ArticleScientific reports2019
The effect of chronic cerebral hypoperfusion on the pathology of Alzheimer's disease: A positron emission tomography study in rats.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 96 citations in OpenAlex.
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- Temporal Evolution of Brain Inflammation in the Bilateral Common Carotid Artery Stenosis Model of Chronic Cerebral Hypoperfusion.Journal of inflammation research · 2026Review
- Quantifying White Matter Hyperintensities: Automated Volumetry Compared with Visual Grading Scales.Medicina (Kaunas, Lithuania) · 2025Article
- The vascular contribution to cognitive decline in ageing and dementia.Nature reviews. Neuroscience · 2025Review
- Alzheimer's Disease-Thrombosis Comorbidity: A Growing Body of Evidence from Patients and Animal Models.Cells · 2025Review
- Adaptive Immune Dyshomeostasis as a Mediator of Vascular Cognitive Decline: Unraveling Neurovascular Crosstalk.Aging and disease · 2025Review
- Astrocyte-driven vasoconstriction impairs glymphatic clearance in a human tauopathy-on-chip model.APL bioengineering · 2025Article
- Glucose uptake in pigment glia suppresses Tau-induced inflammation and photoreceptor degeneration.Disease models & mechanisms · 2025Article
- Cerebral Hemodynamic Impairment and Cognitive Dysfunction inJournal of the American Heart Association · 2025Observational
- Associations of plasma biomarkers with cerebral perfusion and structure in Alzheimer's disease.Translational psychiatry · 2025Article
- The cerebral blood flow response to neuroactivation is reduced in cognitively normal men with β-amyloid accumulation.Alzheimer's research & therapy · 2025Article
- The therapeutic effects and mechanisms of glucagon-like peptide-1 receptor agonists in neurocognitive disorders.Therapeutic advances in neurological disorders · 2025Review
- Western diet-induced visceral adipose tissue inflammation promotes Alzheimer's disease pathology via microglial activation in a mouse model.Frontiers in aging neuroscience · 2025Article
- Association between cardiovascular disease risk, regional brain age gap, and cognition in healthy adults.Frontiers in aging neuroscience · 2025Article
- Characterizing vascular function in mouse models of Alzheimer's disease, atherosclerosis, and mixed Alzheimer's and atherosclerosis.Neurophotonics · 2025Article
- Hypertension and cerebral blood flow in the development of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
9 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebrovascular disease is a potential risk factor for Alzheimer's disease (AD). Although acute cerebral hypoperfusion causes neuronal necrosis and infarction, chronic cerebral hypoperfusion induces apoptosis in neurons, but its effects on the cognitive impairment are not clear. The purpose of this study was to evaluate the effects of chronic cerebral hypoperfusion on AD pathology and cerebral glucose metabolism. A model of chronic cerebral hypoperfusion was established by ligating the common carotid arteries bilaterally in adult male rats (CAL group). Sham-operated rats underwent the same procedures without artery ligation (control group). At 12 weeks after ligation, expression levels of amyloid-β (Aβ) and hyperphosphorylated tau (p-tau), as well as the regional cerebral glucose metabolism, were evaluated using Western blots and positron emission tomography with fluorine-18 fluorodeoxyglucose, respectively. The expression levels of Aβ in the frontal cortex and hippocampus and of p-tau in the temporal cortex were significantly higher in the CAL group than those in the control group. The cerebral glucose metabolism of the amygdala, entorhinal cortex, and hippocampus was significantly decreased in the CAL group compared to that in the control. These results suggest that chronic cerebral hypoperfusion can induce AD pathology and may play a significant role in AD development.
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