise mechanism of FMT in the treatment of AD remains elusive. In this study, FMT was performed by transplanting fecal microbiota from healthy wild-type mice into APP/PS1 mice (APPswe, PSEN1dE9) to assess the effectiveness of FMT in mitigating AD-associated inflammation and to reveal its precise mechanism of action. The results demonstrated that FMT treatment improved cognitive function and reduced the expression levels of inflammatory factors by regulating the TLR4/MyD88/NF-κB signaling pathway in mice, which was accompanied by the restoration of gut microbial dysbiosis. These findings suggest that FMT has the potential to ameliorate AD symptoms and delay the disease progression in APP/PS1 mice.
AbstractList	Alzheimer's disease (AD) is a prevalent and progressive neurodegenerative disorder that is the leading cause of dementia. The underlying mechanisms of AD have not yet been completely explored. Neuroinflammation, an inflammatory response mediated by certain mediators, has been exhibited to play a crucial role in the pathogenesis of AD. Additionally, disruption of the gut microbiota has been found to be associated with AD, and fecal microbiota transplantation (FMT) has emerged as a potential therapeutic approach. However, the precise mechanism of FMT in the treatment of AD remains elusive. In this study, FMT was performed by transplanting fecal microbiota from healthy wild-type mice into APP/PS1 mice (APPswe, PSEN1dE9) to assess the effectiveness of FMT in mitigating AD-associated inflammation and to reveal its precise mechanism of action. The results demonstrated that FMT treatment improved cognitive function and reduced the expression levels of inflammatory factors by regulating the TLR4/MyD88/NF-κB signaling pathway in mice, which was accompanied by the restoration of gut microbial dysbiosis. These findings suggest that FMT has the potential to ameliorate AD symptoms and delay the disease progression in APP/PS1 mice.Alzheimer's disease (AD) is a prevalent and progressive neurodegenerative disorder that is the leading cause of dementia. The underlying mechanisms of AD have not yet been completely explored. Neuroinflammation, an inflammatory response mediated by certain mediators, has been exhibited to play a crucial role in the pathogenesis of AD. Additionally, disruption of the gut microbiota has been found to be associated with AD, and fecal microbiota transplantation (FMT) has emerged as a potential therapeutic approach. However, the precise mechanism of FMT in the treatment of AD remains elusive. In this study, FMT was performed by transplanting fecal microbiota from healthy wild-type mice into APP/PS1 mice (APPswe, PSEN1dE9) to assess the effectiveness of FMT in mitigating AD-associated inflammation and to reveal its precise mechanism of action. The results demonstrated that FMT treatment improved cognitive function and reduced the expression levels of inflammatory factors by regulating the TLR4/MyD88/NF-κB signaling pathway in mice, which was accompanied by the restoration of gut microbial dysbiosis. These findings suggest that FMT has the potential to ameliorate AD symptoms and delay the disease progression in APP/PS1 mice. Alzheimer's disease (AD) is a prevalent and progressive neurodegenerative disorder that is the leading cause of dementia. The underlying mechanisms of AD have not yet been completely explored. Neuroinflammation, an inflammatory response mediated by certain mediators, has been exhibited to play a crucial role in the pathogenesis of AD. Additionally, disruption of the gut microbiota has been found to be associated with AD, and fecal microbiota transplantation (FMT) has emerged as a potential therapeutic approach. However, the precise mechanism of FMT in the treatment of AD remains elusive. In this study, FMT was performed by transplanting fecal microbiota from healthy wild-type mice into APP/PS1 mice (APPswe, PSEN1dE9) to assess the effectiveness of FMT in mitigating AD-associated inflammation and to reveal its precise mechanism of action. The results demonstrated that FMT treatment improved cognitive function and reduced the expression levels of inflammatory factors by regulating the TLR4/MyD88/NF-κB signaling pathway in mice, which was accompanied by the restoration of gut microbial dysbiosis. These findings suggest that FMT has the potential to ameliorate AD symptoms and delay the disease progression in APP/PS1 mice. Abstract Alzheimer’s disease (AD) is a prevalent and progressive neurodegenerative disorder that is the leading cause of dementia. The underlying mechanisms of AD have not yet been completely explored. Neuroinflammation, an inflammatory response mediated by certain mediators, has been exhibited to play a crucial role in the pathogenesis of AD. Additionally, disruption of the gut microbiota has been found to be associated with AD, and fecal microbiota transplantation (FMT) has emerged as a potential therapeutic approach. However, the precise mechanism of FMT in the treatment of AD remains elusive. In this study, FMT was performed by transplanting fecal microbiota from healthy wild-type mice into APP/PS1 mice (APPswe, PSEN1dE9) to assess the effectiveness of FMT in mitigating AD-associated inflammation and to reveal its precise mechanism of action. The results demonstrated that FMT treatment improved cognitive function and reduced the expression levels of inflammatory factors by regulating the TLR4/MyD88/NF-κB signaling pathway in mice, which was accompanied by the restoration of gut microbial dysbiosis. These findings suggest that FMT has the potential to ameliorate AD symptoms and delay the disease progression in APP/PS1 mice.
ArticleNumber	2
Author	Li, Xiang Ye, Shiqing Wu, Qilong Wan, Xinxin Lou, Yongliang Ding, Qingyong
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Keywords	Short-chain fatty acids Microbiota-gut-brain axis Inflammation Alzheimer’s disease Fecal microbiota transplantation Intestinal microbiota
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Snippet	Alzheimer’s disease (AD) is a prevalent and progressive neurodegenerative disorder that is the leading cause of dementia. The underlying mechanisms of AD have... Alzheimer's disease (AD) is a prevalent and progressive neurodegenerative disorder that is the leading cause of dementia. The underlying mechanisms of AD have... Abstract Alzheimer’s disease (AD) is a prevalent and progressive neurodegenerative disorder that is the leading cause of dementia. The underlying mechanisms of...
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SubjectTerms	Alzheimer Disease - microbiology Alzheimer Disease - therapy Alzheimer's disease Amyloid beta-Protein Precursor - genetics Animals Behavioral Therapy Biomedical and Life Sciences Biomedicine Brain research Cognitive ability Cytokines Dementia disorders Design of experiments Disease Disease Models, Animal Dysbacteriosis Ethanol Fecal microbiota transplantation Fecal Microbiota Transplantation - methods Fecal microflora Feces Gastrointestinal Microbiome - physiology Gut-brain axis Hypotheses Inflammation Inflammation - metabolism Inflammation - therapy Intestinal microbiota Intestinal microflora Investigations Laboratory animals Male Memory Metabolites Mice Mice, Inbred C57BL Mice, Transgenic Microbiota Microbiota-gut-brain axis Mutation MyD88 protein Myeloid Differentiation Factor 88 - metabolism Neurodegenerative diseases Neurology Neurosciences NF-kappa B - metabolism NF-κB protein Pathogenesis Permeability Presenilin 1 Presenilin-1 - genetics Psychiatry Short-chain fatty acids Signal transduction Signal Transduction - physiology Software TLR4 protein Toll-Like Receptor 4 - metabolism Toll-like receptors Transgenic animals Transgenic mice Transplantation Transplants & implants Tumor necrosis factor-TNF
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Title	Fecal microbiota transplantation attenuates Alzheimer’s disease symptoms in APP/PS1 transgenic mice via inhibition of the TLR4-MyD88-NF-κB signaling pathway-mediated inflammation
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