Dysregulation of the Gut Microbiota Contributes to Sevoflurane-Induced Cognitive Dysfunction in Aged Mice by Activating the NLRP3 Inflammasome DOI
Shanshan Han,

Ruxi Bian,

Yuxuan Chen

et al.

Molecular Neurobiology, Journal Year: 2024, Volume and Issue: 61(12), P. 10500 - 10516

Published: May 14, 2024

Language: Английский

Water-extracted Lonicera japonica polysaccharide attenuates allergic rhinitis by regulating NLRP3-IL-17 signaling axis DOI
Xinyu Bai, Ping Liu,

Hengyan Shen

et al.

Carbohydrate Polymers, Journal Year: 2022, Volume and Issue: 297, P. 120053 - 120053

Published: Sept. 3, 2022

Language: Английский

Citations

40

Myelin in Alzheimer’s disease: culprit or bystander? DOI Creative Commons
Michel Maître, Hélène Jeltsch‐David, Nwife Getrude Okechukwu

et al.

Acta Neuropathologica Communications, Journal Year: 2023, Volume and Issue: 11(1)

Published: March 31, 2023

Alzheimer's disease (AD) is a neurodegenerative disorder with neuronal and synaptic losses due to the accumulation of toxic amyloid β (Αβ) peptide oligomers, plaques, tangles containing tau (tubulin-associated unit) protein. While familial AD caused by specific mutations, sporadic more common appears result from complex chronic brain neuroinflammation mitochondriopathies, inducing free radicals' accumulation. In aged brain, mutations in DNA several unfolded proteins participate amyloidosis response effect on myelin sheath axons, leading cognitive deficits dementia. Αβ peptides are most frequent form oligomers. Accumulations misfolded during years alters different metabolic mechanisms, induce inflammatory immune responses consequences cells. Myelin composition architecture may appear be an early target for activity Aβ others hydrophobic proteins. this work, we describe possible role alterations genesis onset symptomatology. We propose that some pathophysiological clinical forms arise structural disorders processes myelination/demyelination regions where non-functional important. these forms, primacy deleterious would matter questioning initiating neuropathology primarily fact dysmyelination.

Language: Английский

Citations

38

NLRP3 Inflammasome’s Activation in Acute and Chronic Brain Diseases—An Update on Pathogenetic Mechanisms and Therapeutic Perspectives with Respect to Other Inflammasomes DOI Creative Commons
Anna Chiarini, Li Gui, C Viviani

et al.

Biomedicines, Journal Year: 2023, Volume and Issue: 11(4), P. 999 - 999

Published: March 23, 2023

Increasingly prevalent acute and chronic human brain diseases are scourges for the elderly. Besides lack of therapies, these ailments share a neuroinflammation that is triggered/sustained by different innate immunity-related protein oligomers called inflammasomes. Relevant players such as microglia/monocytes typically exhibit strong NLRP3 inflammasome activation. Hence idea suppression might solve neurodegenerative ailments. Here we review recent Literature about this topic. First, update conditions mechanisms, including RNAs, extracellular vesicles/exosomes, endogenous compounds, ethnic/pharmacological agents/extracts regulating function. Second, pinpoint NLRP3-activating mechanisms known inhibition effects in (ischemia, stroke, hemorrhage), (Alzheimer’s disease, Parkinson’s Huntington’s MS, ALS), virus-induced (Zika, SARS-CoV-2, others) diseases. The available data show (i) disease-specific divergent activate (mainly animal) brains NLRP3; (ii) no evidence proves modifies (yet ad hoc trials ongoing); (iii) findings exclude concurrently activated other-than-NLRP3 inflammasomes functionally replace inhibited NLRP3. Finally, highlight among causes persistent therapies species difference problem disease models preference symptomatic over etiologic therapeutic approaches. Therefore, posit neural cell-based could drive etiological, pathogenetic, advances, NLRP3’s other inflammasomes’ regulation, while minimizing failure risks candidate drug trials.

