Gallic acid ameliorates LPS-induced memory decline by modulating NF-κB, TNF-α, and Caspase 3 gene expression and attenuating oxidative stress and neuronal loss in the rat hippocampus DOI
Maryam Dastan, Ziba Rajaei, Mohammadreza Sharifi

et al.

Metabolic Brain Disease, Journal Year: 2024, Volume and Issue: 40(1)

Published: Nov. 18, 2024

Language: Английский

Current perspectives on microglia-neuron communication in the central nervous system: Direct and indirect modes of interaction DOI Creative Commons
Yue Hu, Weiwei Tao

Journal of Advanced Research, Journal Year: 2024, Volume and Issue: 66, P. 251 - 265

Published: Jan. 7, 2024

The incessant communication that takes place between microglia and neurons is essential the development, maintenance, pathogenesis of central nervous system (CNS). As mobile phagocytic cells, serve a critical role in surveilling scavenging neuronal milieu to uphold homeostasis.

Language: Английский

Citations

15

Role of AIM2 and cGAS-STING signaling in high fat high carbohydrate diet-induced gut dysbiosis associated neurodegeneration DOI
Keya Mallick, Sk Ramiz Islam, V. Krishna

et al.

Life Sciences, Journal Year: 2025, Volume and Issue: 363, P. 123392 - 123392

Published: Jan. 11, 2025

Language: Английский

Citations

1

Indole lactic acid derived from Akkermansia muciniphila activates the aryl hydrocarbon receptor to inhibit ferroptosis in ischemic stroke DOI
Jiahan Wang, Yongzheng Peng, Yarui Liu

et al.

Free Radical Biology and Medicine, Journal Year: 2025, Volume and Issue: unknown

Published: April 1, 2025

Language: Английский

Citations

0

Limosilactobacillus reuteri DSM17938 Attenuates Neuroinflammatory Responses After Spinal Cord Injury by Modulating Tryptophan Metabolism DOI Creative Commons

Qiuyu Cen,

Yanru Cui,

Jing Feng

et al.

Probiotics and Antimicrobial Proteins, Journal Year: 2025, Volume and Issue: unknown

Published: April 26, 2025

Spinal cord injury (SCI) disrupts gut flora and exacerbates neuroinflammation. Evidence supports the important role of intestinal microbiota in SCI. This study evaluated neuroprotective effect Limosilactobacillus reuteri (L. reuteri) DSM 17938 on SCI its potential anti-inflammatory mechanism. The was disorganised following SCI, with a significant decrease abundance probiotic bacteria such as L. reuteri. DSM17938 treatment improved spinal pathology enhanced locomotor functional recovery SCI-model rats. Moreover, it modulated tryptophan metabolism by promoting indole-3-carboxaldehyde production. In addition, inhibits polarization M1 microglia reduces production IL-6, IL-1 β, TNF-α to alleviate It also activates aryl hydrocarbon receptor (AhR) signalling via upregulating AhR CYP1A1 expression, tight junction protein synthesis. summary, promotes modulating activate barrier repair attenuate microglial activation neuroinflammation, suggesting strategy for clinical adjuvant treatment.

Language: Английский

Citations

0

Therapeutic application of nicotinamide: As a potential target for inhibiting fibrotic scar formation following spinal cord injury DOI Creative Commons
Ce Zhang, Qiang Shao, Ying Zhang

et al.

CNS Neuroscience & Therapeutics, Journal Year: 2024, Volume and Issue: 30(7)

Published: July 1, 2024

We aimed to confirm the inhibitory effect of nicotinamide on fibrotic scar formation following spinal cord injury in mice using functional metabolomics.

Language: Английский

Citations

2

Necrotizing Enterocolitis and Neurodevelopmental Impairments: Microbiome, Gut, and Brain Entanglements DOI Creative Commons
Cuilee Sha, Zhaosheng Jin,

Stella Y. Ku

et al.

Biomolecules, Journal Year: 2024, Volume and Issue: 14(10), P. 1254 - 1254

Published: Oct. 4, 2024

There is significant communication and interdependence among the gut, microbiome, brain during development. Diseases, such as necrotizing enterocolitis (NEC), highlight how injury to immature gastrointestinal tract leads long-term neurological consequences, due vulnerabilities of in early stages life. A better understanding developing gut–microbiota–brain axis needed both prevent treat devastating consequences these disease processes. The a bidirectional pathway that includes metabolic, nervous, endocrine, immune components. In this review, we discuss gut development, microbiome colonization maturation, interactions influence neurodevelopment context NEC. We describe components gut–brain an integral member relationship. Finally, explore derangements within affect normal development function other systems neurodevelopmental for patients.

