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Cerebrovascular pathology in Down syndrome and Alzheimer disease
Head E, Phelan MJ, Doran E, Kim RC, Poon WW, Schmitt FA, Lott IT.. Acta neuropathologica communications, 2017-12-01
Topic: Amyloid, tau and blood-test diagnosis
Plain-language summary
People with Down syndrome (DS) are at high risk for developing Alzheimer disease (AD) with age. Typically, by age 40 years, most people with DS have sufficient neuropathology for an AD diagnosis. Interestingly, atherosclerosis and hypertension are atypical in DS with age, suggesting the lack of these vascular risk factors may be associated with reduced cerebrovascular pathology. However, because the extra copy of APP leads to increased beta-amyloid peptide (Aβ) accumulation in DS, we hypothesized that there would be more extensive and widespread cerebral amyloid angiopathy (CAA) with age in DS relative to sporadic AD. To test this hypothesis CAA, atherosclerosis and arteriolosclerosis were used as measures of cerebrovascular pathology and compared in post mortem tissue from individuals with DS (n = 32), sporadic AD (n = 80) and controls (n = 37). CAA was observed with significantly higher frequencies in brains of individuals with DS compared to sporadic AD and controls. Atherosclerosis and arteriolosclerosis were rare in the cases with DS. CAA in DS may be a target for future interventional clinical trials.
What this study adds
Evidence grade: Low
The record lists 32 participants. Comparing post mortem brain tissue, this study found cerebral amyloid angiopathy was significantly more frequent in people with Down syndrome than in sporadic Alzheimer's disease or controls, while atherosclerosis and arteriolosclerosis were rare in Down syndrome. The authors suggest cerebral amyloid angiopathy in Down syndrome may be a target for future clinical trials, but no intervention was tested.
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
Head, E., Phelan, M. J., Doran, E., Kim, R. C., Poon, W. W., Schmitt, F. A., et al. (2017). Cerebrovascular pathology in Down syndrome and Alzheimer disease. Acta neuropathologica communications. https://doi.org/10.1186/s40478-017-0499-4
Vancouver
Head E, Phelan MJ, Doran E, Kim RC, Poon WW, Schmitt FA, et al. Cerebrovascular pathology in Down syndrome and Alzheimer disease. Acta neuropathologica communications. 2017. doi:10.1186/s40478-017-0499-4. PMID: 29195510.
BibTeX
@article{head2017-29195510,
author = {Head, E. and Phelan, M. J. and Doran, E. and Kim, R. C. and Poon, W. W. and Schmitt, F. A. and Lott, I. T.},
title = {{Cerebrovascular pathology in Down syndrome and Alzheimer disease}},
journal = {Acta neuropathologica communications},
year = {2017},
doi = {10.1186/s40478-017-0499-4},
pmid = {29195510},
url = {https://doi.org/10.1186/s40478-017-0499-4}
}
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 names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- Interestingly, atherosclerosis and hypertension are atypical in DS with age, suggesting the lack of these vascular risk factors may be associated with reduced cerebrovascular pathology.
- CAA was observed with significantly higher frequencies in brains of individuals with DS compared to sporadic AD and controls.
Why it matters
Comparing post mortem brain tissue, this study found cerebral amyloid angiopathy was significantly more frequent in people with Down syndrome than in sporadic Alzheimer's disease or controls, while atherosclerosis and arteriolosclerosis were rare in Down syndrome. The authors suggest cerebral amyloid angiopathy in Down syndrome may be a target for future clinical trials, but no intervention was tested.
Study details
- Participants32
- Evidence strengthLow
How this study scored 51/100
Published in a peer-reviewed journal. Scored zero for study design, effect reported and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Acta neuropathologica communications) |
| Journal's citation record | 1 / 4 | Acta Neuropathologica Communications: journal h-index 129 (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 | 2017 — within 10 year(s) of the newest study here |
| Sample size | 1 / 4 | 32 participants |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 3 / 3 | Studied in people (participant count stated) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 105 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 9.5 citations a year over 11 year(s) since 2017 |
| Impact for its field and year | 3 / 6 | Cited 4.7× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 15 other studies in this library |
| Still being cited | 2 / 4 | Cited 49 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Ira T. Lott: h-index 58 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of California, Irvine: institution h-index 1,195 (OpenAlex) |
| Multicenter collaboration | 2 / 3 | PubMed indexes it as a multicentre study |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 29195510) |
| Free to read | 2 / 2 | Free to read |
| Total | 51 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1186/s40478-017-0499-4
- PubMed: 29195510
- Original source →
- Free full text: Acta Neuropathologica Communications →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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