Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5739063 | Progress in Neurobiology | 2017 | 27 Pages |
Abstract
The interaction between the nervous and immune systems during aging is an area of avid interest, but many aspects remain unclear. This is due, not only to the complexity of the aging process, but also to a mutual dependency and reciprocal causation of alterations and diseases between both the nervous and immune systems. Aging of the brain drives whole body systemic aging, including aging-related changes of the immune system. In turn, the immune system aging, particularly immunosenescence and T cell aging initiated by thymic involution that are sources of chronic inflammation in the elderly (termed inflammaging), potentially induces brain aging and memory loss in a reciprocal manner. Therefore, immunotherapeutics including modulation of inflammation, vaccination, cellular immune therapies and “protective autoimmunity” provide promising approaches to rejuvenate neuroinflammatory disorders and repair brain injury. In this review, we summarize recent discoveries linking the aging immune system with the development of neurodegeneration. Additionally, we discuss potential rejuvenation strategies, focusing aimed at targeting the aging immune system in an effort to prevent acute brain injury and chronic neurodegeneration during aging.
Keywords
ADCCNSAIDSLPSCOXMOGCTLMBPAPCsAβmTORTCrTCVNF-kBMIRi.p.APPEAEMCAONSCsNFTGM-CSFi.v.MBLNT-3GCsTregRRMsPOCDNOS2NLRP3SASPTREM2IL-βT-cell vaccineGnRHTGF-βCTFSC-terminal fragmentsAPP/PS1BDNFC/EBPROSamyloid-betaantibody dependent cell-mediated cytotoxicityAntigen presenting cellsexperimental autoimmune encephalomyelitisApoeapolipoprotein EPostoperative cognitive dysfunctionamyotrophic lateral sclerosisinflammationmiddle cerebral artery occlusionimmunotherapyinterferonIFNInterleukin-βsenescence-associated beta-galactosidaseAlzheimer’s diseaseALSParkinson’s diseasetransforming growth factor-betalong-term potentiationLTPNeurodegenerationtumor necrosis factor-alphaintraperitonealIntravenousNon-steroidal anti-inflammatory drugsImmune systemCNSmicroRNAsAgingBBBRegulatory T cellCMVcytomegaloviruscentral nervous systemgranulocyte-macrophage colony-stimulating factorBrain-derived neurotrophic factornuclear factor kappa-light-chain-enhancer of activated B cellsSenescence-associated secretory phenotypeCytotoxic T lymphocytesMannan-binding lectinLipopolysaccharidesBlood-brain barrierMacrophageCerebrospinal fluidCSFMHCmajor histocompatibility complexMultiple sclerosisneurofibrillary tanglesneurotrophin-3wild-typenitric oxide synthaseMechanistic target of rapamycinGonadotropin-releasing hormoneMøHIVhuman immunodeficiency virusCCAAT/enhancer binding proteinC-reactive proteinCRPMyelin basic proteinamyloid precursor proteinnod-like receptor protein 3Glucocorticoidsmyelin oligodendrocyte glycoproteinReactive oxygen speciestriggering receptor expressed on myeloid cells 2T cell receptorglucocorticoid receptor
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Authors
Zhanfeng Liang, Yang Zhao, Linhui Ruan, Linnan Zhu, Kunlin Jin, Qichuan Zhuge, Dong-Ming Su, Yong Zhao,