ReviewFrontiers in neuroscience2018
Neuroprotection Targeting Protein Misfolding on Chronic Cerebral Hypoperfusion in the Context of Metabolic Syndrome.
Review in Frontiers in neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Development and validation of a LASSO-derived prognostic model predicting postoperative cognitive dysfunction risk in off-pump coronary artery bypass grafting patients.Journal of thoracic disease · 2026Article
- CaCommunications chemistry · 2025Article
- Neuroprotection from protein misfolding in cerebral hypoperfusion concurrent with metabolic syndrome. A translational perspective.Frontiers in neuroscience · 2023Review
- Editorial: Neurological comorbidity in metabolic syndrome.Frontiers in neuroscience · 2023Article
- Triptolide protects against white matter injury induced by chronic cerebral hypoperfusion in mice.Acta pharmacologica Sinica · 2022Article
- Stress Response Is the Main Trigger of Sporadic Amyloidoses.International journal of molecular sciences · 2021Review
- Nicotinamide Improves Cognitive Function in Mice With Chronic Cerebral Hypoperfusion.Frontiers in neurology · 2021Article
- Adipokines, Cardiovascular Risk, and Therapeutic Management in Obesity and Psoriatic Arthritis.Frontiers in immunology · 2020Review
- Role of Oxidative Stress and Metal Toxicity in the Progression of Alzheimer's Disease.Current neuropharmacology · 2020Review
- Ambiguous Effects of Autophagy Activation Following Hypoperfusion/Ischemia.International journal of molecular sciences · 2018Review
- AAV-Syn-BDNF-EGFP Virus Construct Exerts Neuroprotective Action on the Hippocampal Neural Network during Hypoxia In Vitro.International journal of molecular sciences · 2018Article
- Role of Prenatal Hypoxia in Brain Development, Cognitive Functions, and Neurodegeneration.Frontiers in neuroscience · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.