Obesity-Induced Neuroinflammation: Beyond the Hypothalamus

Trends in Neurosciences, Journal Year: 2017, Volume and Issue: 40(4), P. 237 - 253

Published: March 18, 2017

Language: Английский

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Immune mediators in the brain and peripheral tissues in autism spectrum disorder

Nature reviews. Neuroscience, Journal Year: 2015, Volume and Issue: 16(8), P. 469 - 486

Published: July 20, 2015

Language: Английский

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Roles of inflammation, neurogenic inflammation, and neuroinflammation in pain

Journal of Anesthesia, Journal Year: 2018, Volume and Issue: 33(1), P. 131 - 139

Published: Nov. 17, 2018

Language: Английский

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Neuropeptide substance P and the immune response

Cellular and Molecular Life Sciences, Journal Year: 2016, Volume and Issue: 73(22), P. 4249 - 4264

Published: June 17, 2016

Language: Английский

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Role of TLR4 in the gut-brain axis in Parkinson’s disease: a translational study from men to mice

Gut, Journal Year: 2018, Volume and Issue: 68(5), P. 829 - 843

Published: Dec. 15, 2018

Objective Recent evidence suggesting an important role of gut-derived inflammation in brain disorders has opened up new directions to explore the possible gut-brain axis neurodegenerative diseases. Given prominence dysbiosis and colonic dysfunction patients with Parkinson’s disease (PD), we propose that toll-like receptor 4 (TLR4)-mediated intestinal could contribute central PD-related neurodegeneration. Design To test this hypothesis performed studies both human tissue a murine model PD. Inflammation, immune activation microbiota composition were measured samples from subjects PD healthy controls rotenone or vehicle-treated mice. further assess TLR4 signalling PD-induced neuroinflammation, used TLR4-knockout (KO) mice conjunction oral administration Results Patients have barrier disruption, enhanced markers microbial translocation higher pro-inflammatory gene profiles biopsy compared controls. In regard, found increased expression bacterial endotoxin-specific ligand TLR4, CD3+ T cells, cytokine biopsies, characterised by decrease abundance SCFA-producing bacteria Rotenone treatment TLR4-KO revealed less inflammation, motor dysfunction, neuroinflammation neurodegeneration, relative rotenone-treated wild-type animals despite presence dysbiotic Conclusion Taken together, these suggest TLR4-mediated plays and/or which may be one key factors leading neurodegeneration

Language: Английский

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Roles of microglia in brain development, tissue maintenance and repair

Brain, Journal Year: 2015, Volume and Issue: 138(5), P. 1138 - 1159

Published: March 29, 2015

The emerging roles of microglia are currently being investigated in the healthy and diseased brain with a growing interest their diverse functions. In recent years, it has been demonstrated that not only immunocentric, but also neurobiological can impact neural development maintenance neuronal cell function both pathological contexts. disease context, there is widespread consensus dynamic cells potential to contribute central nervous system damage repair. Indeed, number studies have found microenvironmental conditions selectively modify unique phenotypes One novel mechanism garnered involves regulation microglial by microRNAs, which therapeutic implications such as enhancing microglia-mediated suppression injury promoting repair following inflammatory injury. Furthermore, recently published articles identified molecular signatures myeloid cells, suggesting distinct population compared other lineage access under conditions. Thus, new opportunities exist help distinguish permit study functions health disease.

Language: Английский

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Estrogens, Neuroinflammation, and Neurodegeneration

Endocrine Reviews, Journal Year: 2016, Volume and Issue: 37(4), P. 372 - 402

Published: May 19, 2016

Inflammatory activation of microglia is a hallmark several disorders the central nervous system. In addition to protecting brain against inflammatory insults, are neuroprotective and play significant role in maintaining neuronal connectivity, but prolongation an status may limit beneficial functions these immune cells. The finding that estrogen receptors present monocyte-derived cells estrogens prevent control response raise question this sex steroid plays manifestation progression pathologies have clear difference prevalence, such as multiple sclerosis, Parkinson's disease, Alzheimer's disease. review aims provide critical current literature on actions involvement selected neurological disorders. This understanding highlights research area should be expanded identify appropriate replacement therapies slow diseases.

Language: Английский

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Does inflammation have a role in migraine?

Nature Reviews Neurology, Journal Year: 2019, Volume and Issue: 15(8), P. 483 - 490

Published: July 1, 2019

Language: Английский

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Factors controlling permeability of the blood–brain barrier

Cellular and Molecular Life Sciences, Journal Year: 2015, Volume and Issue: 73(1), P. 57 - 77

Published: Sept. 24, 2015

Language: Английский

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Chronic stress-induced gut dysfunction exacerbates Parkinson's disease phenotype and pathology in a rotenone-induced mouse model of Parkinson's disease

Neurobiology of Disease, Journal Year: 2018, Volume and Issue: 135, P. 104352 - 104352

Published: Dec. 20, 2018

Recent evidence provides support for involvement of the microbiota-gut-brain axis in Parkinson's disease (PD) pathogenesis. We propose that a pro-inflammatory intestinal milieu, due to hyper-permeability and/or microbial dysbiosis, initiates or exacerbates PD One factor can cause and dysbiosis is chronic stress which has been shown accelerate neuronal degeneration motor deficits Parkinsonism rodent models. hypothesized stress-induced barrier dysfunction lead milieu phenotype low-dose oral rotenone mice model. To test this hypothesis, received unpredictable restraint (RS) 12 weeks, during last six weeks also daily administration (10 mg/kg/day) orally. The initial RS caused significantly higher urinary cortisol, hyperpermeability, decreased abundance putative "anti-inflammatory" bacteria (Lactobacillus) compared non-stressed mice. Rotenone alone (i.e., without RS) disrupted colonic expression tight junction protein ZO-1, increased oxidative (N-tyrosine), myenteric plexus enteric glial cell GFAP α-synuclein (α-syn) levels colon controls. Restraint exacerbated these rotenone-induced changes. Specifically, potentiated effects including: 1) hyper-permeability, 2) disruption proteins (ZO-1, Occludin, Claudin1), 3) 4) inflammation cells (GFAP + glia cells), 5) α-syn, 6) relative fecal Akkermansia (mucin-degrading Gram-negative bacteria), 7) endotoxemia. In addition, promoted number brain reduced resting microglia dystrophic/phagocytic as well (FJ-C+) dying substantia nigra (SN), lipopolysaccharide (LPS) reactivity SN, dopamine (DA) DA metabolites (DOPAC, HVA) striatum control Our findings model stress-induced, gut-derived, via dysfunctional axis.

Language: Английский

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