Evidence map›Paper›PMID 31177226›Full record

ArticleJournal of Alzheimer's disease : JAD2019

Disentangling Heterogeneity in Alzheimer's Disease: Two Empirically-Derived Subtypes.

Anna E Blanken, Shubir Dutt, Yanrong Li, Daniel A Nation, Alzheimer’s Disease Neuroimaging Initiative

Abstract read
PubMed Full text at PMC Publisher
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 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–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

9 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Heterogeneity in Alzheimer's Disease Diagnosis and Progression Rates: Implications for Therapeutic Trials.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
    Review
  6. Review
  7. Article
  8. Article
  9. 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.

Anna E BlankenDepartment of Psychology, University of Southern California, Los Angeles, CA, USA.
Shubir DuttDepartment of Psychology, University of Southern California, Los Angeles, CA, USA.
Yanrong LiDepartment of Psychology, University of Southern California, Los Angeles, CA, USA.
Daniel A NationDepartment of Psychology, University of Southern California, Los Angeles, CA, USA.
Alzheimer’s Disease Neuroimaging Initiative

Funding

VASCULAR RISK AND COGNITIVE STATUS IN A LATINO POPULATIONP50AG005142 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BRASKIE, MEREDITH NICOLE · 1985 to 2019
$41.0M
Vascular Contributions to Dementia and Genetic Risk Factors for Alzheimer's DiseaseP01AG052350 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ARTHUR W TOGA · 2016 to 2026
$28.4M
Vascular Reserve and Protective Mechanisms in Aging and Alzheimer’s Dementia RiskR21AG055034 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI NATION, DANIEL A · 2017 to 2018
$454k
NIA NIH HHS P01 AG052350NIA NIH HHS P50 AG005142NIA NIH HHS R21 AG055034
6 · The paper itself

Abstract

backgroundClinical-pathological Alzheimer's disease (AD) subtypes may help distill heterogeneity in patient presentation. To date, no studies have utilized neuropsychological and biological markers to identify preclinical subtypes with longitudinal stability.

objectiveThe objective of this study was to empirically derive AD endophenotypes using a combination of cognitive and biological markers.

methodsHierarchical cluster analysis grouped dementia-free older adults using memory, executive and language abilities, and cerebrospinal fluid amyloid-β and phosphorylated tau. Brain volume differences, neuropsychological trajectory, and progression to dementia were compared, controlling for age, gender, education, and apolipoprotein E4 (ApoE4).

resultsSubgroups included asymptomatic-normal (n = 653) with unimpaired cognition and subthreshold biomarkers, typical AD (TAD; n = 191) showing marked memory decline, high ApoE4 rates and abnormal biomarkers, and atypical AD (AAD; n = 132) with widespread cognitive decline, intermediate biomarker levels, older age, less education and more white matter lesions. Cognitive profiles showed longitudinal stability with corresponding patterns of cortical atrophy, despite nearly identical rates of progression to AD dementia.

conclusionTwo clinical-pathological AD subtypes are identified with potential implications for preventative efforts.

Indexed as

EndophenotypesAgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesBiomarkersBrainCognitionDisease ProgressionFemaleHumansMagnetic Resonance ImagingMaleNeuroimagingNeuropsychological TestsPeptide FragmentsAmyloid beta-PeptidesBiomarkersPeptide Fragmentstau ProteinsAlzheimer’s diseaseatypical ADcluster analysisheterogeneityneuroimaging

Identifiers

PMID31177226
PMCPMC8820245

What OpenQuestion holds

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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.