ArticleMolecular neurobiology2018
Chronic Cerebral Hypoperfusion Induced Synaptic Proteome Changes in the rat Cerebral Cortex.
Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- A review of animal models of vascular dementia.Molecular biology reports · 2026Review
- Exploring synaptic density patterns in cerebral small vessel disease: insights from [European journal of nuclear medicine and molecular imaging · 2026Article
- Synaptic Vesicle-Related Proteins and Ubiquilin 2 in Cortical Synaptosomes Mediate Cognitive Impairment in Vascular Dementia Rats.Molecular neurobiology · 2025Article
- Integrated analysis of chromatin and transcriptomic profiling of the striatum after cerebral hypoperfusion in mice.BMC genomics · 2025Article
- Intermittent fasting reprograms the brain proteome to prevent synaptic degeneration and cognitive impairment in vascular dementia.Theranostics · 2025Article
- The Phenotype Changes of Astrocyte During Different Ischemia Conditions.Brain sciences · 2024Article
- I-C-F-6 attenuates chronic cerebral hypoperfusion-induced neurological injury in mice by modulating microglia polarization.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- A circRNA ceRNA network involved in cognitive dysfunction after chronic cerebral hypoperfusion.Aging · 2024Article
- Peripheral blood diagnostic markers of chronic cerebral hypoperfusion.American journal of translational research · 2024Article
- ChemR23 activation attenuates cognitive impairment in chronic cerebral hypoperfusion by inhibiting NLRP3 inflammasome-induced neuronal pyroptosis.Cell death & disease · 2023Article
- Review
- The role of Shunaoxin pills in the treatment of chronic cerebral hypoperfusion and its main pharmacodynamic components.Open medicine (Warsaw, Poland) · 2022Article
- Limb Remote Ischemic Conditioning Ameliorates Cognitive Impairment in Rats with Chronic Cerebral Hypoperfusion by Regulating Glucose Transport.Aging and disease · 2021Article
- Article
- Acupuncture accelerates neural regeneration and synaptophysin production after neural stem cells transplantation in mice.World journal of stem cells · 2020Article
- Chronic stepwise cerebral hypoperfusion differentially induces synaptic proteome changes in the frontal cortex, occipital cortex, and hippocampus in rats.Scientific reports · 2020Article
- Machine learning analysis of whole mouse brain vasculature.Nature methods · 2020Article
- Dendritic Localization and Exocytosis of NAAG in the Rat Hippocampus.Cerebral cortex (New York, N.Y. : 1991) · 2020Article
- The Effects of GABAergic System under Cerebral Ischemia: Spotlight on Cognitive Function.Neural plasticity · 2020Review
- Dysfunction of Cerebrovascular Endothelial Cells: Prelude to Vascular Dementia.Frontiers in aging neuroscience · 2018Review
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Chronic cerebral hypoperfusion (CCH) evokes mild cognitive impairment (MCI) and contributes to the progression of vascular dementia and Alzheimer's disease (AD). How CCH induces these neurodegenerative processes that may spread along the synaptic network and whether they are detectable at the synaptic proteome level of the cerebral cortex remains to be established. In the present study, we report the synaptic protein changes in the cerebral cortex after stepwise bilateral common carotid artery occlusion (BCCAO) induced CCH in the rat. The occlusions were confirmed with magnetic resonance angiography 5 weeks after the surgery. Synaptosome fractions were prepared using sucrose gradient centrifugation from cerebral cortex dissected 7 weeks after the occlusion. The synaptic protein differences between the sham operated and CCH groups were analyzed with label-free nanoUHPLC-MS/MS. We identified 46 proteins showing altered abundance due to CCH. In particular, synaptic protein and lipid metabolism, as well as GABA shunt-related proteins showed increased while neurotransmission and synaptic assembly-related proteins showed decreased protein level changes in CCH rats. Protein network analysis of CCH-induced protein alterations suggested the importance of increased synaptic apolipoprotein E (APOE) level as a consequence of CCH. Therefore, the change in APOE level was confirmed with Western blotting. The identified synaptic protein changes would precede the onset of dementia-like symptoms in the CCH model, suggesting their importance in the development of vascular dementia.
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