Evidence map›Paper›PMID 37085326›Full record

ArticleNeurology2023

Genetic Moderation of the Association of β-Amyloid With Cognition and MRI Brain Structure in Alzheimer Disease.

Philip S Insel, Atul Kumar, Oskar Hansson, Niklas Mattsson-Carlgren, Alzheimer's Disease Neuroimaging Initiative

Open access · hybridAbstract read
In one paragraph

Article in Neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Concomitant presence of a novel ARPP21 variant and CNVs in Chinese familial amyotrophic lateral sclerosis-frontotemporal dementia patients.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Article
  3. Review
  4. 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

5 authors at 2 institutions in 2 countries.

Philip S InselFrom the Clinical Memory Research Unit (P.S.I., A.K., O.H., N.M.-C.), Faculty of Medicine, Lund University, Sweden; Department of Psychiatry and Behavioral Sciences (P.S.I.), University of California, San Francisco; Memory Clinic (O.H.), Department of Neurology (N.M.-C.), Skåne University Hospital, and Wallenberg Center for Molecular Medicine (N.M.-C.), Lund University, Sweden. philip.insel@ucsf.edu.
Atul KumarFrom the Clinical Memory Research Unit (P.S.I., A.K., O.H., N.M.-C.), Faculty of Medicine, Lund University, Sweden; Department of Psychiatry and Behavioral Sciences (P.S.I.), University of California, San Francisco; Memory Clinic (O.H.), Department of Neurology (N.M.-C.), Skåne University Hospital, and Wallenberg Center for Molecular Medicine (N.M.-C.), Lund University, Sweden.
Oskar HanssonFrom the Clinical Memory Research Unit (P.S.I., A.K., O.H., N.M.-C.), Faculty of Medicine, Lund University, Sweden; Department of Psychiatry and Behavioral Sciences (P.S.I.), University of California, San Francisco; Memory Clinic (O.H.), Department of Neurology (N.M.-C.), Skåne University Hospital, and Wallenberg Center for Molecular Medicine (N.M.-C.), Lund University, Sweden.
Niklas Mattsson-CarlgrenFrom the Clinical Memory Research Unit (P.S.I., A.K., O.H., N.M.-C.), Faculty of Medicine, Lund University, Sweden; Department of Psychiatry and Behavioral Sciences (P.S.I.), University of California, San Francisco; Memory Clinic (O.H.), Department of Neurology (N.M.-C.), Skåne University Hospital, and Wallenberg Center for Molecular Medicine (N.M.-C.), Lund University, Sweden.ORCID 0000-0002-8885-7724
Alzheimer's Disease Neuroimaging Initiative
Lund University · SEUniversity of California, San Francisco · US

Funding

Alzheimer's Disease Neuroimaging Initiative - SupplementU01AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI WEINER, MICHAEL W · 2004 to 2015
$121.0M
RECRUITMENT COREU19AG010483 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FELDMAN, HOWARD · 2013 to 2020
$80.6M
Vascular factors, physical activity, and inflammation as modulators of neurodegenerative and cognitive trajectories (Project 2)P01AG036694 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI Hyun-Sik Yang · 2010 to 2026
$50.2M
Anti-Amyloid Treatment in Asymptomatic Alzheimer's Disease (A4) Open-Label Extension StudyR01AG063689 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI AISEN, PAUL S., SPERLING, REISA A. · 2019 to 2024
$30.8M
UC Davis Alzheimer's Disease Core CenterP30AG010129 · NIA · UNIVERSITY OF CALIFORNIA DAVIS · PI DECARLI, CHARLES · 1991 to 2020
$28.3M
Estimating Long-Term Disease Trajectories from Short-Term DataR01AG049750 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI DONOHUE, MICHAEL C · 2016 to 2019
$1.6M
"MR Morphometrics and Cognitive Decline Rate in Large-Scale Aging Studies"K01AG030514 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CARMICHAEL, OWEN T. · 2008 to 2012
$495k
NIA NIH HHS K01 AG030514NIA NIH HHS P01 AG036694NIA NIH HHS P30 AG010129NIA NIH HHS R01 AG049750NIA NIH HHS R01 AG063689NIA NIH HHS U01 AG024904NIA NIH HHS U19 AG010483
6 · The paper itself

Abstract

BACKGROUND AND

objectivesThere is considerable heterogeneity in the association between increasing β-amyloid (Aβ) pathology and early cognitive dysfunction in preclinical Alzheimer disease (AD). At this stage, some individuals show no signs of cognitive dysfunction, while others show clear signs of decline. The factors explaining this heterogeneity are particularly important for understanding progression in AD but remain largely unknown. In this study, we examined an array of genetic variants that may influence the relationships among Aβ, brain structure, and cognitive performance in 2 large cohorts.

methodsIn 2,953 cognitively unimpaired participants from the Anti-Amyloid Treatment in Asymptomatic Alzheimer disease (A4) study, interactions between genetic variants and 18F-Florbetapir PET standardized uptake value ratio (SUVR) to predict the Preclinical Alzheimer Cognitive Composite (PACC) were assessed. Genetic variants identified in the A4 study were evaluated in the Alzheimer Disease Neuroimaging Initiative (ADNI, N = 527) for their association with longitudinal cognition and brain atrophy in both cognitively unimpaired participants and those with mild cognitive impairment.

resultsIn the A4 study, 4 genetic variants significantly moderated the association between Aβ load and cognition. Minor alleles of 3 variants were associated with additional decreases in PACC scores with increasing Aβ SUVR (rs78021285, β = -2.29, SE = 0.40, DISCUSSION: Patterns of increased cognitive dysfunction and accelerated atrophy due to specific genetic variation may explain some of the heterogeneity in cognition in preclinical and prodromal AD. The genetic variant near

Indexed as

Alzheimer DiseaseCognitive DysfunctionAmyloid beta-PeptidesAtrophyBrainCognitionHumansMagnetic Resonance ImagingPositron-Emission TomographyAmyloid beta-Peptides

Identifiers

PMID37085326
PMCPMC10351305
OpenAlexW4366609292

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.