Home › Research › Biomarkers
Cerebral amyloid angiopathy: pathogenetic mechanisms and link to dense amyloid plaques
S Kumar-Singh. Genes, brain, and behavior, 2008-02
Topic: Disease mechanisms in lab and animal studies
Cerebral amyloid angiopathy (CAA) of the amyloid-beta (Abeta) type is the most common form of sporadic CAA and is now also accepted as an early and integral part of Alzheimer's disease (AD) pathogenesis. Cerebral amyloid angiopathy is a risk factor for haemorrhagic stroke and is believed to independently contribute to dementia. Rare forms of hereditary cerebral amyloidosis caused by mutations within the Abeta domain of amyloid precursor protein (APP) have been identified, where mutant Abeta preferably deposits in vessels because of a decreased fibrillogenic potential and/or increased vasotopicity. A review of factors involved in CAA caused by wild-type Abeta suggests that increased Abeta levels in brain without an increased Abeta42/Abeta40 ratio is one of the most important prerequisites for vascular amyloidosis. This is exemplified by CAA observed in APP duplication and Down's syndrome patients, neprilysin polymorphism patients and knockout mice and Swedish APP (KM670/671NL) mice. Select presenilin mutations also lead to a prominent CAA, and importantly, presenilin mutations are shown to have varied effects on the production of Abeta40, the predominant amyloid found in CAA. Conversely, APP mutations such as Austrian APP (T714I) drastically decrease Abeta40 production and are deficient in CAA. Apolipoprotein E-epsilon4 is also shown to be a risk factor for CAA, and this might be because of its specific role in the aggregation of Abeta40. Recent data also suggest that dense-core senile plaques in humans and dense plaques in transgenic mice, composed predominantly of Abeta40, associate with vessels. This review highlights some of these aspects of genetics and biochemistry of CAA and pathological descriptions linked to a prominent CAA and/or dense plaques in humans and relevant mouse models and discusses how this knowledge has led to a better understanding of the processes involved in vascular amyloidosis, and in causing dementia, and thus has important therapeutic implications.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Kumar-Singh, S. (2008). Cerebral amyloid angiopathy: pathogenetic mechanisms and link to dense amyloid plaques. Genes, brain, and behavior. https://doi.org/10.1111/j.1601-183x.2007.00380.x
Vancouver
Kumar-Singh S. Cerebral amyloid angiopathy: pathogenetic mechanisms and link to dense amyloid plaques. Genes, brain, and behavior. 2008. doi:10.1111/j.1601-183x.2007.00380.x. PMID: 18184371.
BibTeX
@article{kumarsingh2008-18184371,
author = {Kumar-Singh, S},
title = {{Cerebral amyloid angiopathy: pathogenetic mechanisms and link to dense amyloid plaques}},
journal = {Genes, brain, and behavior},
year = {2008},
doi = {10.1111/j.1601-183x.2007.00380.x},
pmid = {18184371},
url = {https://doi.org/10.1111/j.1601-183x.2007.00380.x}
}
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
- A review of factors involved in CAA caused by wild-type Abeta suggests that increased Abeta levels in brain without an increased Abeta42/Abeta40 ratio is one of the most important prerequisites for vascular amyloidosis.
- Recent data also suggest that dense-core senile plaques in humans and dense plaques in transgenic mice, composed predominantly of Abeta40, associate with vessels.
New to this subject? Start with our plain-English guide: Blood tests & biomarkers →
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 randomized / 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, multicenter 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 (Genes, brain, and behavior) |
| 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 | 2008 — 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 | — / 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 |
| Multicenter collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 18184371) |
| 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 | — |
What each of these 20 components measures, and what this score is not →
Read the original
Free copy unknown: no free-copy check has an answer for this record yet. That does not mean it is paywalled.
Related
Studies in the library that share something with this one. The line above each title says what.
Related studies in Biomarkers
Also tagged “presenilin”
344 studies in the library carry the topic tag “presenilin”; these are this study's neighbours in a fixed, alphabetical-by-hash tour of them, not the closest in content. All 344 tagged studies.