Evidence map›Paper›PMID 25249975›Full record

ArticleFrontiers in aging neuroscience2014

APOE and COMT polymorphisms are complementary biomarkers of status, stability, and transitions in normal aging and early mild cognitive impairment.

Roger A Dixon, Correne A DeCarlo, Stuart W S MacDonald, David Vergote, Jack Jhamandas, David Westaway

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Article in Frontiers in aging neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

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

  1. Pooled it
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  4. IBRO reports · 2019
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  10. Memory Resilience to Alzheimer's Genetic Risk: Sex Effects in Predictor Profiles.The journals of gerontology. Series B, Psychological sciences and social sciences · 2017
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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

6 authors.

Roger A DixonDepartment of Psychology, University of Alberta Edmonton, AB, Canada ; Neuroscience and Mental Health Institute, University of Alberta Edmonton, AB, Canada.
Correne A DeCarloDepartment of Psychology, University of Victoria Victoria, BC, Canada.
Stuart W S MacDonaldDepartment of Psychology, University of Victoria Victoria, BC, Canada.
David VergoteCentre for Prions and Protein Folding Diseases, University of Alberta Edmonton, AB, Canada.
Jack JhamandasNeuroscience and Mental Health Institute, University of Alberta Edmonton, AB, Canada ; Department of Medicine (Neurology), University of Alberta Edmonton, AB, Canada.
David WestawayNeuroscience and Mental Health Institute, University of Alberta Edmonton, AB, Canada ; Centre for Prions and Protein Folding Diseases, University of Alberta Edmonton, AB, Canada.

Funding

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

Abstract

objectiveResearch has reported associations among selected genetic susceptibility biomarkers and risk of (a) normal cognitive aging decrements, (b) established mild cognitive impairment (MCI), and (c) sporadic Alzheimer's disease (AD). In focusing on the transitional normal-to-early MCI phase, we examine associations among three theoretically relevant polymorphisms (APOE [rs429358, rs7412], BDNF [rs6265], COMT [rs4680]) and both baseline cognitive status (MCI vs. normal aging) and two-wave (four-year) longitudinal stability or change profiles. The latter included three profiles: (a) stable as normal aging, (b) stable or chronic impairment (MCI-to-MCI), and (c) emergence of impairment (normal-to-MCI).

methodGenotyped older adults (n = 237 at baseline; age range = 64-91; 62% women) from the Victoria Longitudinal Study were examined for (a) independent and interactive associations of three genetic polymorphisms with (b) two objectively classified cognitive status groups (not-impaired controls (NIC) and MCI) at (c) both baseline and across a two-wave (four-year) longitudinal interval.

resultsFirst, logistic regression revealed that the presence of at least one APOE ε4 allele (the risk factor for AD) was linked to greater baseline risk of objective MCI. Second, multinomial logistic regression revealed that (a) the presence of an APOE ε4 allele was associated with an increased risk of 4-year MCI status stability (chronicity), and (b) the COMT homozygous risk genotype (G/G or Val/Val) was associated with an increased risk of both MCI-to-MCI stability (chronicity) and emerging NIC-to-MCI conversion. DISCUSSION: Both chronicity and emergence of objectively classified early cognitive impairment may be genetically heterogeneous phenomena, with influences from a panel of both normal cognitive aging (COMT) and AD-related (APOE) polymorphisms.

Indexed as

APOEBDNFCOMTmild cognitive impairmentVictoria Longitudinal Study

Identifiers

PMID25249975
PMCPMC4155788

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LicenceCC BY
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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.