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Hypertension induces brain β-amyloid accumulation, cognitive impairment, and memory deterioration through activation of receptor for advanced glycation end products in brain vasculature
Carnevale D, Mascio G, D'Andrea I, Fardella V, Bell RD, Branchi I, Pallante F, Zlokovic B et al.. Hypertension (Dallas, Tex. : 1979), 2012-05-21
Topic: Brain proteins, microglia and lab models
Although epidemiological data associate hypertension with a strong predisposition to develop Alzheimer disease, no mechanistic explanation exists so far. We developed a model of hypertension, obtained by transverse aortic constriction, leading to alterations typical of Alzheimer disease, such as amyloid plaques, neuroinflammation, blood-brain barrier dysfunction, and cognitive impairment, shown here for the first time. The aim of this work was to investigate the mechanisms involved in Alzheimer disease of hypertensive mice.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Carnevale, D., Mascio, G., D'Andrea, I., Fardella, V., Bell, R. D., Branchi, I., et al. (2012). Hypertension induces brain β-amyloid accumulation, cognitive impairment, and memory deterioration through activation of receptor for advanced glycation end products in brain vasculature. Hypertension (Dallas, Tex. : 1979). https://doi.org/10.1161/hypertensionaha.112.195511
Vancouver
Carnevale D, Mascio G, D'Andrea I, Fardella V, Bell RD, Branchi I, et al. Hypertension induces brain β-amyloid accumulation, cognitive impairment, and memory deterioration through activation of receptor for advanced glycation end products in brain vasculature. Hypertension (Dallas, Tex. : 1979). 2012. doi:10.1161/hypertensionaha.112.195511. PMID: 22615109.
BibTeX
@article{carnevale2012-22615109,
author = {Carnevale, D. and Mascio, G. and D'Andrea, I. and Fardella, V. and Bell, R. D. and Branchi, I. and Pallante, F. and Zlokovic, B. and others},
title = {{Hypertension induces brain β-amyloid accumulation, cognitive impairment, and memory deterioration through activation of receptor for advanced glycation end products in brain vasculature}},
journal = {Hypertension (Dallas, Tex. : 1979)},
year = {2012},
doi = {10.1161/hypertensionaha.112.195511},
pmid = {22615109},
url = {https://doi.org/10.1161/hypertensionaha.112.195511}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
Key findings
- We developed a model of hypertension, obtained by transverse aortic constriction, leading to alterations typical of Alzheimer disease, such as amyloid plaques, neuroinflammation, blood-brain barrier dysfunction, and cognitive impairment, shown here for the first time.
- The aim of this work was to investigate the mechanisms involved in Alzheimer disease of hypertensive mice.
- We focused on receptor for advanced glycation end products (RAGE) that critically regulates Aβ transport at the blood-brain barrier and could be influenced by vascular factors.
- The hypertensive challenge had an early and sustained effect on RAGE upregulation in brain vessels of the cortex and hippocampus.
Why it matters
This study in mice found that hypertension led to amyloid plaques, neuroinflammation, blood-brain barrier dysfunction, and cognitive impairment through activation of RAGE in brain blood vessels. This is animal research and does not yet show whether treating hypertension or targeting RAGE would prevent or treat Alzheimer's disease in people.
Study details
- Evidence strengthLow
How this study scored 48/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people 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 | 1 / 5 | 2012 — within 20 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 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 241 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 15.1 citations a year over 16 year(s) since 2012 |
| Impact for its field and year | 4 / 6 | Cited 9.7× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 12 other studies in this library |
| Still being cited | 2 / 4 | Cited 45 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Giuseppe Lembo: h-index 59 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of Southern California: institution h-index 1,521 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 6 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 22615109) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 48 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1161/hypertensionaha.112.195511
- PubMed: 22615109
- Original source →
- Free full text: Hypertension →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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