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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Getting a diagnosis

Topic: Amyloid, tau and blood-test diagnosis

Cerebral amyloid angiopathy (CAA) may result from focal to widespread amyloid-β protein (Aβ) deposition within leptomeningeal and intracortical cerebral blood vessels. In addition, pericapillary Aβ refers to Aβ depositions in the glia limitans and adjacent neuropil, whereas in capillary CAA Aβ depositions are present in the capillary wall. CAA may cause lobar intracerebral haemorrhages and microbleeds. Hypoperfusion and reduced vascular autoregulation due to CAA might cause infarcts and white matter lesions. CAA thus causes vascular lesions that potentially lead to (vascular) dementia and may further contribute to dementia by impeding the clearance of solutes out of the brain and transport of nutrients across the blood brain barrier. Severe CAA is an independent risk factor for cognitive decline. The clinical diagnosis of CAA is based on the assessment of associated cerebrovascular lesions. In addition, perivascular spaces in the white matter and reduced concentrations of both Aβ(40) and Aβ(42) in cerebrospinal fluid may prove to be suggestive for CAA. Transgenic mouse models that overexpress human Aβ precursor protein show parenchymal Aβ and CAA, thus corroborating the current concept of CAA pathogenesis: neuronal Aβ enters the perivascular drainage pathway and may accumulate in vessel walls due to increased amounts and/or decreased clearance of Aβ, respectively. We suggest that pericapillary Aβ represents early impairment of the perivascular drainage pathway while capillary CAA is associated with decreased transendothelial clearance of Aβ. CAA plays an important role in the multimorbid condition of the ageing brain but its contribution to neurodegeneration remains to be elucidated.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Attems, J., Jellinger, K., Thal, D. R., & Van Nostrand, W. (2011). Review: sporadic cerebral amyloid angiopathy. Neuropathology and applied neurobiology. https://doi.org/10.1111/j.1365-2990.2010.01137.x

Vancouver

Attems J, Jellinger K, Thal DR, Van Nostrand W. Review: sporadic cerebral amyloid angiopathy. Neuropathology and applied neurobiology. 2011. doi:10.1111/j.1365-2990.2010.01137.x. PMID: 20946241.

BibTeX

@article{attems2011-20946241,
  author  = {Attems, J. and Jellinger, K. and Thal, D. R. and Van Nostrand, W.},
  title   = {{Review: sporadic cerebral amyloid angiopathy}},
  journal = {Neuropathology and applied neurobiology},
  year    = {2011},
  doi     = {10.1111/j.1365-2990.2010.01137.x},
  pmid    = {20946241},
  url     = {https://doi.org/10.1111/j.1365-2990.2010.01137.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

Why it matters

This review describes how cerebral amyloid angiopathy can cause vascular lesions that may lead to dementia and may contribute to dementia by impeding clearance of solutes and transport of nutrients across the blood brain barrier. It notes that severe cerebral amyloid angiopathy is an independent risk factor for cognitive decline, and suggests that pericapillary amyloid-β represents early impairment of the perivascular drainage pathway.

Study details

How this study scored 43/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 1 of 4; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 1 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomized / blinded 0 of 2; Times cited 6 of 7; Citations per year 4 of 5; Impact for its field and year 3 of 6; Cited by studies here 3 of 6; Still being cited 2 of 4; Senior author's track record 1 of 4; Institution's track record 1 of 3; Multicenter collaboration 1 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 43 of 100.43 of 100 points earned57 not earned

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.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Neuropathology and applied neurobiology)
Journal's citation record 1 / 4 Neuropathology and Applied Neurobiology: journal h-index 143 (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 2011 — 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 371 times (OpenAlex, 2026-10-10)
Citations per year 4 / 5 21.8 citations a year over 17 year(s) since 2011
Impact for its field and year 3 / 6 Cited 7.8× 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 48 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 1 / 4 Last-listed author William Van Nostrand: h-index 7 (OpenAlex, whole career)
Institution's track record 1 / 3 Stony Brook University: institution h-index 963 (OpenAlex)
Multicenter collaboration 1 / 3 OpenAlex lists 3 institution(s) in 3 countries
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 20946241)
Free to read 0 / 2 Behind a paywall — scores zero
Total 43 / 100 —

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