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Neurovascular mechanisms and blood-brain barrier disorder in Alzheimer's disease
Bell RD, Zlokovic BV.. Acta neuropathologica, 2009-03-25
Topic: Amyloid, tau and blood-test diagnosis
Plain-language summary
Vascular dysfunction has a critical role in Alzheimer's disease (AD). Recent data from brain imaging studies in humans and animal models suggest that cerebrovascular dysfunction may precede cognitive decline and onset of neurodegenerative changes in AD and AD models. Cerebral hypoperfusion and impaired amyloid beta-peptide (Abeta) clearance across the blood-brain barrier (BBB) may contribute to the onset and progression of dementia AD type.
What this study adds
Evidence grade: Low
This is a narrative review. This review describes evidence that cerebrovascular dysfunction, including cerebral hypoperfusion and impaired amyloid-beta clearance across the blood-brain barrier, may precede cognitive decline and contribute to the onset and progression of Alzheimer's disease. It proposes mechanisms for future investigation but reports no treatment, cure or prevention.
Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Bell, R. D., & Zlokovic, B. V. (2009). Neurovascular mechanisms and blood-brain barrier disorder in Alzheimer's disease. Acta neuropathologica. https://doi.org/10.1007/s00401-009-0522-3
Vancouver
Bell RD, Zlokovic BV. Neurovascular mechanisms and blood-brain barrier disorder in Alzheimer's disease. Acta neuropathologica. 2009. doi:10.1007/s00401-009-0522-3. PMID: 19319544.
BibTeX
@article{bell2009-19319544,
author = {Bell, R. D. and Zlokovic, B. V.},
title = {{Neurovascular mechanisms and blood-brain barrier disorder in Alzheimer's disease}},
journal = {Acta neuropathologica},
year = {2009},
doi = {10.1007/s00401-009-0522-3},
pmid = {19319544},
url = {https://doi.org/10.1007/s00401-009-0522-3}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- Recent data from brain imaging studies in humans and animal models suggest that cerebrovascular dysfunction may precede cognitive decline and onset of neurodegenerative changes in AD and AD models.
- Cerebral hypoperfusion and impaired amyloid beta-peptide (Abeta) clearance across the blood-brain barrier (BBB) may contribute to the onset and progression of dementia AD type.
- Decreased cerebral blood flow (CBF) negatively affects the synthesis of proteins required for memory and learning, and may eventually lead to neuritic injury and neuronal death.
- Impaired clearance of Abeta from the brain by the cells of the neurovascular unit may lead to its accumulation on blood vessels and in brain parenchyma.
Why it matters
This review describes evidence that cerebrovascular dysfunction, including cerebral hypoperfusion and impaired amyloid-beta clearance across the blood-brain barrier, may precede cognitive decline and contribute to the onset and progression of Alzheimer's disease. It proposes mechanisms for future investigation but reports no treatment, cure or prevention.
Study details
- Evidence strengthLow
How this study scored 53/100
Published in a leading specialty journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Acta neuropathologica) |
| Journal's citation record | 3 / 4 | Acta Neuropathologica: journal h-index 287 (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 | 2009 — 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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 865 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 45.5 citations a year over 19 year(s) since 2009 |
| Impact for its field and year | 5 / 6 | Cited 35.3× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 19 other studies in this library |
| Still being cited | 3 / 4 | Cited 78 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Berislav V. Zloković: h-index 118 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Rochester: institution h-index 1,195 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 19319544) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 53 / 100 | — |
What each of these 20 components measures, and what this score is not →
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