ArticleFrontiers in aging neuroscience2014
Chronic cerebral hypoperfusion causes decrease of O-GlcNAcylation, hyperphosphorylation of tau and behavioral deficits in mice.
Article in Frontiers in aging neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed.
- Pulse pressure as a predictor of Alzheimer's disease biomarkers and cognitive decline: The moderating role of APOE ε4.The journal of prevention of Alzheimer's disease · 2025Trial
- Gene expression and brain pathology at the early stages of bilateral chronic cerebral hypoperfusion in the female mouse brain.Experimental neurology · 2026Article
- A review of animal models of vascular dementia.Molecular biology reports · 2026Review
- Exploring the role of zolpidem in alleviating cognitive and motor impairments in chronic cerebral hypoperfusion: a rat model study with in vivo and in silico insights.Experimental animals · 2026Article
- Genomic and proteomic conversion of brain ischemia to Alzheimer's disease.Frontiers in cell and developmental biology · 2026Review
- Neutrophil stalling does not mediate the increase in tau phosphorylation and the cognitive impairment associated with high salt diet.Cardiovascular research · 2025Article
- Neuronal deterioration associated with hyperexcitability under mild chronic cerebral hypoperfusion.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2025Article
- Review
- The pathophysiology of mixed Alzheimer's disease and vascular dementia.Theranostics · 2025Review
- Is the Relationship Between Cardiovascular Disease and Alzheimer's Disease Genetic? A Scoping Review.Genes · 2024Article
- Hexahydrocurcumin Attenuates Neuronal Injury and Modulates Synaptic Plasticity in Chronic Cerebral Hypoperfusion in Rats.Molecular neurobiology · 2024Article
- Two-photon optogenetics-based assessment of neuronal connectivity in healthy and chronic hypoperfusion mice.Neurophotonics · 2024Article
- Echocardiographic measures of the left heart and cerebrospinal fluid biomarkers of Alzheimer's disease pathology in cognitively intact adults: The CABLE study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Orthostatic Hypotension Promotes the Progression From Mild Cognitive Impairment to Dementia in Type 2 Diabetes Mellitus.The Journal of clinical endocrinology and metabolism · 2024Article
- Therapeutic potential of berries in age-related neurological disorders.Frontiers in pharmacology · 2024Review
- Elevated amyloid beta peptides and total tau in cerebrospinal fluid in individuals with Creatine transporter deficiency.Molecular genetics and metabolism reports · 2023Article
- Lipopolysaccharide-Induced Delirium-like Behaviour in a Rat Model of Chronic Cerebral Hypoperfusion Is Associated with Increased Indoleamine 2,3-Dioxygenase Expression and Endotoxin Tolerance.International journal of molecular sciences · 2023Article
- Mumefural Improves Recognition Memory and Alters ERK-CREB-BDNF Signaling in a Mouse Model of Chronic Cerebral Hypoperfusion.Nutrients · 2023Article
- An Altered Neurovascular System in Aging-Related Eye Diseases.International journal of molecular sciences · 2022Review
- Combination of indirect revascularization and endothelial progenitor cell transplantation improved cerebral perfusion and ameliorated tauopathy in a rat model of bilateral ICA ligation.Stem cell research & therapy · 2022Article
5 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors.
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Abstract
Chronic cerebral hypoperfusion (CCH) is one of the causes of vascular dementia (VaD) and is also an etiological factor for Alzheimer's disease (AD). However, how CCH causes cognitive impairment and contributes to Alzheimer's pathology is poorly understood. Here we produced a mouse model of CCH by unilateral common carotid artery occlusion (UCCAO) and studied the behavioral changes and brain abnormalities in mice 2.5 months after UCCAO. We found that CCH caused significant short-term memory deficits and mild long-term spatial memory impairment, as well as decreased level of protein O-GlcNAcylation, increased level of tau phosphorylation, dysregulated synaptic proteins and insulin signaling, and selective neurodegeneration in the brain. These findings provide mechanistic insight into the effects of CCH on memory and cognition and the likely link between AD and VaD.
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