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Molecular Mechanisms of ER Stress and UPR in the Pathogenesis of Alzheimer’s Disease

dc.contributor.authorUddin M.S.
dc.contributor.authorTewari D.
dc.contributor.authorSharma G.
dc.contributor.authorKabir M.T.
dc.contributor.authorBarreto G.E.
dc.contributor.authorBin-Jumah M.N.
dc.contributor.authorPerveen A.
dc.contributor.authorAbdel-Daim M.M.
dc.contributor.authorAshraf G.M.
dc.date.accessioned2020-09-02T22:29:30Z
dc.date.available2020-09-02T22:29:30Z
dc.date.issued2020
dc.identifier10.1007/s12035-020-01929-y
dc.identifier.citation57, 7, 2902-2919
dc.identifier.issn08937648
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6469
dc.descriptionAlzheimer’s disease (AD) is a progressive neurodegenerative disease involving aggregation of misfolded proteins inside the neuron causing prolonged cellular stress. The neuropathological hallmarks of AD include the formation of senile plaques and neurofibrillary tangles in specific brain regions that lead to synaptic loss and neuronal death. The exact mechanism of neuron dysfunction in AD remains obscure. In recent years, endoplasmic reticulum (ER) dysfunction has been implicated in neuronal degeneration seen in AD. Apart from AD, many other diseases also involve misfolded proteins aggregations in the ER, a condition referred to as ER stress. The response of the cell to ER stress is to activate a group of signaling pathways called unfolded protein response (UPR) that stimulates a particular transcriptional program to restore ER function and ensure cell survival. ER stress also involves the generation of reactive oxygen species (ROS) that, together with mitochondrial ROS and decreased effectiveness of antioxidant mechanisms, producing a condition of chronic oxidative stress. The unfolded proteins may not always produce a response that leads to the restoration of cellular functions, but they may also lead to inflammation by a set of different pathways with deleterious consequences. In this review, we extensively discuss the role of ER stress and how to target it using different pharmacological approaches in AD development and onset. © 2020, Springer Science+Business Media, LLC, part of Springer Nature.
dc.language.isoen
dc.publisherSpringer
dc.subjectAlzheimer’s disease
dc.subjectAmyloid β
dc.subjectEndoplasmic reticulum
dc.subjectTau
dc.subjectUnfolded protein response
dc.subjectactivating transcription factor 4
dc.subjectactivating transcription factor 6
dc.subjectADAM10 endopeptidase
dc.subjectadenosine triphosphatase (calcium)
dc.subjectamyloid beta protein
dc.subjectamyloid precursor protein
dc.subjectanthra[1,9 cd]pyrazol 6(2h) one
dc.subjectbeta secretase 1
dc.subjectcalcium calmodulin dependent protein kinase II
dc.subjectdibenzoylmethane derivative
dc.subjectglucose regulated protein 78
dc.subjectglutathione
dc.subjectglycogen synthase kinase 3 inhibitor
dc.subjectgrowth arrest and DNA damage inducible protein 153
dc.subjectgsk 2606414
dc.subjectinitiation factor 2
dc.subjectinitiation factor 2alpha
dc.subjectinositol 1,4,5 trisphosphate receptor
dc.subjectpancreatic ER kinase
dc.subjectprotein disulfide isomerase
dc.subjectprotein IRE1
dc.subjectprotein kinase
dc.subjectprotein tyrosine kinase inhibitor
dc.subjectreactive oxygen metabolite
dc.subjectresveratrol
dc.subjecttau protein
dc.subjecttranscription factor Nrf2
dc.subjecttrazodone
dc.subjectunclassified drug
dc.subjectunindexed drug
dc.subjectX box binding protein 1
dc.subjectAlzheimer disease
dc.subjectapoptosis
dc.subjectautophagy (cellular)
dc.subjectbrain mitochondrion
dc.subjectcalcium signaling
dc.subjectendoplasmic reticulum
dc.subjectendoplasmic reticulum stress
dc.subjectgene expression
dc.subjectgene overexpression
dc.subjecthippocampus
dc.subjecthuman
dc.subjecthyperphosphorylation
dc.subjectimmunohistochemistry
dc.subjectnerve cell necrosis
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectpathogenesis
dc.subjectphosphorylation
dc.subjectprotein aggregation
dc.subjectprotein degradation
dc.subjectprotein expression
dc.subjectprotein folding
dc.subjectprotein phosphorylation
dc.subjectprotein protein interaction
dc.subjectReview
dc.subjecttemporal cortex
dc.subjectunfolded protein response
dc.subjectupregulation
dc.subjectWestern blotting
dc.titleMolecular Mechanisms of ER Stress and UPR in the Pathogenesis of Alzheimer’s Disease
dc.typeReview


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