Language: Английский

Citations

2

Brain organoid models for studying the function of iPSC-derived microglia in neurodegeneration and brain tumours DOI Creative Commons
Angélica María Sabogal-Guáqueta,

Teresa Mitchell-Garcia,

Jasmijn Hunneman

et al.

Neurobiology of Disease, Journal Year: 2024, Volume and Issue: unknown, P. 106742 - 106742

Published: Nov. 1, 2024

Language: Английский

Citations

2

The relationship between acrylamide and neurodegenerative diseases: gut microbiota as a new intermediate cue DOI
Xinrui Xu, Siyu Wei,

Mengyi Lin

et al.

Critical Reviews in Food Science and Nutrition, Journal Year: 2024, Volume and Issue: unknown, P. 1 - 13

Published: Dec. 13, 2024

Acrylamide (AA), a compound formed during the thermal processing of high-carbohydrate foods, has been implicated in onset and progression neurodegenerative diseases. An increasing number reports support that gut microbiota plays significant role brain function diseases, suggesting it may act as mediator between AA exposure development Available studies have shown intake affects composition integrity intestinal barrier, both which are often thought to be associated with pathogenesis given numerous evidences linking brain. Based on current understanding, this paper discusses induces diseases by disrupting structure barrier. Furthermore, explores interaction probiotics exposure, well potential for polysaccharides polyphenols improve microenvironment, provides novel perspectives modulating caused through diet.

Language: Английский

Citations

2

Should We Consider Neurodegeneration by Itself or in a Triangulation with Neuroinflammation and Demyelination? The Example of Multiple Sclerosis and Beyond DOI Open Access
Océane Perdaens, Vincent Van Pesch

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(23), P. 12637 - 12637

Published: Nov. 25, 2024

Neurodegeneration is preeminent in many neurological diseases, and still a major burden we fail to manage patient's care. Its pathogenesis complicated, intricate, far from being completely understood. Taking multiple sclerosis as an example, propose that neurodegeneration neither cause nor consequence by itself. Mitochondrial dysfunction, leading energy deficiency ion imbalance, plays key role neurodegeneration, partly caused the oxidative stress generated microglia astrocytes. Nodal paranodal disruption, with or without myelin alteration, further involved. Myelin loss exposes axons directly inflammatory environment. Moreover, oligodendrocytes provide singular metabolic trophic support axons, but do not emerge unscathed pathological events, primary defects cell apoptosis secondary neuroinflammation axonal damage. Hereby, failure might be overlooked contributor neurodegeneration. Thus, complex interplay between neuroinflammation, demyelination, wherein each primarily secondarily involved, offer more comprehensive understanding of help establishing novel therapeutic strategies for diseases beyond.

Language: Английский

Citations

1

Indole‐3‐Carboxaldehyde Inhibits Inflammatory Response and Lipid Accumulation in Macrophages Through the miR‐1271‐5p/HDAC9 Pathway DOI Creative Commons
Wei Luo,

Jun Meng,

Xiao‐Hua Yu

et al.

Journal of Cellular and Molecular Medicine, Journal Year: 2024, Volume and Issue: 28(24)

Published: Dec. 1, 2024

ABSTRACT Indole‐3‐carboxaldehyde (ICA), a microbiota‐derived tryptophan metabolite, has been reported to protect against atherosclerosis. However, the molecular mechanisms for its atheroprotective effect remain largely unknown. This study aimed explore influence of ICA on lipid accumulation and inflammatory response in THP‐1 macrophage‐derived foam cells. Our results showed that administration upregulated expression miR‐1271‐5p, ATP binding cassette transporter A1 (ABCA1) ABCG1, downregulated histone deacetylase 9 (HDAC9) inhibited macrophage accumulation. treatment also facilitated polarisation M2 phenotype alleviated response, as evidenced by decreased IL‐6 levels increased IL‐10 levels. HDAC9 was identified direct target miR‐1271‐5p. overexpression or miR‐1271‐5p knockdown ABCA1 ABCG1 well response. Taken together, these suggest can suppress mitigate macrophages activating miR‐1271‐5p/HDAC9 signalling cascade, thereby providing new explanations how reduces

Language: Английский

Citations

1