Language: Английский

Citations

23

The contribution of age-related changes in the gut-brain axis to neurological disorders DOI Creative Commons
Romeesa Khan, Claudia M. Di Gesù, June‐Young Lee

et al.

Gut Microbes, Journal Year: 2024, Volume and Issue: 16(1)

Published: Jan. 18, 2024

Trillions of microbes live symbiotically in the host, specifically mucosal tissues such as gut. Recent advances metagenomics and metabolomics have revealed that gut microbiota plays a critical role regulation host immunity metabolism, communicating through bidirectional interactions microbiota-gut-brain axis (MGBA). The regulates both systemic contributes to neurodevelopment behaviors host. With aging, composition changes, emerging studies linked these shifts microbial populations age-related neurological diseases (NDs). Preclinical demonstrated microbiota-targeted therapies can improve behavioral outcomes by modulating microbial, metabolomic, immunological profiles. In this review, we discuss pathways brain-to-gut or gut-to-brain signaling summarize metabolites across lifespan disease. We highlight recent investigating 1) changes with aging; 2) how aging maternal microbiome affect offspring health; 3) contribution chronic (e.g., Parkinson's disease, Alzheimer's disease cerebral amyloidosis), acute brain injury, including ischemic stroke traumatic injury.

Language: Английский

Citations

15

Lactobacillus plantarum PS128 prevents cognitive dysfunction in Alzheimer’s disease mice by modulating propionic acid levels, glycogen synthase kinase 3 beta activity, and gliosis DOI Creative Commons

Hei-Jen Huang,

Jie-Ling Chen,

Jian-Fu Liao

et al.

BMC Complementary Medicine and Therapies, Journal Year: 2021, Volume and Issue: 21(1)

Published: Oct. 9, 2021

According to recent evidence, psychobiotics exert beneficial effects on central nervous system-related diseases, such as mental disorders. Lactobacillus plantarum PS128 (PS128), a novel psychobiotic strain, improves motor function, depression, and anxiety behaviors. However, the mechanisms of in Alzheimer's disease (AD) remain be explored.The goal current study was evaluate further elucidate its mechanism AD mice.PS128 (1010 colony-forming unit (CFU)/ml) administered via oral gavage (o.g.) 6-month-old male wild-type B6 3 × Tg-AD mice (harboring PS1M146V, APPswe TauP30IL transgenes) that received an intracerebroventricular injection streptozotocin (icv-STZ, mg/kg) or vehicle (saline) for 33 days. After serial behavioral tests, fecal short-chain fatty acid levels AD-related pathology were assessed these mice.Our findings show accelerated cognitive dysfunction associated with increasing glycogen synthase kinase beta (GSK3β) activity, tau protein phosphorylation at T231 site (pT231), amyloid-β (Aβ) deposition, precursor (AβPP), β-site AβPP-cleaving enzyme (BACE1), gliosis, propionic (PPA) cognition-related neuronal loss decreasing postsynaptic density 95 (PSD95) mice. supplementation effectively prevented damage induced by mice.Based experimental results, accelerates progression mice, primarily which mediated pathways. prevents regulating levels, gliosis Therefore, we suggest is potential strategy prevent and/or delay AD.

Language: Английский

Citations

44

Porphyromonas gingivalis-Induced Cognitive Impairment Is Associated With Gut Dysbiosis, Neuroinflammation, and Glymphatic Dysfunction DOI Creative Commons
Li Chi, Cheng Xiao, Lishan Lin

et al.

