CNS inflammation and neurodegeneration

Chitnis, Tanuja; Weiner, Howard L.

doi:10.1172/jci90609

Cited by 384 publications

(278 citation statements)

References 175 publications

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“…; Kim et al . ; Chitnis and Weiner ; Labzin et al . ; Fehily and Fitzgerald ; Mizuma and Yenari ; Neal and Richardson ; Franklin et al .…”

Section: Concluding Remarks and Perspectivesmentioning

confidence: 99%

“…The disorders considered in the present review are caused by different etiologic factors and display a variety of symptoms that could hardly be reconducted to a unifying pattern. However, regardless of the origin of these diseases, the involvement of processes which share aspects reasonably attributable to inflammation is detectable in their underlying pathogenic mechanisms (Giovannoni et al 2007;Wilcock and Griffin 2013;King et al 2014;Ochoa-Cortes et al 2016;Hamlett et al 2018;Stark et al 2016;Chitnis and Weiner 2017;Labzin et al 2018;Fehily and Fitzgerald 2017;Mizuma and Yenari 2017;Neal and Richardson 2017;Franklin et al 2017;Prata et al 2017;Santos and Ferreira 2017;Joshi and Singh 2017;Thelin et al 2017a;Majd et al 2017;Zhang et al 2017;Zolezzi and Inestrosa 2017). This consideration has also been the object of a recent valuable review (Skaper et al 2018).…”

Section: Concluding Remarks and Perspectivesmentioning

confidence: 99%

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The S100B story: from biomarker to active factor in neural injury

Michetti

D’Ambrosi

Toesca

et al. 2018

Journal of Neurochemistry

268

238

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S100B is a Ca -binding protein mainly concentrated in astrocytes. Its levels in biological fluids (cerebrospinal fluid, peripheral and cord blood, urine, saliva, amniotic fluid) are recognized as a reliable biomarker of active neural distress. Although the wide spectrum of diseases in which the protein is involved (acute brain injury, neurodegenerative diseases, congenital/perinatal disorders, psychiatric disorders) reduces its specificity, its levels remain an important aid in monitoring the trend of the disorder. Mounting evidence now points to S100B as a Damage-Associated Molecular Pattern molecule which, when released at high concentration, through its Receptor for Advanced Glycation Endproducts, triggers tissue reaction to damage in a series of different neural disorders. This review addresses this novel scenario, presenting data indicating that S100B levels and/or distribution in the nervous tissue of patients and/or experimental models of different neural disorders, for which the protein is used as a biomarker, are directly related to the progress of the disease: acute brain injury (ischemic/hemorrhagic stroke, traumatic injury), neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis), congenital/perinatal disorders (Down syndrome, spinocerebellar ataxia-1), psychiatric disorders (schizophrenia, mood disorders), inflammatory bowel disease. In many cases, over-expression/administration of the protein induces worsening of the disease, whereas its deletion/inactivation produces amelioration. This review points out that the pivotal role of the protein resulting from these data, opens the perspective that S100B may be regarded as a therapeutic target for these different diseases, which appear to share some common features reasonably attributable to neuroinflammation, regardless their origin.

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“…; Kim et al . ; Chitnis and Weiner ; Labzin et al . ; Fehily and Fitzgerald ; Mizuma and Yenari ; Neal and Richardson ; Franklin et al .…”

Section: Concluding Remarks and Perspectivesmentioning

confidence: 99%

Section: Concluding Remarks and Perspectivesmentioning

confidence: 99%

The S100B story: from biomarker to active factor in neural injury

Michetti

D’Ambrosi

Toesca

et al. 2018

Journal of Neurochemistry

268

238

View full text Add to dashboard Cite

show abstract

“…Chronic activation of inflammatory mechanisms associated with aging is a shared feature of many neurodegenerative diseases, such as Parkinson's, Huntington's, and Alzheimer's disease (AD) (1)(2)(3). The presence of amyloidb (Ab) peptides induces the production and release of proinflammatory cytokines by neurons and astrocytes (4,5) which shift microglia from a surveillance/maintenance mode into active phagocytosis (6)(7)(8).…”

mentioning

confidence: 99%

“…Microglia are the immunocompetent cells in the CNS and are also involved in removal of damaged neurons and dysfunctional synapses in both normal and pathologic nervous tissue (9)(10)(11)(12)(13)(14). Activated microglia perform phagocytosis of Ab deposits, contributing to Ab clearance and removal of cytotoxic debris from the brain (1,6,12,(14)(15)(16). However, sustained microglial activation may increase Ab deposition, intensify neurodegeneration (2,3), and phagocytose healthy neurons (10,11,14,17,18).…”

mentioning

confidence: 99%

Microglial distribution, branching, and clearance activity in aged rat hippocampus are affected by astrocyte meshwork integrity: evidence of a novel cell‐cell interglial interaction

et al. 2018

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Aging and neurodegenerative diseases share a condition of neuroinflammation entailing the production of endogenous cell debris in the CNS that must be removed by microglia (i.e., resident macrophages), to restore tissue homeostasis. In this context, extension of microglial cell branches toward cell debris underlies the mechanisms of microglial migration and phagocytosis. Amoeboid morphology and the consequent loss of microglial branch functionality characterizes dysregulated microglia. Microglial migration is assisted by another glial population, the astroglia, which forms a dense meshwork of cytoplasmic projections. Amoeboid microglia and disrupted astrocyte meshwork are consistent traits in aged CNS. In this study, we assessed a possible correlation between microglia and astroglia morphology in rat models of chronic neuroinflammation and aging, by 3‐dimensional confocal analysis implemented with particle analysis. Our findings suggest that a microglia‐astroglia interaction occurs in rat hippocampus via cell‐cell contacts, mediating microglial cell branching in the presence of inflammation. In aged rats, the impairment of such an interaction correlates with altered distribution, morphology, and inefficient clearance by microglia. These data support the idea that generally accepted functional boundaries between microglia and astrocytes should be re‐evaluated to better understand how their functions overlap and interact.—Lana, D., Ugolini, F., Wenk, G. L., Giovannini, M. G., Zecchi‐Orlandini, S., Nosi, D. Microglial distribution, branching, and clearance activity in aged rat hippocampus are affected by astrocyte meshwork integrity: evidence of a novel cell‐cell interglial interaction. FASEB J. 33, 4007–4020 (2019). http://www.fasebj.org

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“…Activation of microglial cells marks neuroinflammation, an early sign of neuronal dysfunction 38,39 . We have previously shown that microglia stained with antibodies to the Iba inflammatory marker accumulate in the hippocampus of Npc1 nmf164 mice 10 .…”

Section: Assessment Of Chronic Tcf-treatment In Cerebellar and Hippocmentioning

confidence: 99%