Evidence map›Paper›PMID 26756273›Full record

ReviewAmerican journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics2017

Genetics of psychosis of Alzheimer disease.

Chintan Shah, Mary Ann A DeMichele-Sweet, Robert A Sweet

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.9field-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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. GWAS links APOE to neuropsychiatric symptoms in mild cognitive impairment and dementia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  3. The neural signatures of psychoses in Alzheimer's disease: a neuroimaging genetics approach.European archives of psychiatry and clinical neuroscience · 2023
    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

3 authors at 2 institutions in 1 country.

Chintan ShahDepartment of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania.
Mary Ann A DeMichele-SweetDepartment of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania.
Robert A SweetDepartment of Psychiatry and Neurology, University of Pittsburgh, Pittsburgh, Pennsylvania.
University of Pittsburgh · USMental Illness Research, Education and Clinical Centers · US

Funding

TREATMENT OF DEPRESSION IN ALZHEIMER'S DISEASEP50AG005133 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KAMBOH, M. ILYAS · 1985 to 2019
$43.0M
Prediction of Psychosis in Alzheimer DiseaseR01AG027224 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SWEET, ROBERT A · 2007 to 2021
$10.8M
NIA NIH HHS P50 AG005133NIA NIH HHS R01 AG027224
6 · The paper itself

Abstract

Psychotic symptoms, comprised of delusions and hallucinations, occur in about half of individuals with Alzheimer disease (AD with psychosis, AD+P). These individuals have greater agitation, aggression, depression, functional impairment, and mortality than individuals without psychosis (AD-P). Although the exact etiopathogenesis of AD+P is unclear, the rapidly developing field of genomics continues to expand our understanding of this disease. Several independent studies have demonstrated familial aggregation and heritability of AD+P. Linkage studies have been suggestive of loci on several chromosomes associated with AD+P. Association studies examining apolipoprotein E gene, the best established genetic risk factor for late-onset AD, did not find any significant association of this gene with AD+P. Other candidate gene studies focusing on monoamine neurotransmitter systems have yielded equivocal results. A genome-wide association study and studies examining copy number variations recently have detected suggestive associations, but have been underpowered. Approaches to increase sizes of AD+P samples for genome wide association studies are discussed. © 2016 Wiley Periodicals, Inc.

Indexed as

AgedAlzheimer DiseaseApolipoproteins EDNA Copy Number VariationsFemaleGenetic LinkageGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMalePsychotic DisordersApolipoproteins EAlzheimer diseasegenome-wide associationheritabilitypsychosis

Identifiers

PMID26756273
PMCPMC5154859
OpenAlexW2236956758

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.