Evidence map›Paper›PMID 30594928›Full record

ArticleJournal of Alzheimer's disease : JAD2019

Cerebral Amyloid Angiopathy and Neuritic Plaque Pathology Correlate with Cognitive Decline in Elderly Non-Demented Individuals.

Michael Malek-Ahmadi, Kewei Chen, Sylvia E Perez, Elliott J Mufson

Open access · greenAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

  1. Cerebral proteome adaptations to amyloid angiopathy are prevented by carbonic anhydrase inhibitors.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  2. Article
  3. A New Hypothesis for Alzheimer's Disease: The Lipid Invasion Model.Journal of Alzheimer's disease reports · 2022
    Article
  4. Review
  5. Article
  6. Article
  7. Individualized clinical management of patients at risk for Alzheimer's dementia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2019
    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

4 authors at 2 institutions in 1 country.

Michael Malek-AhmadiBanner Alzheimer's Institute, Phoenix, AZ, USA.
Kewei ChenBanner Alzheimer's Institute, Phoenix, AZ, USA.
Sylvia E PerezDepartment of Neurobiology, Barrow Neurological Institute, Phoenix, AZ, USA.
Elliott J MufsonDepartment of Neurobiology, Barrow Neurological Institute, Phoenix, AZ, USA.
Banner Alzheimer’s InstituteBarrow Neurological Institute · US

Funding

SUPPLEMENT TO RUSH ALZHEIMERS DISEASE CENTER COREP30AG010161 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 1991 to 2020
$49.1M
TAU, AB, SYNUCLEIN AND NITRATIVE/OXIDATIVE DAMAGE IN MCIP01AG014449 · NIA · UNIVERSITY OF PITTSBURGH · PI IKONOMOVIC, MILOS D · 1997 to 2024
$39.7M
Cellular and Molecular Medial Temporal Lobe Pathology in Elderly PreMCI subjectsR01AG043375 · NIA · ST. JOSEPH'S HOSPITAL AND MEDICAL CENTER · PI GINSBERG, STEPHEN D, MUFSON, ELLIOTT JAY · 2013 to 2017
$3.6M
Neuroprotective microRNA pathwaysR21AG042146 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI COUNTS, SCOTT E · 2012 to 2013
$409k
NIA NIH HHS P01 AG014449NIA NIH HHS P30 AG010161NIA NIH HHS R01 AG043375NIA NIH HHS R21 AG042146
6 · The paper itself

Abstract

backgroundCerebral amyloid angiopathy (CAA) is a vascular neuropathology commonly reported in non-cognitively impaired (NCI), mild cognitive impairment, and Alzheimer's disease (AD) brains. However, it is unknown whether similar findings are present in non-demented elderly subjects.

objectiveThis study determined the association between CAA and cognition among elderly NCI subjects with varying levels of AD pathology.

methodsData from 182 cases that received a diagnosis of NCI at their first clinical assessment were obtained from the Rush Religious Orders study (RROS). A cognitive composite score was used to measure cognitive decline. CAA was dichotomized as present or absent. Cases were also dichotomized according to CERAD neuropathological diagnosis and Braak staging. A mixed model-repeated measures analysis assessed decline on the cognitive composite score.

resultsCAA, alone, was not associated with cognitive decline [-0.87 (95% CI: -3.33, 1.58), p = 0.49]. However, among those with CAA, the High CERAD group had significantly greater decline relative to the Low CERAD group [-4.08 (95% CI: -7.10, -1.06), p = 0.008]. The High and Low CERAD groups were not significantly different [-1.77 (95% CI: -6.14, 2.60), p = 0.43] in those without CAA. Composite score decline in the High and Low Braak groups with [-1.32 (95% CI: -4.40, 1.75), p = 0.40] or without [0.27 (95% CI: -4.01, 4.56), p = 0.90] CAA was not significantly different.

conclusionThe current data shows that an interaction between CAA and plaque load is associated with greater decline on a cognitive composite score used to test non-cognitively impaired elderly participants in AD prevention trials.

Indexed as

AgedAged, 80 and overCerebral Amyloid AngiopathyCognitionCognitive DysfunctionExecutive FunctionFemaleHumansMaleNeuritesNeuropsychological TestsPlaque, AmyloidAmyloiddementiaepisodic memoryexecutive functionneuropathologypreclinicalpreventionvascular

Identifiers

PMID30594928
PMCPMC7717643
OpenAlexW2907786298

What OpenQuestion holds

Textmetadata
LicenceTDM
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.