ArticleNeurochemical research2017
Chronic Cerebral Hypoperfusion Promotes Amyloid-Beta Pathogenesis via Activating β/γ-Secretases.
Article in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
- Toll-Like Receptor 4-Mediated Neuroinflammation: Updates on Pathological Roles and Therapeutic Strategies in Chronic Cerebral Hypoperfusion.Molecular neurobiology · 2025Review
- The Conceivable Role of Metabolic Syndrome in the Pathogenesis of Alzheimer's Disease: Cellular and Subcellular Alterations in Underpinning a Tale of Two.Neuromolecular medicine · 2025Review
- Antiageing strategy for neurodegenerative diseases: from mechanisms to clinical advances.Signal transduction and targeted therapy · 2025Review
- Association between hemoglobin-to-red blood cell distribution width ratio and cognitive function in older US adults: a cross-sectional study based on the NHANES 2011-2014.Frontiers in aging neuroscience · 2025Article
- Amyloid-β and heart failure in Alzheimer's disease: the new vistas.Frontiers in medicine · 2025Review
- New insight on the potential detrimental effect of metabolic syndrome on the Alzheimer disease neuropathology: Mechanistic role.Journal of cellular and molecular medicine · 2024Review
- Vascular Function and Ion Channels in Alzheimer's Disease.Microcirculation (New York, N.Y. : 1994) · 2024Review
- Microvascular Contributions to Alzheimer Disease Pathogenesis: Is Alzheimer Disease Primarily an Endotheliopathy?Biomolecules · 2023Review
- Altered O-GlcNAcylation and mitochondrial dysfunction, a molecular link between brain glucose dysregulation and sporadic Alzheimer's disease.Neural regeneration research · 2023Article
- Gastrodin and Gastrodigenin Improve Energy Metabolism Disorders and Mitochondrial Dysfunction to Antagonize Vascular Dementia.Molecules (Basel, Switzerland) · 2023Article
- Abnormal circadian blood pressure regulation and cognitive impairment in α-synucleinopathies.Hypertension research : official journal of the Japanese Society of Hypertension · 2022Review
- Cognitive Impairments and blood-brain Barrier Damage in a Mouse Model of Chronic Cerebral Hypoperfusion.Neurochemical research · 2022Article
- Article
- Capsaicin Ameliorates the Loosening of Mitochondria-Associated Endoplasmic Reticulum Membranes and Improves Cognitive Function in Rats With Chronic Cerebral Hypoperfusion.Frontiers in cellular neuroscience · 2022Article
- Metabolomic analysis of vascular cognitive impairment due to hepatocellular carcinoma.Frontiers in neurology · 2022Article
- Cerebral blood flow, tau imaging, and memory associations in cognitively unimpaired older adults.Cerebral circulation - cognition and behavior · 2022Article
- Dietary Spray-Dried Porcine Plasma Reduces Neuropathological Alzheimer's Disease Hallmarks in SAMP8 Mice.Nutrients · 2021Article
- Article
- Detrimental effects of long-term elevated serum uric acid on cognitive function in rats.Scientific reports · 2021Article
- Role of Neuron and Glia in Alzheimer's Disease and Associated Vascular Dysfunction.Frontiers in aging neuroscience · 2021Article
Corrections and comments
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Authors and funding
5 authors at 5 institutions in 1 country.
Funding
Abstract
Chronic cerebral hypoperfusion (CCH) contributes to the Alzheimer's-like pathogenesis, but the relationship between CCH and the occurrence of Alzheimer's disease (AD) remains obscure. The aim is to elucidate the potential pathophysiological mechanism in the field of amyloid-beta (Aβ) pathology induced by CCH. A rat model of CCH has been developed with permanent bilateral occlusion of common carotid arteries (BCCAO). The cognitive function of rats was tested by the Morris water maze. The levels of Aβ (Aβ40 and Aβ42) and soluble amyloid precursor protein (sAPP: sAPPα and sAPPβ) were determined by enzyme linked immunosorbent assay. The expression of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), presenilin1 (PS1), nicastrin (NCT), anterior pharynx-defective 1alpha (Aph-1α) and presenilin enhancer 2 (Pen-2), sAPPα and sAPPβ were detected by Western blotting. Morris water maze test showed that CCH induced decline in learning and memory related to Aβ levels in the hippocampus. The levels of sAPPα, ADAM10 and ADAM17 in the hippocampus of CCH rats were higher than the control ones (P < 0.05); the levels of sAPPβ, BACE and BACE1 increased more than the control ones (P < 0.05). CCH intervention (1-week or 4-week) markedly increased the expression of PS1, Aph-1α and Pen-2 in the hippocampus of rats, but had no effect on NCT. CCH contributed to cognitive impairment and altered the amyloidogenic and non-amyloidogenic pathway of APP processing by boosting the activity of β-secretase/γ-secretase and α-secretase respectively. The non-amyloidogenic pathway can't overcome the damage role of the amyloidogenic pathway in the process of chronic cerebral hypoperfusion which promotes amyloid-beta pathogenesis.
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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.