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dc.contributor.authorUddin M.S.
dc.contributor.authorKabir M.T.
dc.contributor.authorMamun A.A.
dc.contributor.authorBarreto G.E.
dc.contributor.authorRashid M.
dc.contributor.authorPerveen A.
dc.contributor.authorAshraf G.M.
dc.date.accessioned2020-09-02T22:29:29Z
dc.date.available2020-09-02T22:29:29Z
dc.date.issued2020
dc.identifier10.1016/j.intimp.2020.106479
dc.identifier.citation84, , -
dc.identifier.issn15675769
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6464
dc.descriptionAlzheimer's disease (AD) is one of the most prevalent neurodegenerative diseases characterized by the formation of extracellular amyloid beta (Aβ) plaques and intracellular neurofibrillary tangles (NFTs). Growing evidence suggested that there is an association between neuronal dysfunction and neuroinflammation (NI) in AD, coordinated by the chronic activation of astrocytes and microglial cells along with the subsequent excessive generation of the proinflammatory molecule. Therefore, a better understanding of the relationship between the nervous and immune systems is important in order to delay or avert the neurodegenerative events of AD. The inflammatory/immune pathways and the mechanisms to control these pathways may provide a novel arena to develop new drugs in order to target NI in AD. In this review, we represent the influence of cellular mediators which are involved in the NI process, with regards to the progression of AD. We also discuss the processes and the current status of multiple anti-inflammatory agents which are used in AD and have gone through or going through clinical trials. Moreover, new prospects for targeting NI in the development of AD drugs have also been highlighted. © 2020 Elsevier B.V.
dc.language.isoen
dc.publisherElsevier B.V.
dc.subjectAlzheimer's disease
dc.subjectAnti-inflammatory agents
dc.subjectImmune system
dc.subjectNeuroinflammation
dc.subjectProinflammatory molecules
dc.subjectadvanced glycation end product receptor
dc.subjectamyloid beta protein
dc.subjectangiotensin 1 receptor
dc.subjectantiinflammatory agent
dc.subjectazeliragon
dc.subjectcandesartan
dc.subjectcytokine
dc.subjectetanercept
dc.subjectgc 021109
dc.subjectgranulocyte macrophage colony stimulating factor
dc.subjectimmunoglobulin
dc.subjectminocycline
dc.subjectneflamapimod
dc.subjectnonsteroid antiinflammatory agent
dc.subjectnootropic agent
dc.subjectpioglitazone
dc.subjectprostaglandin synthase
dc.subjectrosiglitazone
dc.subjectsargramostim
dc.subjecttelmisartan
dc.subjectthalidomide
dc.subjectunclassified drug
dc.subjectAlzheimer disease
dc.subjectantiinflammatory activity
dc.subjectcytokine release
dc.subjectdisease exacerbation
dc.subjectdrug targeting
dc.subjecthuman
dc.subjectinsulin resistance
dc.subjectmacroglia
dc.subjectmediator
dc.subjectmicroglia
dc.subjectmononuclear cell
dc.subjectnerve cell
dc.subjectnervous system inflammation
dc.subjectnonhuman
dc.subjectpriority journal
dc.subjectprotein expression
dc.subjectReview
dc.subjectsignal transduction
dc.titlePharmacological approaches to mitigate neuroinflammation in Alzheimer's disease
dc.typeReview


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