Mostrar el registro sencillo del ítem
Neuroprotection targeting protein misfolding on chronic cerebral hypoperfusion in the context of metabolic syndrome
dc.contributor.author | Herrera M.I. | |
dc.contributor.author | Udovin L.D. | |
dc.contributor.author | Toro-Urrego N. | |
dc.contributor.author | Kusnier C.F. | |
dc.contributor.author | Luaces J.P. | |
dc.contributor.author | Otero-Losada M. | |
dc.contributor.author | Capani F. | |
dc.date.accessioned | 2020-09-02T22:20:27Z | |
dc.date.available | 2020-09-02T22:20:27Z | |
dc.date.issued | 2018 | |
dc.identifier | 10.3389/fnins.2018.00339 | |
dc.identifier.citation | 12, MAY, - | |
dc.identifier.issn | 16624548 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12728/4877 | |
dc.description | Metabolic 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.iso | en | |
dc.publisher | Frontiers Media S.A. | |
dc.subject | Chaperones | |
dc.subject | Chronic cerebral hypoperfusion | |
dc.subject | Endoplasmic reticulum stress | |
dc.subject | Metabolic syndrome | |
dc.subject | Neurodegenerative diseases | |
dc.subject | Neuroprotection | |
dc.subject | Protein misfolding | |
dc.subject | activating transcription factor 6 | |
dc.subject | amyloid beta protein | |
dc.subject | baclofen | |
dc.subject | cyclohexylcarbamic acid 3' carbamoylbiphenyl 3 yl ester | |
dc.subject | inositol requiring enzyme 1 alpha | |
dc.subject | lipoxin A4 methyl ester | |
dc.subject | melatonin | |
dc.subject | n stearoyl levo tyrosine | |
dc.subject | neuroprotective agent | |
dc.subject | palmidrol | |
dc.subject | proteasome | |
dc.subject | protein RNA like endoplasmic reticulum kinase | |
dc.subject | tau protein | |
dc.subject | ubiquitin | |
dc.subject | unclassified drug | |
dc.subject | X box binding protein 1 | |
dc.subject | Alzheimer disease | |
dc.subject | APOE gene | |
dc.subject | atherosclerosis | |
dc.subject | autophagy | |
dc.subject | behavior disorder | |
dc.subject | bilateral common carotid artery occlusion | |
dc.subject | brain atrophy | |
dc.subject | brain blood flow | |
dc.subject | brain disease | |
dc.subject | brain perfusion | |
dc.subject | carotid artery obstruction | |
dc.subject | chaperone-mediated autophagy | |
dc.subject | chronic cerebral hypoperfusion | |
dc.subject | cognitive defect | |
dc.subject | disease association | |
dc.subject | endoplasmic reticulum stress | |
dc.subject | genetic risk | |
dc.subject | hippocampal atrophy | |
dc.subject | human | |
dc.subject | hyperglycemia | |
dc.subject | hypertension | |
dc.subject | hypertriglyceridemia | |
dc.subject | hypoxia | |
dc.subject | insulin resistance | |
dc.subject | lipid diet | |
dc.subject | macroautophagy | |
dc.subject | metabolic syndrome X | |
dc.subject | nerve degeneration | |
dc.subject | neuroprotection | |
dc.subject | non insulin dependent diabetes mellitus | |
dc.subject | nonhuman | |
dc.subject | obesity | |
dc.subject | oxidative stress | |
dc.subject | oxygen glucose deprivation | |
dc.subject | pathogenesis | |
dc.subject | protein deficiency | |
dc.subject | protein function | |
dc.subject | protein homeostasis | |
dc.subject | protein misfolding | |
dc.subject | protein misfolding disorder | |
dc.subject | protein phosphorylation | |
dc.subject | risk factor | |
dc.subject | Short Survey | |
dc.subject | signal transduction | |
dc.subject | unfolded protein response | |
dc.subject | vascular disease | |
dc.title | Neuroprotection targeting protein misfolding on chronic cerebral hypoperfusion in the context of metabolic syndrome | |
dc.type | Short Survey |