Evidence map›Paper›PMID 33617650›Full record

ArticleJournal of neuropathology and experimental neurology2021

Vascular Lesions, APOE ε4, and Tau Pathology in Alzheimer Disease.

Jodie B Nichols, Michael Malek-Ahmadi, Pierre N Tariot, Geidy E Serrano, Lucia I Sue, Thomas G Beach

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neuropathology and experimental neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. How does type 2 diabetes modify the risk of Alzheimer's disease?Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  3. Article
  4. Article
  5. The influence of APOEActa neuropathologica · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Significance of cerebral amyloid angiopathy and other co-morbidities in Lewy body diseases.Journal of neural transmission (Vienna, Austria : 1996) · 2021
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Jodie B NicholsFrom the Arizona College of Osteopathic Medicine, Midwestern University, Glendale, Arizona, USA.
Michael Malek-AhmadiBanner Alzheimer's Institute, Phoenix, Arizona, USA.
Pierre N TariotBanner Alzheimer's Institute, Phoenix, Arizona, USA.
Geidy E SerranoBanner Sun Health Research Institute, Sun City, Arizona, USA.
Lucia I SueBanner Sun Health Research Institute, Sun City, Arizona, USA.
Thomas G BeachBanner Sun Health Research Institute, Sun City, Arizona, USA.
Banner Sun Health Research Institute · USAlzheimer's Association · USMidwestern University · US

Funding

Research Education ComponentP30AG019610 · NIA · SUN HEALTH RESEARCH INSTITUTE · PI GONZALEZ HERNANDEZ, GRACIELA · 2001 to 2020
$32.5M
National Brain and Tissue Resource for Parkinson's Disease and Related DisordersU24NS072026 · NINDS · BANNER SUN HEALTH RESEARCH INSTITUTE · PI BEACH, THOMAS G · 2011 to 2015
$7.8M
NIA NIH HHS P30 AG019610NINDS NIH HHS U24 NS072026
6 · The paper itself

Abstract

We sought to determine the associations among cerebral amyloid angiopathy (CAA), white matter rarefaction (WMR), circle of Willis atherosclerosis (CWA), and total microinfarct number with Braak neurofibrillary stage in postmortem individuals with and without Alzheimer disease (AD). Data from 355 cases of autopsied individuals with Braak stage I-VI who had antemortem consensus diagnoses of cognitively unimpaired (n = 183), amnestic mild cognitive impairment (n = 31), and AD dementia (n = 141) were used. The association between Braak stage and vascular lesions were individually assessed using multivariable linear regression that adjusted for age at death, APOE ε4 carrier status, sex, education, and neuritic plaque density. CAA (p = 0.007) and WMR (p < 0.001) were associated with Braak stage, independent of amyloid load; microinfarct number and CWA showed no association. Analyses of the interactions between APOE ε4 carrier status and vascular lesions found that greater WMR and positive ε4 carrier status were associated with higher Braak stages. These results suggest that CAA and WMR are statistically linked to the severity of AD-related NFT pathology. The statistical link between WMR and NFT load may be strengthened by the presence of APOE ε4 carrier status. An additional finding was that Lewy body pathology was most prevalent in higher Braak stages.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseApolipoprotein E4Circle of WillisDatabases, FactualFemaleHeterozygoteHumansMaletau ProteinsVascular DiseasesApolipoprotein E4MAPT protein, humantau ProteinsBraak stageCerebral amyloid angiopathyMild cognitive impairmentNeurofibrillary tanglesWhite matter rarefaction

Identifiers

PMID33617650
PMCPMC7899190
OpenAlexW3131445577

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.