ArticleOncotarget2016
Severe chronic cerebral hypoperfusion induces microglial dysfunction leading to memory loss in APPswe/PS1 mice.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Loss of ovarian hormones is detrimental in early disease stages of mouse models of Alzheimer's disease and multi-etiology dementia.Biology of sex differences · 2025Article
- Endothelial PDGF-D contributes to neurovascular protection after ischemic stroke by rescuing pericyte functions.Cellular and molecular life sciences : CMLS · 2024Article
- What type of cell death occurs in chronic cerebral hypoperfusion? A review focusing on pyroptosis and its potential therapeutic implications.Frontiers in cellular neuroscience · 2023Review
- Pathophysiology of blood brain barrier dysfunction during chronic cerebral hypoperfusion in vascular cognitive impairment.Theranostics · 2022Review
- Neurotrophic signaling deficiency exacerbates environmental risks for Alzheimer's disease pathogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Cognitive Dysfunction after Heart Disease: A Manifestation of the Heart-Brain Axis.Oxidative medicine and cellular longevity · 2021Review
- Multifocal Cerebral Microinfarcts Modulate Early Alzheimer's Disease Pathology in a Sex-Dependent Manner.Frontiers in immunology · 2021Article
- Neurovascular Alterations in Vascular Dementia: Emphasis on Risk Factors.Frontiers in aging neuroscience · 2021Article
- Heart and Brain: Complex Relationships for Left Ventricular Dysfunction.Current cardiology reports · 2020Review
- Heterogeneous Disease Progression in a Mouse Model of Vascular Cognitive Impairment.International journal of molecular sciences · 2020Article
- Optical coherence tomography-based assessment of retinal vascular pathology in cerebral small vessel disease.Neurological research and practice · 2020Article
- Canonical Wnt Pathway Maintains Blood-Brain Barrier Integrity upon Ischemic Stroke and Its Activation Ameliorates Tissue Plasminogen Activator Therapy.Molecular neurobiology · 2019Article
- Melatonin Improves Memory Deficits in Rats with Cerebral Hypoperfusion, Possibly, Through Decreasing the Expression of Small-Conductance CaNeurochemical research · 2019Article
- Fatigue, Sleep, and Autoimmune and Related Disorders.Frontiers in immunology · 2019Review
- Small Vessels Are a Big Problem in Neurodegeneration and Neuroprotection.Frontiers in neurology · 2019Review
- Vascular Endothelial Growth Factor Isoform-B Stimulates Neurovascular Repair After Ischemic Stroke by Promoting the Function of Pericytes via Vascular Endothelial Growth Factor Receptor-1.Molecular neurobiology · 2018Article
- Effects of Cerebral Blood Flow and White Matter Integrity on Cognition in CADASIL Patients.Frontiers in psychiatry · 2018Article
- Better Correlation of Cognitive Function to White Matter Integrity than to Blood Supply in Subjects with Leukoaraiosis.Frontiers in aging neuroscience · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral vasculature plays a key role in controlling brain homeostasis. Cerebral vasculature dysfunction, associated to irregularities in cerebral blood perfusion, has been proposed to directly contribute to Alzheimer's disease (AD) pathogenesis. More precisely, chronic cerebral hypoperfusion, which impairs brain homeostasis, was demonstrated to take place even before cognitive decline. However, the mechanisms underlying the implication of chronic cerebral hypoperfusion in AD pathogenesis remain elusive. Therefore, this study aims at investigating the role of severe chronic cerebral hypoperfusion (SCCH) in AD pathogenesis. For this purpose, SCCH was induced in young APPswe/PS1 in order to evaluate the progression of AD-like pathology in these mice. We observed that SCCH accelerated the cognitive decline of young APPswe/PS1 mice, which was associated with an increased amyloid plaque number in brain parenchyma. In addition, SCCH reduced the activity of extracellular signal-regulated kinases 1/2 (ERK1/2), which has been shown to play an important role in the adaptive responses of neurons. Importantly, SCCH impaired the function of microglial cells, which are implicated in amyloid-β (Aβ) elimination. In vitro approaches underlined the ability of a low-glucose microenvironment to decrease the general activity and phagocytic capacity of microglia. By using a new model of SCCH, our study unravels new insights into the implication of severe chronic cerebral hypoperfusion in AD pathogenesis, mainly by altering microglial cell activity and consequently Aβ clearance.
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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.