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dc.contributor.authorUddin, Md Sahab
dc.contributor.authorTewari, Devesh
dc.contributor.authorSharma, Gaurav
dc.contributor.authorKabir, Md Tanvir
dc.contributor.authorBarreto, George E
dc.contributor.authorBin-Jumah, May N
dc.contributor.authorPerveen, Asma
dc.contributor.authorAbdel-Daim, Mohamed M
dc.contributor.authorAshraf, Ghulam Md
dc.date.accessioned2022-05-03T00:46:30Z
dc.date.available2022-05-03T00:46:30Z
dc.date.issued2020
dc.identifier.issn0893-7648
dc.identifier.doi10.1007/s12035-020-01929-y
dc.identifier.urihttp://hdl.handle.net/10072/414243
dc.description.abstractAlzheimer’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.
dc.description.peerreviewedYes
dc.languageEnglish
dc.publisherSpringer
dc.relation.ispartofpagefrom2902
dc.relation.ispartofpageto2919
dc.relation.ispartofissue7
dc.relation.ispartofjournalMolecular Neurobiology
dc.relation.ispartofvolume57
dc.subject.fieldofresearchNeurosciences
dc.subject.fieldofresearchClinical and health psychology
dc.subject.fieldofresearchCognitive and computational psychology
dc.subject.fieldofresearchBiochemistry and cell biology
dc.subject.fieldofresearchcode3209
dc.subject.fieldofresearchcode5203
dc.subject.fieldofresearchcode5204
dc.subject.fieldofresearchcode3101
dc.subject.keywordsScience & Technology
dc.subject.keywordsLife Sciences & Biomedicine
dc.subject.keywordsNeurosciences
dc.subject.keywordsNeurosciences & Neurology
dc.subject.keywordsEndoplasmic reticulum
dc.subject.keywordsUnfolded protein response
dc.subject.keywordsAmyloid β
dc.subject.keywordsTau
dc.subject.keywordsAlzheimer’s disease
dc.titleMolecular mechanisms of ER stress and UPR in the pathogenesis of Alzheimer's disease
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationUddin, MS; Tewari, D; Sharma, G; Kabir, MT; Barreto, GE; Bin-Jumah, MN; Perveen, A; Abdel-Daim, MM; Ashraf, GM, Molecular mechanisms of ER stress and UPR in the pathogenesis of Alzheimer's disease, Molecular Neurobiology, 2020, 57 (7), pp. 2902-2919
dcterms.dateAccepted2020-05-01
dc.date.updated2022-04-27T22:31:15Z
gro.hasfulltextNo Full Text
gro.griffith.authorKabir, Md. Tanvir


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