Frontiers in Cellular and Infection Microbiology, Journal Year: 2021, Volume and Issue: 11

Published: Dec. 1, 2021

Background Periodontal pathogen and gut microbiota are closely associated with the pathogenesis of Alzheimer’s disease (AD). Porphyromonas gingivalis (Pg), keystone periodontal pathogen, can induce cognitive impairment. The has a connection communication brain, which is an important aspect gut–brain axis (GBA). In present study, we investigate whether Pg induces impairment through disturbing GBA. Methods this was orally administered to mice, three times week for 1 month. effects administration on brain were evaluated behaviors, microbiota, immune cells, glymphatic pathway clearance, neuroinflammation. Results induced dysbiosis microbiota. α-diversity parameters did not show significant change after administration. β-diversity demonstrated that compositions different between Pg-administered control groups. At species level, group displayed lower abundance Parabacteroides gordonii Ruminococcus callidus than group, but higher Mucispirillum schaedleri . proportions lymphocytes in periphery myeloid cells infiltrating increased Pg-treated animals. addition, solute clearance efficiency system decreased. Neurons hippocampus cortex regions reduced mice treated Pg. Microglia, astrocytes, apoptotic increased. Furthermore, amyloid plaque appeared mice. Conclusions These findings indicate may play role dysbiosis, neuroinflammation, impairment, turn lead

Language: Английский

Citations

42

Targeting gut microbiota to alleviate neuroinflammation in Alzheimer’s disease DOI
Vu Thu Thuy Nguyen, Kristina Endres

Advanced Drug Delivery Reviews, Journal Year: 2022, Volume and Issue: 188, P. 114418 - 114418

Published: July 3, 2022

Language: Английский

Citations

36

Implications of gut and oral microbiota in neuroinflammatory responses in Alzheimer's disease DOI Creative Commons
Laura Bello-Corral,

Lisa Alves-Gomes,

Jesús Antonio Fernández-Fernández

et al.

Life Sciences, Journal Year: 2023, Volume and Issue: 333, P. 122132 - 122132

Published: Oct. 2, 2023

A diverse and stable microbiota promotes a healthy state, nevertheless, an imbalance in gut or oral bacterial composition, called dysbiosis, can cause gastrointestinal disorders, systemic inflammatory states oxidative stress, among others. Recently, dysbiosis has been linked to Alzheimer's disease (AD), which is considered the most common form of dementia public health priority due its high prevalence incidence. The aim this review highlight implications neuroinflammation characteristic AD pathology subsequent cognitive impairment. It systematic current literature obtained by searching PubMed, Web Science Scopus databases. intestinal patients leads increased permeability barrier activates immune cells central nervous system translocation microbiota-derived metabolites and/or bacteria into circulation leading neuronal loss, thus generating impairment AD. presence Porphyromonas gingivalis beta-amyloid peptide accumulation.

Language: Английский

Citations

22

Review of microbiota gut brain axis and innate immunity in inflammatory and infective diseases DOI Creative Commons
Chongshan Yuan, Yuhong He,

Kunyu Xie

et al.

Frontiers in Cellular and Infection Microbiology, Journal Year: 2023, Volume and Issue: 13

Published: Oct. 4, 2023

The microbiota gut brain (MGB) axis has been shown to play a significant role in the regulation of inflammatory and infective diseases. Exploring structure communication mode MGB is crucial for understanding its diseases, studying signaling pathways regulatory methods diseases also profound significance future clinical research. This article reviews composition, mechanism including Parkinson’s disease (PD), Alzheimer’s (AD), multiple sclerosis (MS), autism spectrum disorder (ASD), depression, psoriasis, irritable bowel syndrome (IBS), (IBD). In addition, our investigation delved into functions inflammasome, IFN-I, NF-κB, PARK7/DJ-1 innate immune pathway context Ultimately, we discussed efficacy various interventions, fecal transplantation (FMT), antibiotics, probiotics, prebiotics, synbiotics, postbiotics, management Understanding might make positive effects treatment

Language: Английский

Citations

21

Interactions between gut microbes and NLRP3 inflammasome in the gut-brain axis DOI
Yang Ding, Zixu Wang, Yaoxing Chen

et al.

Computational and Structural Biotechnology Journal, Journal Year: 2023, Volume and Issue: 21, P. 2215 - 2227

Published: Jan. 1, 2023

Language: Английский

Citations

20