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Cerebral autoregulation, beta amyloid, and white matter hyperintensities are interrelated
Adam M Brickman, Vanessa A Guzman, Miguel Gonzalez-Castellon, Qolamreza Razlighi, Yian Gu, Atul Narkhede, Sarah Janicki, Masanori Ichise et al.. Neuroscience letters, 2015-03-04
Topic: Plasma and spinal-fluid biomarkers
Emerging studies link vascular risk factors and cerebrovascular health to the prevalence and rates of progression in Alzheimer's disease (AD). The brain's ability to maintain constant blood flow across a range of cerebral perfusion pressures, or autoregulation, may both promote and result from small vessel cerebrovascular disease and AD-related amyloid pathology. Here, we examined the relationship among cerebral autoregulation, small vessel cerebrovascular disease, and amyloid deposition in 14 non-demented older adults. Reduced cerebral autoregulation, was associated with increased amyloid deposition and increased white matter hyperintensity volume, which, in turn were positively associated with each other. For the first time in humans, we demonstrate an interrelationship among AD pathology, small vessel cerebrovascular disease, and cerebral autoregulation. Vascular factors and AD pathology are not independent but rather appear to interact.
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APA 7th
Brickman, A. M., Guzman, V. A., Gonzalez-Castellon, M., Razlighi, Q., Gu, Y., Narkhede, A., et al. (2015). Cerebral autoregulation, beta amyloid, and white matter hyperintensities are interrelated. Neuroscience letters. https://doi.org/10.1016/j.neulet.2015.03.005
Vancouver
Brickman AM, Guzman VA, Gonzalez-Castellon M, Razlighi Q, Gu Y, Narkhede A, et al. Cerebral autoregulation, beta amyloid, and white matter hyperintensities are interrelated. Neuroscience letters. 2015. doi:10.1016/j.neulet.2015.03.005. PMID: 25748319.
BibTeX
@article{brickman2015-25748319,
author = {Brickman, Adam M and Guzman, Vanessa A and Gonzalez-Castellon, Miguel and Razlighi, Qolamreza and Gu, Yian and Narkhede, Atul and Janicki, Sarah and Ichise, Masanori and others},
title = {{Cerebral autoregulation, beta amyloid, and white matter hyperintensities are interrelated}},
journal = {Neuroscience letters},
year = {2015},
doi = {10.1016/j.neulet.2015.03.005},
pmid = {25748319},
url = {https://doi.org/10.1016/j.neulet.2015.03.005}
}
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Key findings
- The brain's ability to maintain constant blood flow across a range of cerebral perfusion pressures, or autoregulation, may both promote and result from small vessel cerebrovascular disease and AD-related amyloid pathology.
- Reduced cerebral autoregulation, was associated with increased amyloid deposition and increased white matter hyperintensity volume, which, in turn were positively associated with each other.
Study details
- Evidence strengthLow
How this study scored 38/100
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. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record, multi-centre collaboration and free to read, so those were left out: it earned 21 of the 56 points we could judge it on, which is 38 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neuroscience letters) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| 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 | 2015 — 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 | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 25748319) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 21 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 21 of the 56 points we could judge it on is 38 out of 100. |
| Total | 38 / 100 | — |
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