Modulation of Alzheimer’s disease brain pathology in mice by gut bacterial depletion: the role of IL-17a

Hao, Wenlin; Luo, Qinghua; Tomic, Inge; Quan, Wenqiang; Hartmann, Tobias; Menger, Michael D.; Fassbender, Klaus; Liu, Yang

doi:10.1080/19490976.2024.2363014

Cited by 3 publications

(1 citation statement)

References 86 publications

(137 reference statements)

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“…Furthermore, IL-17A has been shown to induce neural damage directly when administered to primary hippocampal neurons, and its inhibition via neutralizing antibodies can ameliorate Aβ-induced neurotoxicity and cognitive decline by downregulating the TRAF6/NF-κB pathway 66 . Additionally, the depletion of gut bacteria, which reduces IL-17A-expressing T cells, has been found to lower cerebral Aβ levels and inhibit inflammatory activation in the brain, highlighting the gut-brain axis's role in AD pathophysiology 68 .…”

Section: Validation On Identified Biomarkersmentioning

confidence: 99%

mosGraphGPT: a foundation model for multi-omic signaling graphs using generative AI

Zhang,

Huang,

Chen

et al. 2024

Preprint

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Generative pretrained models represent a significant advancement in natural language processing and computer vision, which can generate coherent and contextually relevant content based on the pre-training on large general datasets and fine-tune for specific tasks. Building foundation models using large scale omic data is promising to decode and understand the complex signaling language patterns within cells. Different from existing foundation models of omic data, we build a foundation model,mosGraphGPT, for multi-omic signaling (mos) graphs, in which the multi-omic data was integrated and interpreted using a multi-level signaling graph. The model was pretrained using multi-omic data of cancers in The Cancer Genome Atlas (TCGA), and fine-turned for multi-omic data of Alzheimer’s Disease (AD). The experimental evaluation results showed that the model can not only improve the disease classification accuracy, but also is interpretable by uncovering disease targets and signaling interactions. And the model code are uploaded via GitHub with link:https://github.com/mosGraph/mosGraphGPT

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Section: Validation On Identified Biomarkersmentioning

confidence: 99%

mosGraphGPT: a foundation model for multi-omic signaling graphs using generative AI

Zhang,

Huang,

Chen

et al. 2024

Preprint

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A review of the roles of pathogens in Alzheimer’s disease

Zhao,

Wang,

Shen

et al. 2024

Front. Neurosci.

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Alzheimer’s disease (AD) is one of the leading causes of dementia and is characterized by memory loss, mental and behavioral abnormalities, and impaired ability to perform daily activities. Even as a global disease that threatens human health, effective treatments to slow the progression of AD have not been found, despite intensive research and significant investment. In recent years, the role of infections in the etiology of AD has sparked intense debate. Pathogens invade the central nervous system through a damaged blood–brain barrier or nerve trunk and disrupt the neuronal structure and function as well as homeostasis of the brain microenvironment through a series of molecular biological events. In this review, we summarize the various pathogens involved in AD pathology, discuss potential interactions between pathogens and AD, and provide an overview of the promising future of anti-pathogenic therapies for AD.

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Novelties on Neuroinflammation in Alzheimer’s Disease–Focus on Gut and Oral Microbiota Involvement

Popescu,

Munteanu,

Anghelescu

et al. 2024

IJMS

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Recent studies underscore the role of gut and oral microbiota in influencing neuroinflammation through the microbiota–gut–brain axis, including in Alzheimer’s disease (AD). This review aims to provide a comprehensive synthesis of recent findings on the involvement of gut and oral microbiota in the neuroinflammatory processes associated with AD, emphasizing novel insights and therapeutic implications. This review reveals that dysbiosis in AD patients’ gut and oral microbiota is linked to heightened peripheral and central inflammatory responses. Specific bacterial taxa, such as Bacteroides and Firmicutes in the gut, as well as Porphyromonas gingivalis in the oral cavity, are notably altered in AD, leading to significant changes in microglial activation and cytokine production. Gut microbiota alterations are associated with increased intestinal permeability, facilitating the translocation of endotoxins like lipopolysaccharides (LPS) into the bloodstream and exacerbating neuroinflammation by activating the brain’s toll-like receptor 4 (TLR4) pathways. Furthermore, microbiota-derived metabolites, including short-chain fatty acids (SCFAs) and amyloid peptides, can cross the blood-brain barrier and modulate neuroinflammatory responses. While microbial amyloids may contribute to amyloid-beta aggregation in the brain, certain SCFAs like butyrate exhibit anti-inflammatory properties, suggesting a potential therapeutic avenue to mitigate neuroinflammation. This review not only highlights the critical role of microbiota in AD pathology but also offers a ray of hope by suggesting that modulating gut and oral microbiota could represent a novel therapeutic strategy for reducing neuroinflammation and slowing disease progression.

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Modulation of Alzheimer’s disease brain pathology in mice by gut bacterial depletion: the role of IL-17a

Cited by 3 publications

References 86 publications

mosGraphGPT: a foundation model for multi-omic signaling graphs using generative AI

mosGraphGPT: a foundation model for multi-omic signaling graphs using generative AI

A review of the roles of pathogens in Alzheimer’s disease

Novelties on Neuroinflammation in Alzheimer’s Disease–Focus on Gut and Oral Microbiota Involvement

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