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High Systolic Blood Pressure Induces Cerebral Microvascular Endothelial Dysfunction, Neurovascular Unit Damage, and Cognitive Decline in Mice
de Montgolfier O, Pinçon A, Pouliot P, Gillis MA, Bishop J, Sled JG, Villeneuve L, Ferland G et al.. Hypertension (Dallas, Tex. : 1979), 2019-01-01
Topic: Brain proteins, microglia and lab models
A chronic and gradual increase in pulse pressure (PP) is associated with cognitive decline and dementia in older individuals, but the mechanisms remain ill-defined. We hypothesized that a chronic elevation of PP would cause brain microvascular endothelial mechanical stress, damage the neurovascular unit, and ultimately induce cognitive impairment in mice, potentially contributing to the progression of vascular dementia and Alzheimer disease. To test our hypothesis, male control wild-type mice and Alzheimer disease model APP/PS1 (amyloid precursor protein/presenilin 1) mice were exposed to a transverse aortic constriction for 6 weeks, creating a PP overload in the right carotid (ipsilateral).
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APA 7th
de Montgolfier, O., Pinçon, A., Pouliot, P., Gillis, M. A., Bishop, J., Sled, J. G., et al. (2019). High Systolic Blood Pressure Induces Cerebral Microvascular Endothelial Dysfunction, Neurovascular Unit Damage, and Cognitive Decline in Mice. Hypertension (Dallas, Tex. : 1979). https://doi.org/10.1161/hypertensionaha.118.12048
Vancouver
de Montgolfier O, Pinçon A, Pouliot P, Gillis MA, Bishop J, Sled JG, et al. High Systolic Blood Pressure Induces Cerebral Microvascular Endothelial Dysfunction, Neurovascular Unit Damage, and Cognitive Decline in Mice. Hypertension (Dallas, Tex. : 1979). 2019. doi:10.1161/hypertensionaha.118.12048. PMID: 30571552.
BibTeX
@article{demontgolfier2019-30571552,
author = {de Montgolfier, O. and Pinçon, A. and Pouliot, P. and Gillis, M. A. and Bishop, J. and Sled, J. G. and Villeneuve, L. and Ferland, G. and others},
title = {{High Systolic Blood Pressure Induces Cerebral Microvascular Endothelial Dysfunction, Neurovascular Unit Damage, and Cognitive Decline in Mice}},
journal = {Hypertension (Dallas, Tex. : 1979)},
year = {2019},
doi = {10.1161/hypertensionaha.118.12048},
pmid = {30571552},
url = {https://doi.org/10.1161/hypertensionaha.118.12048}
}
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Key findings
- We hypothesized that a chronic elevation of PP would cause brain microvascular endothelial mechanical stress, damage the neurovascular unit, and ultimately induce cognitive impairment in mice, potentially contributing to the progression of vascular dementia and Alzheimer disease.
- To test our hypothesis, male control wild-type mice and Alzheimer disease model APP/PS1 (amyloid precursor protein/presenilin 1) mice were exposed to a transverse aortic constriction for 6 weeks, creating a PP overload in the right carotid (ipsilateral).
- We show that the transverse aortic constriction procedure associated with high PP induces a cascade of vascular damages in the ipsilateral parenchymal microcirculation: in wild-type mice, it impairs endothelial dilatory and blood brain barrier functions and causes microbleeds, a reduction in microvascular density, microvascular cell death by apoptosis, leading to severe hypoperfusion and parenchymal cell senescence.
- These damages were associated with brain inflammation and a significant reduction in learning and spatial memories.
Why it matters
In mice, six weeks of high pulse pressure caused brain microvascular endothelial dysfunction, neurovascular unit damage, and cognitive decline in both wild-type and APP/PS1 mice. This is animal research and does not show a treatment, cure, or prevention for Alzheimer's disease in people.
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Study details
- Evidence strengthLow
How this study scored 45/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Hypertension (Dallas, Tex. : 1979)) |
| Journal's citation record | 3 / 4 | Hypertension: journal h-index 369 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 2 / 5 | 2019 — within 10 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Laboratory or animal study (title names “mice”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 112 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 12.4 citations a year over 9 year(s) since 2019 |
| Impact for its field and year | 3 / 6 | Cited 4.0× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 1 other studies in this library |
| Still being cited | 2 / 4 | Cited 36 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Éric Thorin: h-index 43 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of Toronto: institution h-index 1,923 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 7 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 30571552) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 45 / 100 | — |
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