Neuroinflammation pathways: a general review

Shabab, Tara; Khanabdali, Ramin; Moghadamtousi, Soheil Zorofchian; Kadir, Habsah Abdul; Mohan, Gokula

doi:10.1080/00207454.2016.1212854

Cited by 457 publications

(369 citation statements)

References 49 publications

Supporting

Mentioning

323

Contrasting

Unclassified

Order By: Relevance

“…On the surface of microglial cells, TLR4 activates several signal pathways, which leads to NF-κB activation in the end [29, 48]. In an inactive form, NF-κB bound to I-κB proteins, an interaction that regulates its activity in the cytoplasm.…”

Section: Discussionmentioning

confidence: 99%

Wogonin prevents TLR4-NF-κB-medicated neuro-inflammation and improves retinal ganglion cells survival in retina after optic nerve crush

Yang

et al. 2016

Oncotarget

View full text Add to dashboard Cite

Chronic neuro-inflammation is involved in the death of retinal ganglion cells (RGCs) in glaucoma. The aim of this study is to determine whether wogonin can suppress inflammatory responses and rescue RGCs death after optic nerve crush (ONC), an ideal animal model of glaucoma. Wogonin was administered intraperitoneally 10 min after establishment of ONC model. In this study, wogonin treatment reduced RGCs loss and inhibited RGCs apoptosis demonstrated by the increased Brn3a labeling RGCs at day 14 and the decreased cleaved caspase-3 expression at day 7 after ONC, respectively. In ONC model, number of GFAP-positive glial cells and iba1-positive microglial cells were increased, combined of the elevated level of pro-inflammatory cytokines released in retina at day 7. However, most of these responses were inhibited after wogonin treatment. The level of TLR4 expression, NF-κB-P65 nucleus location and NF-κB-P65 phosphorylation were increased in retina at day 1 after ONC, which was significantly reduced after wogonin treatment. These results demonstrated that wogonin protected RGCs survival and suppressed neuro-inflammation in retina after ONC by inhibiting TLR4-NF-κB pathways. We conclude that wogonin could be a possible strategy for the treatment of glaucoma.

show abstract

Section: Discussionmentioning

confidence: 99%

Wogonin prevents TLR4-NF-κB-medicated neuro-inflammation and improves retinal ganglion cells survival in retina after optic nerve crush

Yang

et al. 2016

Oncotarget

View full text Add to dashboard Cite

show abstract

“…Moreover, neuroinflammation induced by lipopolysaccharide injection or traumatic brain injury exacerbated Tau pathology in transgenic mouse models of tauopathies [213-215]. Interestingly, numerous Tau kinases can be activated through inflammatory pathways such as JNK, ERK, Akt, or p38 [216]. These data suggest that neuroinflammation could contribute to, and maybe initiate, Tau pathology [217, 218].…”

Section: Brain Insulin Resistance In Ad and Tauopathies: Cause Or Conmentioning

confidence: 99%

Mutual Relationship between Tau and Central Insulin Signalling: Consequences for AD and Tauopathies?

et al. 2018

View full text Add to dashboard Cite

Alzheimer disease (AD) is a progressive neurodegenerative disorder mainly characterized by cognitive deficits and neuropathological changes such as Tau lesions and amyloid plaques, but also associated with non-cognitive symptomatology. Metabolic and neuroendocrine abnormalities, such as alterations in body weight, brain insulin impairments, and lower brain glucose metabolism, which often precede clinical diagnosis, have been extensively reported in AD patients. However, the origin of these symptoms and their relation to pathology and cognitive impairments remain misunderstood. Insulin is a hormone involved in the control of energy homeostasis both peripherally and centrally, and insulin-resistant state has been linked to increased risk of dementia. It is now well established that insulin resistance can exacerbate Tau lesions, mainly by disrupting the balance between Tau kinases and phosphatases. On the other hand, the emerging literature indicates that Tau protein can also modulate insulin signalling in the brain, thus creating a detrimental vicious circle. The following review will highlight our current understanding of the role of insulin in the brain and its relation to Tau protein in the context of AD and tauopathies. Considering that insulin signalling is prone to be pharmacologically targeted at multiple levels, it constitutes an appealing approach to improve both insulin brain sensitivity and mitigate brain pathology with expected positive outcome in terms of cognition.

show abstract

“…Although there is a huge variety in central nervous system-associated injuries or symptoms, the mechanisms of neurodegeneration are quite similar. Among possible mechanisms considered essential in the contribution or the maintenance of neuroprotection, the most promising ones to serve as targets for therapeutic interventions are inflammation, apoptosis, mitochondrial dysfunction, protein aggregation and excitotoxicity [13]. …”

Section: Neuroprotectionmentioning

confidence: 99%

The Molecular Pathway of Argon-Mediated Neuroprotection

Ulbrich

Goebel

2016

IJMS

View full text Add to dashboard Cite

The noble gas argon has attracted increasing attention in recent years, especially because of its neuroprotective properties. In a variety of models, ranging from oxygen-glucose deprivation in cell culture to complex models of mid-cerebral artery occlusion, subarachnoid hemorrhage or retinal ischemia-reperfusion injury in animals, argon administration after individual injury demonstrated favorable effects, particularly increased cell survival and even improved neuronal function. As an inert molecule, argon did not show signs of adverse effects in the in vitro and in vivo model used, while being comparably cheap and easy to apply. However, the molecular mechanism by which argon is able to exert its protective and beneficial characteristics remains unclear. Although there are many pieces missing to complete the signaling pathway throughout the cell, it is the aim of this review to summarize the known parts of the molecular pathways and to combine them to provide a clear insight into the cellular pathway, starting with the receptors that may be involved in mediating argons effects and ending with the translational response.

show abstract

Neuroinflammation pathways: a general review

Cited by 457 publications

References 49 publications

Wogonin prevents TLR4-NF-κB-medicated neuro-inflammation and improves retinal ganglion cells survival in retina after optic nerve crush

Wogonin prevents TLR4-NF-κB-medicated neuro-inflammation and improves retinal ganglion cells survival in retina after optic nerve crush

Mutual Relationship between Tau and Central Insulin Signalling: Consequences for AD and Tauopathies?

The Molecular Pathway of Argon-Mediated Neuroprotection

Contact Info

Product

Resources

About