Evidence map›Paper›PMID 29480189›Full record

ArticleJournal of Alzheimer's disease : JAD2018

A Network of Genetic Effects on Non-Demented Cognitive Aging: Alzheimer's Genetic Risk (CLU + CR1 + PICALM) Intensifies Cognitive Aging Genetic Risk (COMT + BDNF) Selectively for APOEɛ4 Carriers.

Shraddha Sapkota, Roger A Dixon

Open access · greenAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. APOE ε4 carrier status moderates the effect of lifestyle factors on cognitive reserve.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  6. Article
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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

2 authors at 1 institution in 1 country.

Shraddha SapkotaNeuroscience and Mental Health Institute, University of Alberta, Edmonton, Canada.
Roger A DixonNeuroscience and Mental Health Institute, University of Alberta, Edmonton, Canada.
Women and Children’s Health Research Institute · CA

Funding

LONGITUDINAL STUDY OF COGNITIVE AGINGR01AG008235 · NIA · UNIVERSITY OF VICTORIA · PI DIXON, ROGER A · 1989 to 2017
$2.3M
CIHRNIA NIH HHS R01 AG008235
6 · The paper itself

Abstract

backgroundTrajectories of complex neurocognitive phenotypes in preclinical aging may be produced differentially through selective and interactive combinations of genetic risk.

objectiveWe organize three possible combinations into a "network" of genetic risk indices derived from polymorphisms associated with normal and impaired cognitive aging, as well as Alzheimer's disease (AD). Specifically, we assemble and examine three genetic clusters relevant to non-demented cognitive trajectories: 1) Apolipoprotein E (APOE), 2) a Cognitive Aging Genetic Risk Score (CA-GRS; Catechol-O-methyltransferase + Brain-derived neurotrophic factor), and 3) an AD-Genetic Risk Score (AD-GRS; Clusterin + Complement receptor 1 + Phosphatidylinositol-binding clathrin assembly protein).

methodWe use an accelerated longitudinal design (n = 634; age range = 55-95 years) to test whether AD-GRS (low versus high) moderates the effect of increasing CA-GRS risk on executive function (EF) performance and change as stratified by APOE status (ɛ4+ versus ɛ4-).

resultsAPOEɛ4 carriers with high AD-GRS had poorer EF performance at the centering age (75 years) and steeper 9-year decline with increasing CA-GRS but this association was not present in APOEɛ4 carriers with low AD-GRS.

conclusionsAPOEɛ4 carriers with high AD-GRS are at elevated risk of cognitive decline when they also possess higher CA-GRS risk. Genetic risk from both common cognitive aging and AD-related indices may interact in intensification networks to differentially predict (1) level and trajectories of EF decline and (2) potential selective vulnerability for transitions into impairment and dementia.

Indexed as

Cognitive AgingAgedAged, 80 and overAlzheimer DiseaseApolipoprotein E4Brain-Derived Neurotrophic FactorCanadaCatechol O-MethyltransferaseClusterinCognitive DysfunctionExecutive FunctionFemaleGenetic Predisposition to DiseaseHeterozygoteHumansLongitudinal StudiesApolipoprotein E4BDNF protein, humanBrain-Derived Neurotrophic FactorCatechol O-MethyltransferaseCLU protein, humanClusterinCOMT protein, humanCR1 protein, humanMonomeric Clathrin Assembly ProteinsPICALM protein, humanReceptors, Complement 3bAlzheimer’s diseaseApolipoprotein Ecognitive agingexecutive functiongenetic riskVictoria Longitudinal Study

Identifiers

PMID29480189
PMCPMC5830167
OpenAlexW2791802626

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.