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http://purl.uniprot.org/citations/31286344http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31286344http://www.w3.org/2000/01/rdf-schema#comment"Neuroinflammation plays an early and prominent role in the pathology of Alzheimer's disease (AD). Tumor necrosis factor-α-induced protein 8-like 2 (TIPE2) has been identified as a negative regulator of innate and adaptive immunity. However, whether TIPE2 affects cognitive functions in AD-like mouse models remains unknown. In this study, we compared the gene and protein expressions of TIPE2 between the APP/PS1 mice and the age-matched wild type (WT) mice at different stages of development using western blot and RT-qPCR. The hippocampal expression of the TIPE2 mRNA and protein in APP/PS1 mice was higher than that of the WT mice starting from 6 months to 10 months. However, the difference of the TIPE2 expression between the APP/PS1 mice and the WT mice declined in a time-dependent manner. The spatial learning and memory deficit from the 8-month-old APP/PS1 mice was observed in the Y-maze test and fear conditioning task. Interestingly, overexpression of TIPE2 by intra-hippocampal injection of AAV-TIPE2 into APP/PS1 mice resulted in an improvement of learning and memory and reduced expression of inflammatory cytokines, such as TNF-α, IL-6 and IL-1β, and increased expression of anti-inflammatory cytokines, such as IL-10 and Arg-1. Taken together, our findings show that the TIPE2 expression level was negatively correlated with the pathogenesis of Alzheimer's disease, and overexpression of TIPE2 attenuates cognitive deficits in APP/PS1 mice, suggesting TIPE2 is a potential target for pharmacological intervention and improvement of cognitive deficits. Graphical Abstract ."xsd:string
http://purl.uniprot.org/citations/31286344http://purl.org/dc/terms/identifier"doi:10.1007/s11481-019-09861-2"xsd:string
http://purl.uniprot.org/citations/31286344http://purl.uniprot.org/core/author"Zhang F."xsd:string
http://purl.uniprot.org/citations/31286344http://purl.uniprot.org/core/author"Zhang R."xsd:string
http://purl.uniprot.org/citations/31286344http://purl.uniprot.org/core/author"Wang L."xsd:string
http://purl.uniprot.org/citations/31286344http://purl.uniprot.org/core/author"Yang Z."xsd:string
http://purl.uniprot.org/citations/31286344http://purl.uniprot.org/core/author"Xu Z."xsd:string
http://purl.uniprot.org/citations/31286344http://purl.uniprot.org/core/author"Wang N."xsd:string
http://purl.uniprot.org/citations/31286344http://purl.uniprot.org/core/author"Ju C."xsd:string
http://purl.uniprot.org/citations/31286344http://purl.uniprot.org/core/author"Miao Y."xsd:string
http://purl.uniprot.org/citations/31286344http://purl.uniprot.org/core/author"Shao W."xsd:string
http://purl.uniprot.org/citations/31286344http://purl.uniprot.org/core/date"2019"xsd:gYear
http://purl.uniprot.org/citations/31286344http://purl.uniprot.org/core/name"J Neuroimmune Pharmacol"xsd:string
http://purl.uniprot.org/citations/31286344http://purl.uniprot.org/core/pages"519-529"xsd:string
http://purl.uniprot.org/citations/31286344http://purl.uniprot.org/core/title"Overexpression of TIPE2, a Negative Regulator of Innate and Adaptive Immunity, Attenuates Cognitive Deficits in APP/PS1 Mice."xsd:string
http://purl.uniprot.org/citations/31286344http://purl.uniprot.org/core/volume"14"xsd:string
http://purl.uniprot.org/citations/31286344http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/31286344
http://purl.uniprot.org/citations/31286344http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/31286344
http://purl.uniprot.org/uniprot/#_Q9D8Y7-mappedCitation-31286344http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31286344
http://purl.uniprot.org/uniprot/Q9D8Y7http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/31286344