Evidence map›Paper›PMID 26189833›Full record

ArticleMolecular neurobiology2016

PLD3 in Alzheimer's Disease: a Modest Effect as Revealed by Updated Association and Expression Analyses.

Deng-Feng Zhang, Yu Fan, Dong Wang, Rui Bi, Chen Zhang, Yiru Fang, Yong-Gang Yao

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
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  12. National science review · 2019
    Article
  13. Genetic association of the cytochrome c oxidase-related genes with Alzheimer's disease in Han Chinese.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018
    Article
  14. 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

7 authors at 4 institutions in 1 country.

Deng-Feng ZhangKey Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences & Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, 650223, China.
Yu FanKey Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences & Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, 650223, China.
Dong WangKey Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences & Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, 650223, China.
Rui BiKey Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences & Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, 650223, China.
Chen ZhangDivision of Mood Disorders, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Yiru FangDivision of Mood Disorders, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Yong-Gang YaoKey Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences & Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, 650223, China. yaoyg@mail.kiz.ac.cn.
Kunming Institute of Zoology · CNShanghai Mental Health Center · CNUniversity of Chinese Academy of Sciences · CNChinese Academy of Sciences · CN

Funding

National Centralized Repository for Alzheimer's Disease and Related Dementias (NCRAD)U24AG021886 · NIA · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI TATIANA M. FOROUD · 2002 to 2026
$119.8M
NATIONAL ALZHEIMERS COORDINATING CENTER (NACC)U01AG016976 · NIA · UNIVERSITY OF WASHINGTON · PI KUKULL, WALTER ANTHONY · 1999 to 2020
$72.8M
Alzheimer's Disease Genetics ConsortiumU01AG032984 · NIA · UNIVERSITY OF PENNSYLVANIA · PI SCHELLENBERG, GERARD DAVID · 2009 to 2024
$60.4M
CHARGE Consortium: Omics Discovery for CVD and Aging PhenotypesR01HL105756 · NHLBI · UNIVERSITY OF WASHINGTON · PI Bruce M Psaty, NICHOLAS L SMITH · 2011 to 2026
$9.5M
Collaborative GWAS of Dementia, AD and related MRI and Cognitive EndophenotypesR01AG033193 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SESHADRI, SUDHA · 2009 to 2016
$4.4M
COLON CANCER SURVIVORS--MEDICATIONS &RISK OF RECURRENCER01CA081220 · NCI · HENRY FORD HEALTH SYSTEM · PI JOHNSON, CHRISTINE C · 2000 to 2004
$1.9M
AGES STUDY-THE REYKJAVIK STUDY OF HEALTHY AGING FOR THE NEW MILLENNIUM-26012100N01AG012100 · NIA · ICELANDIC HEART ASSOCIATION · 2002 to 2004
–
Medical Research Council 503480NCI NIH HHS R01 CA081220NHLBI NIH HHS R01 HL105756NIA NIH HHS N01 AG012100NIA NIH HHS R01 AG033193NIA NIH HHS U01 AG016976NIA NIH HHS U01 AG032984NIA NIH HHS U24 AG021886Wellcome Trust 082604/2/07/Z
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common form of dementia. Numerous genome-wide association studies (GWASs) have found several AD susceptibility common loci but with limited effect size. Recent next-generation sequencing studies of large AD pedigrees had identified phospholipase D3 (PLD3) p.V232M as the potentially functional rare variant with causal effect. However, four follow-up replication studies (Brief Communications Arising on Nature) questioned that PLD3 V232M might not be so important in AD. In this study, we re-analyzed all public-available genetic (rare and common variants) and expression data of PLD3, and screened coding variants within PLD3 in probands of 18 Han Chinese families with AD, to clarify the exact involvement of PLD3 in AD. Two closest homologues of PLD3, PLD1 and PLD2, were also analyzed to comprehensively understand the role of phospholipase D members in AD. We found that PLD3 variant V232M was associated with AD risk in overall sample sets (∼40,000 subjects) with a modest to moderate effect size (odds ratio [OR] = 1.53). Our results also showed that common variants and mRNA expression alterations of PLD2 play a role in AD genetic risk and pathology. Although we provided a systematic view of the involvement of PLD3 in AD at the genetic, mRNA expression, and protein levels, we could not define the exact causal or essential role of PLD3 rare variants in AD based on currently available data.

Indexed as

Gene Expression RegulationGenetic Predisposition to DiseaseGenome-Wide Association StudyAlzheimer DiseaseAmino Acid SequenceAsian PeopleBrainConserved SequenceEthnicityExodeoxyribonucleasesHumansMeta-Analysis as TopicModels, GeneticMutationPhospholipase DProtein Structure, SecondaryExodeoxyribonucleasesPhospholipase Dphospholipase D2PLD3 protein, humanAlzheimer’s diseaseCommon variantMeta-analysisPLD3Rare variant

Identifiers

PMID26189833
OpenAlexW962033880

What OpenQuestion holds

Textmetadata
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.