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dc.contributor.authorUddin M.S.
dc.contributor.authorKabir M.T.
dc.contributor.authorAl Mamun A.
dc.contributor.authorAbdel-Daim M.M.
dc.contributor.authorBarreto G.E.
dc.contributor.authorAshraf G.M.
dc.date.accessioned2020-09-02T22:29:28Z
dc.date.available2020-09-02T22:29:28Z
dc.date.issued2019
dc.identifier10.1007/s12035-018-1237-z
dc.identifier.citation56, 4, 2450-2465
dc.identifier.issn08937648
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6461
dc.descriptionAlzheimer’s disease (AD) is an immutable neurodegenerative disease featured by the two hallmark brain pathologies that are the extracellular amyloid ß (Aß) and intraneuronal tau protein. People carrying the APOE4 allele are at high risk of AD concerning the ones carrying the ε3 allele, while the ε2 allele abates risk. ApoE isoforms exert a central role in controlling the transport of brain lipid, neuronal signaling, mitochondrial function, glucose metabolism, and neuroinflammation. Regardless of widespread indispensable studies, the appropriate function of APOE in AD etiology stays ambiguous. Existing proof recommends that the disparate outcomes of ApoE isoforms on Aβ accretion and clearance have a distinct function in AD pathogenesis. ApoE–lipoproteins combine diverse cell-surface receptors to transport lipids and moreover to lipophilic Aβ peptide, that is believed to begin deadly events that generate neurodegeneration in the AD. ApoE has great influence in tau pathogenesis, tau-mediated neurodegeneration, and neuroinflammation, as well as α-synucleinopathy, lipid metabolism, and synaptic plasticity despite the presence of Aβ pathology. ApoE4 shows the deleterious effect for AD while the lack of ApoE4 is defensive. Therapeutic strategies primarily depend on APOE suggest to lessen the noxious effects of ApoE4 and reestablish the protective aptitudes of ApoE. This appraisal represents the critical interactions of APOE and AD pathology, existing facts on ApoE levels in the central nervous system (CNS), and the credible active stratagems for AD therapy by aiming ApoE. This review also highlighted utmost ApoE targeting therapeutic tactics that are crucial for controlling Alzheimer’s pathogenesis. © 2018, Springer Science+Business Media, LLC, part of Springer Nature.
dc.language.isoen
dc.publisherHumana Press Inc.
dc.subjectAlzheimer’s disease
dc.subjectAmyloid β
dc.subjectAPOE4
dc.subjectNeurofibrillary tangles
dc.subjectSenile plaques
dc.subjectTauopathy
dc.subjectABC transporter A1
dc.subjectalpha synuclein
dc.subjectamyloid beta protein
dc.subjectamyloid precursor protein
dc.subjectapolipoprotein E
dc.subjectapolipoprotein E4
dc.subjectfluindostatin
dc.subjectlow density lipoprotein receptor related protein
dc.subjectmonoclonal antibody
dc.subjectn (2,2,2 trifluoroethyl) n [4 (2,2,2 trifluoro 1 hydroxy 1 trifluoromethylethyl)phenyl]benzenesulfonamide
dc.subjectpresenilin 1
dc.subjectpresenilin 2
dc.subjectretinoid X receptor
dc.subjecttau protein
dc.subjectamyloid
dc.subjectapolipoprotein E
dc.subjectapolipoprotein E4
dc.subjectAlzheimer disease
dc.subjectamyloid plaque
dc.subjectamyloidosis
dc.subjectcognitive defect
dc.subjectfrontotemporal dementia
dc.subjectgenetic risk
dc.subjecthippocampus
dc.subjecthomozygote
dc.subjecthuman
dc.subjectlipid metabolism
dc.subjectnerve cell plasticity
dc.subjectnerve degeneration
dc.subjectnervous system inflammation
dc.subjectnonhuman
dc.subjectpathogenesis
dc.subjectprotein aggregation
dc.subjectReview
dc.subjectsenile plaque
dc.subjectsynucleinopathy
dc.subjectAlzheimer disease
dc.subjectanimal
dc.subjectgenetic predisposition
dc.subjectgenetics
dc.subjectmetabolism
dc.subjectpathology
dc.subjectrisk factor
dc.subjectAlzheimer Disease
dc.subjectAmyloid
dc.subjectAnimals
dc.subjectApolipoprotein E4
dc.subjectApolipoproteins E
dc.subjectGenetic Predisposition to Disease
dc.subjectHumans
dc.subjectRisk Factors
dc.titleAPOE and Alzheimer’s Disease: Evidence Mounts that Targeting APOE4 may Combat Alzheimer’s Pathogenesis
dc.typeReview


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