ArticleInternational journal of clinical and experimental medicine2015
Expression of Tau protein in rats with cognitive dysfunction induced by cerebral hypoperfusion.
Article in International journal of clinical and experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Hexahydrocurcumin Attenuates Neuronal Injury and Modulates Synaptic Plasticity in Chronic Cerebral Hypoperfusion in Rats.Molecular neurobiology · 2024Article
- Inhibition of MiR-122 Decreases Cerebral Ischemia-reperfusion Injury by Upregulating DJ-1-Phosphatase and Tensin Homologue Deleted on Chromosome 10 (PTEN)/Phosphonosinol-3 Kinase (PI3K)/AKT.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Embelin Improves the Spatial Memory and Hippocampal Long-Term Potentiation in a Rat Model of Chronic Cerebral Hypoperfusion.Scientific reports · 2019Article
- Cerebral Hypoperfusion and Other Shared Brain Pathologies in Ischemic Stroke and Alzheimer's Disease.Translational stroke research · 2018Review
- Neuroprotection Targeting Protein Misfolding on Chronic Cerebral Hypoperfusion in the Context of Metabolic Syndrome.Frontiers in neuroscience · 2018Review
- Effects of Shaoyao-Gancao Decoction on Infarcted Cerebral Cortical Neurons: Suppression of the Inflammatory Response following Cerebral Ischemia-Reperfusion in a Rat Model.BioMed research international · 2016Article
- Possible Post-Traumatic Focal Dystonia Associated with Tau Pathology Localized to Putamen-Globus Pallidus.Movement disorders clinical practiceArticle
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to investigate the relationship between chronic cerebral hypoperfusion and the occurrence and development of Alzheimer's disease (AD). A cerebral hypoperfusion rat model was established by two vessels occlusion (2VO). The cognitive function of the rats with chronic cerebral hypoperfusion and the expression of p-Tau protein in the hippocampus were observed dynamically. Before the operation, no differences were observed in the cognitive functions of the control and 2VO group (P > 0.05). However, a significant difference was found at 2, 4, 8, and 12 weeks after the operation. The shock number required to reach the "learned" standard in the 2VO group increased remarkably compared with that of the control group (P < 0.01). With the passage of time, the shock number in the model group increased gradually. The p-Tau-positive cells in the CA1 region of the hippocampus also increased markedly in the model group in a time-dependent manner as compared with that in the control group (P < 0.01). Cerebral hypoperfusion can cause and aggravate the phosphorylation of Tau protein in the brain, leading to cognitive dysfunction. Therefore, this protein is an important initiating and promoting factor involved in the development of AD.
Indexed as
Identifiers
26770632PMC4694532W2419239967What OpenQuestion holds
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.