Journal of Neuroinflammation
Papers 3161
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#1Gonzalo Ruiz-Pérez (Universidad Francisco de Vitoria)H-Index: 4
#2Samuel Ruiz de Martı N Esteban (Universidad Francisco de Vitoria)H-Index: 2
Last. María Posada-Ayala (Universidad Francisco de Vitoria)
view all 14 authors...
BACKGROUND The complex pathophysiology of Alzheimer's disease (AD) hampers the development of effective treatments. Attempts to prevent neurodegeneration in AD have failed so far, highlighting the need for further clarification of the underlying cellular and molecular mechanisms. Neuroinflammation seems to play a crucial role in disease progression, although its specific contribution to AD pathogenesis remains elusive. We have previously shown that the modulation of the endocannabinoid system (E...
#1Latarsha Porcher (USC: University of South Carolina)H-Index: 1
#2Sophie Bruckmeier (UMB: University of Maryland, Baltimore)
Last. Michy P. Kelly (USC: University of South Carolina)H-Index: 19
view all 8 authors...
Background null Despite widespread acceptance that neuroinflammation contributes to age-related cognitive decline, studies comparing protein expression of cytokines in the young versus old brains are surprisingly limited in terms of the number of cytokines and brain regions studied. Complicating matters, discrepancies abound-particularly for interleukin 6 (IL-6)-possibly due to differences in sex, species/strain, and/or the brain regions studied. null Methods null As such, we clarified how cytok...
#1Electra Brunialti (University of Milan)H-Index: 6
#2Alessandro Villa (University of Milan)H-Index: 28
Last. Paolo Ciana (University of Milan)H-Index: 38
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BACKGROUND Homozygotic mutations in the GBA gene cause Gaucher's disease; moreover, both patients and heterozygotic carriers have been associated with 20- to 30-fold increased risk of developing Parkinson's disease. In homozygosis, these mutations impair the activity of β-glucocerebrosidase, the enzyme encoded by GBA, and generate a lysosomal disorder in macrophages, which changes morphology towards an engorged phenotype, considered the hallmark of Gaucher's disease. Notwithstanding the key role...
#1Peipei Zhang (University of Freiburg)H-Index: 4
#2Anja Schlecht (University of Freiburg)H-Index: 5
Last. Carmen Härdtner (University of Freiburg)H-Index: 5
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Background null Microglia cells represent the resident innate immune cells of the retina and are important for retinal development and tissue homeostasis. However, dysfunctional microglia can have a negative impact on the structural and functional integrity of the retina under native and pathological conditions. null Methods null In this study, we examined interferon-regulatory factor 8 (Irf8)-deficient mice to determine the transcriptional profile, morphology, and temporospatial distribution of...
#1Keith E. Campagno (UPenn: University of Pennsylvania)H-Index: 5
#2Wennan Lu (UPenn: University of Pennsylvania)H-Index: 21
Last. Claire H. Mitchell (UPenn: University of Pennsylvania)H-Index: 40
view all 10 authors...
BACKGROUND The identification of endogenous signals that lead to microglial activation is a key step in understanding neuroinflammatory cascades. As ATP release accompanies mechanical strain to neural tissue, and as the P2X7 receptor for ATP is expressed on microglial cells, we examined the morphological and molecular consequences of P2X7 receptor stimulation in vivo and in vitro and investigated the contribution of the P2X7 receptor in a model of increased intraocular pressure (IOP). METHODS In...
#1Nahdia S. Jones (Georgetown University)H-Index: 2
#2Katarina Q. Watson (Georgetown University)H-Index: 1
Last. G. William Rebeck (Georgetown University)H-Index: 62
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Background null APOE4 is the strongest genetic risk factor for Alzheimer's disease (AD), and obesity is a strong environmental risk factor for AD. These factors result in multiple central nervous system (CNS) disturbances and significantly increase chances of AD. Since over 20% of the US population carry the APOE4 allele and over 40% are obese, it is important to understand how these risk factors interact to affect neurons and glia in the CNS. null Methods null We fed male and female APOE3 and A...
#1Susana S. CorreiaH-Index: 1
#2Guang LiuH-Index: 4
Last. Andrew CarvalhoH-Index: 2
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BACKGROUND Inflammation in the central nervous system (CNS) is observed in many neurological disorders. Nitric oxide-soluble guanylate cyclase-cyclic guanosine monophosphate (NO-sGC-cGMP) signaling plays an essential role in modulating neuroinflammation. CYR119 is a CNS-penetrant sGC stimulator that amplifies endogenous NO-sGC-cGMP signaling. We evaluated target engagement and the effects of CYR119 on markers of neuroinflammation in vitro in mouse microglial cells and in vivo in quinolinic acid ...
#1Lilan Li (Nantong University)
#2Yu Li (HUST: Huazhong University of Science and Technology)
Last. Ting Yang (Nantong University)
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BACKGROUND Two activation states of reactive astrocytes termed A1 and A2 subtypes emerge at the lesion sites following spinal cord injury (SCI). A1 astrocytes are known to be neurotoxic that participate in neuropathogenesis, whereas A2 astrocytes have been assigned the neuroprotective activity. Heat shock transcription factor 1 (HSF1) plays roles in protecting cells from stress-induced apoptosis and in controlling inflammatory activation. It is unknown whether HSF1 is involved in suppressing the...
Neuromyelitis optica (NMO) is a chronic inflammatory autoimmune disease of the central nervous system (CNS) characterized by acute optic neuritis (ON) and transverse myelitis (TM). NMO is caused by a pathogenic serum IgG antibody against the water channel aquoporin 4 (AQP4) in the majority of patients. AQP4-antibody (AQP4-ab) presence is highly specific, and differentiates NMO from multiple sclerosis. It binds to AQP4 channels on astrocytes, triggering activation of the classical complement casc...
#1Hanhai Zeng (ZJU: Zhejiang University)H-Index: 3
#2Huaijun Chen (ZJU: Zhejiang University)H-Index: 1
Last. Shenglong Cao (ZJU: Zhejiang University)H-Index: 9
view all 13 authors...
Background null Neuroinflammation and oxidative stress plays an important role in the pathogenesis of early brain injury (EBI) after subarachnoid hemorrhage (SAH). This study is the first to show that activation of autophagy protein nuclear receptor binding factor 2 (NRBF2) could reduce endoplasmic reticulum stress (ERS)-associated inflammation and oxidative stress after SAH. null Methods null Male C57BL/6J mice were subjected to endovascular perforation to establish a model of SAH. NRBF2 overex...
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