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dc.contributor.authorHerrera M.I.
dc.contributor.authorUdovin L.D.
dc.contributor.authorToro-Urrego N.
dc.contributor.authorKusnier C.F.
dc.contributor.authorLuaces J.P.
dc.contributor.authorOtero-Losada M.
dc.contributor.authorCapani F.
dc.date.accessioned2020-09-02T22:20:27Z
dc.date.available2020-09-02T22:20:27Z
dc.date.issued2018
dc.identifier10.3389/fnins.2018.00339
dc.identifier.citation12, MAY, -
dc.identifier.issn16624548
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4877
dc.descriptionMetabolic syndrome (MetS) is a cluster of risk factors that lead to microvascular dysfunction and chronic cerebral hypoperfusion (CCH). Long-standing reduction in oxygen and energy supply leads to brain hypoxia and protein misfolding, thereby linking CCH to Alzheimer's disease. Protein misfolding results in neurodegeneration as revealed by studying different experimental models of CCH. Regulating proteostasis network through pathways like the unfolded protein response (UPR), the ubiquitin-proteasome system (UPS), chaperone-mediated autophagy (CMA), and macroautophagy emerges as a novel target for neuroprotection. Lipoxin A4 methyl ester, baclofen, URB597, N-stearoyl-L-tyrosine, and melatonin may pose potential neuroprotective agents for rebalancing the proteostasis network under CCH. Autophagy is one of the most studied pathways of proteostatic cell response against the decrease in blood supply to the brain though the role of the UPR-specific chaperones and the UPS system in CCH deserves further research. Pharmacotherapy targeting misfolded proteins at different stages in the proteostatic pathway might be promising in treating cognitive impairment following CCH. © 2018 Herrera, Udovin, Toro-Urrego, Kusnier, Luaces, Otero-Losada and Capani.
dc.language.isoen
dc.publisherFrontiers Media S.A.
dc.subjectChaperones
dc.subjectChronic cerebral hypoperfusion
dc.subjectEndoplasmic reticulum stress
dc.subjectMetabolic syndrome
dc.subjectNeurodegenerative diseases
dc.subjectNeuroprotection
dc.subjectProtein misfolding
dc.subjectactivating transcription factor 6
dc.subjectamyloid beta protein
dc.subjectbaclofen
dc.subjectcyclohexylcarbamic acid 3' carbamoylbiphenyl 3 yl ester
dc.subjectinositol requiring enzyme 1 alpha
dc.subjectlipoxin A4 methyl ester
dc.subjectmelatonin
dc.subjectn stearoyl levo tyrosine
dc.subjectneuroprotective agent
dc.subjectpalmidrol
dc.subjectproteasome
dc.subjectprotein RNA like endoplasmic reticulum kinase
dc.subjecttau protein
dc.subjectubiquitin
dc.subjectunclassified drug
dc.subjectX box binding protein 1
dc.subjectAlzheimer disease
dc.subjectAPOE gene
dc.subjectatherosclerosis
dc.subjectautophagy
dc.subjectbehavior disorder
dc.subjectbilateral common carotid artery occlusion
dc.subjectbrain atrophy
dc.subjectbrain blood flow
dc.subjectbrain disease
dc.subjectbrain perfusion
dc.subjectcarotid artery obstruction
dc.subjectchaperone-mediated autophagy
dc.subjectchronic cerebral hypoperfusion
dc.subjectcognitive defect
dc.subjectdisease association
dc.subjectendoplasmic reticulum stress
dc.subjectgenetic risk
dc.subjecthippocampal atrophy
dc.subjecthuman
dc.subjecthyperglycemia
dc.subjecthypertension
dc.subjecthypertriglyceridemia
dc.subjecthypoxia
dc.subjectinsulin resistance
dc.subjectlipid diet
dc.subjectmacroautophagy
dc.subjectmetabolic syndrome X
dc.subjectnerve degeneration
dc.subjectneuroprotection
dc.subjectnon insulin dependent diabetes mellitus
dc.subjectnonhuman
dc.subjectobesity
dc.subjectoxidative stress
dc.subjectoxygen glucose deprivation
dc.subjectpathogenesis
dc.subjectprotein deficiency
dc.subjectprotein function
dc.subjectprotein homeostasis
dc.subjectprotein misfolding
dc.subjectprotein misfolding disorder
dc.subjectprotein phosphorylation
dc.subjectrisk factor
dc.subjectShort Survey
dc.subjectsignal transduction
dc.subjectunfolded protein response
dc.subjectvascular disease
dc.titleNeuroprotection targeting protein misfolding on chronic cerebral hypoperfusion in the context of metabolic syndrome
dc.typeShort Survey


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