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dc.contributor.authorBlach-Olszewska Z.
dc.contributor.authorZaczynska E.
dc.contributor.authorGustaw-Rothenberg K.
dc.contributor.authorAvila-Rodrigues M.
dc.contributor.authorBarreto G.E.
dc.contributor.authorLeszek J.
dc.contributor.authorAliev G.
dc.date.accessioned2020-09-02T22:13:12Z
dc.date.available2020-09-02T22:13:12Z
dc.date.issued2015
dc.identifier10.2174/1381612821666150710144829
dc.identifier.citation21, 25, 3582-3588
dc.identifier.issn13816128
dc.identifier.urihttps://hdl.handle.net/20.500.12728/3765
dc.descriptionThe genetic, cellular, and molecular changes associated with Alzheimer disease provide evidence of immune and inflammatory processes involvement in its pathogenesis. These are supported by epidemiological studies, which show some benefit of long-term use of NSAID. The hypothesis that AD is in fact an immunologically mediated and even inflammatory pathological process may be in fact scientifically intriguing. There are several obstacles that suggest the need for more complex view, in the process of targeting inflammation and immunity in AD. In our previous studies we proposed a reliable methodology to assess innate immunity in Alzheimer patients and controls. The methodology is based on the phenomenon of human leukocytes being resistant to viral infection. The unspecific character of the resistance, dependent on interferons and tumor necrosis factor, and occurrence in cells ex vivo indicate that an in vivo mechanism of innate immunity may be involved. The above mentioned resistance could be estimated in a test based on peripheral blood leukocytes infection by vesicular stomachs virus. © 2015 Bentham Science Publishers.
dc.language.isoen
dc.publisherBentham Science Publishers B.V.
dc.subjectAlzheimer disease
dc.subjectHuman peripheral blood leukocytes
dc.subjectInnate immunity
dc.subjectTherapy
dc.subjectcyclooxygenase 2 inhibitor
dc.subjectdonepezil
dc.subjectgalantamine
dc.subjectGinkgo biloba extract
dc.subjectimmunosuppressive agent
dc.subjectnatural product
dc.subjectnonsteroid antiinflammatory agent
dc.subjectsteroid
dc.subjecttumor necrosis factor
dc.subjectcholinesterase inhibitor
dc.subjectimmunologic factor
dc.subjectinterferon
dc.subjectnonsteroid antiinflammatory agent
dc.subjecttumor necrosis factor alpha
dc.subjectAlzheimer disease
dc.subjectArticle
dc.subjectautoimmunity
dc.subjectextract
dc.subjectgene expression
dc.subjecthuman
dc.subjectimmunopathogenesis
dc.subjectimmunosuppressive treatment
dc.subjectinfection resistance
dc.subjectinflammation
dc.subjectinnate immunity
dc.subjectleukocyte
dc.subjectmild cognitive impairment
dc.subjectnonhuman
dc.subjectpriority journal
dc.subjectsteroid therapy
dc.subjectvirus infection
dc.subjectaging
dc.subjectAlzheimer disease
dc.subjectanimal
dc.subjectdrug development
dc.subjectdrug effects
dc.subjectimmunology
dc.subjectinnate immunity
dc.subjectmetabolism
dc.subjectmicroglia
dc.subjectoxidative stress
dc.subjectAging
dc.subjectAlzheimer Disease
dc.subjectAnimals
dc.subjectAnti-Inflammatory Agents, Non-Steroidal
dc.subjectCholinesterase Inhibitors
dc.subjectDrug Discovery
dc.subjectHumans
dc.subjectImmunity, Innate
dc.subjectImmunologic Factors
dc.subjectInterferons
dc.subjectLeukocytes
dc.subjectMicroglia
dc.subjectOxidative Stress
dc.subjectTumor Necrosis Factor-alpha
dc.titleThe innate immunity in alzheimer disease-relevance to pathogenesis and therapy
dc.typeArticle


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