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49/100

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Genetics

Topic: Brain proteins, microglia and lab models

The APOE-ε4 allele correlates with increased risk of Alzheimer disease (AD) and increased parenchymal amyloid plaques. We tested how the APOE genotype correlated with cerebral amyloid angiopathy (CAA) by analyzing 371 brains for parenchymal and meningeal CAA in 4 brain regions (frontal, parietal, temporal, and occipital neocortex). The overall severity of CAA was highest in the occipital lobe. APOE-ε4/4 brains (n = 22) had the highest levels of CAA across regions. In the occipital lobe, nearly all APOE-ε4/4 cases were scored with the highest level of CAA (meninges, 95% of cases; parenchyma, 81%). In this brain region as in others, APOE-ε3/4 brains (n = 115) showed consistently less CAA than APOE-ε4/4 brains (meninges, 43%; parenchyma, 43%). APOE-ε3/3 brains (n = 182) showed even less CAA (meninges, 19%; parenchyma, 19%). Interestingly, APOE-ε2/3 cases (n = 42) had more CAA than APOE-ε3/3 (meninges, 44%; parenchyma, 32%), despite a reduced risk for AD in the APOE-ε2/3 individuals. APOE-ε4/4 brains also had the fewest regions without CAA, whereas APOE-ε3/3 brains had the most. Ordinal regression analyses demonstrated significant impacts of APOE-ε2 and APOE-ε4 on CAA at least in some brain regions. These data demonstrate that APOE genotype correlations with Aβ deposition in CAA only incompletely correspond to other AD-linked brain pathologies.

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APA 7th

Nelson, P. T., Pious, N. M., Jicha, G. A., Wilcock, D. M., Fardo, D. W., Estus, S., et al. (2013). APOE-ε2 and APOE-ε4 correlate with increased amyloid accumulation in cerebral vasculature. Journal of neuropathology and experimental neurology. https://doi.org/10.1097/nen.0b013e31829a25b9

Vancouver

Nelson PT, Pious NM, Jicha GA, Wilcock DM, Fardo DW, Estus S, et al. APOE-ε2 and APOE-ε4 correlate with increased amyloid accumulation in cerebral vasculature. Journal of neuropathology and experimental neurology. 2013. doi:10.1097/nen.0b013e31829a25b9. PMID: 23771217.

BibTeX

@article{nelson2013-23771217,
  author  = {Nelson, P. T. and Pious, N. M. and Jicha, G. A. and Wilcock, D. M. and Fardo, D. W. and Estus, S. and Rebeck, G. W.},
  title   = {{APOE-ε2 and APOE-ε4 correlate with increased amyloid accumulation in cerebral vasculature}},
  journal = {Journal of neuropathology and experimental neurology},
  year    = {2013},
  doi     = {10.1097/nen.0b013e31829a25b9},
  pmid    = {23771217},
  url     = {https://doi.org/10.1097/nen.0b013e31829a25b9}
}

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

The APOE-ε4 allele correlates with increased risk of Alzheimer disease (AD) and increased parenchymal amyloid plaques.
The overall severity of CAA was highest in the occipital lobe.
Ordinal regression analyses demonstrated significant impacts of APOE-ε2 and APOE-ε4 on CAA at least in some brain regions.

Why it matters

In 371 autopsied brains, amyloid in blood-vessel walls (cerebral amyloid angiopathy) was worst in people with two copies of APOE-ε4: in the occipital lobe, 95% of these 22 brains had the highest meningeal score, against 19% of APOE-ε3/3 brains. Unexpectedly, APOE-ε2/3 brains, a genotype linked to lower Alzheimer's risk, had more of this vessel amyloid than ε3/3 (44% vs 19% in the occipital meninges). The authors conclude that APOE's link to vessel amyloid only partly matches its link to other Alzheimer's brain changes; this is an association study of post-mortem tissue, not a test of risk or treatment.

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Study details

Participants22
Evidence strengthLow

How this study scored 49/100

Published in a peer-reviewed journal. Scored zero for study design, effect reported and randomised / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Journal of neuropathology and experimental neurology)
Journal's citation record	2 / 4	Journal of Neuropathology & Experimental Neurology: journal h-index 239 (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	2013 — within 20 year(s) of the newest study here
Sample size	1 / 4	22 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)
Randomised / blinded	0 / 2	No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	5 / 7	Cited 150 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	10.0 citations a year over 15 year(s) since 2013
Impact for its field and year	3 / 6	Cited 4.8× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	3 / 6	Cited by 11 other studies in this library
Still being cited	3 / 4	Cited 53 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	3 / 4	Last-listed author George William Rebeck: h-index 74 (OpenAlex, whole career)
Institution's track record	1 / 3	University of Kentucky: institution h-index 824 (OpenAlex)
Multi-centre collaboration	1 / 3	OpenAlex lists 2 institution(s) in 1 country
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 23771217)
Free to read	0 / 2	Behind a paywall — scores zero
Total	49 / 100	—

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