Evidence map›Paper›PMID 24951455›Full record

ReviewBiological psychiatry2015

Alzheimer's disease risk genes and mechanisms of disease pathogenesis.

Celeste M Karch, Alison M Goate

Open access · greenAbstract readReview
In one paragraph

Review in Biological psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 765 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
765citing papers in PubMed, 3 pooled it
38.2field-weighted citation impact, top 1% 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

765 citing papers in PubMed, 3 syntheses or guidelines pooled it, 1,338 citations in OpenAlex.

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705 more citing papers are in PubMed but not listed here.

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.

Celeste M KarchDepartment of Psychiatry and Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, Missouri.
Alison M GoateDepartment of Psychiatry and Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, Missouri. Electronic address: goatea@psychiatry.wustl.edu.
Hope Center for Neurological Disorders · US

Funding

WASHINGTON UNIVERSITY ALZHEIMERS DISEASE RESEARCH CENTERP50AG005681 · NIA · WASHINGTON UNIVERSITY · PI MORRIS, JOHN · 1985 to 2019
$52.1M
Imaging CoreU01AG032438 · NIA · WASHINGTON UNIVERSITY · PI MORRIS, JOHN · 2008 to 2009
$6.1M
Use of Endophenotypes in the Search for Alzheimer's Disease Risk GenesR01AG035083 · NIA · WASHINGTON UNIVERSITY · PI GOATE, ALISON M · 2010 to 2014
$2.3M
GENETIC DISRUPTION OF TAU METABOLISM IN TAUOPATHIESK01AG046374 · NIA · WASHINGTON UNIVERSITY · PI KARCH, CELESTE MARIE · 2014 to 2018
$568k
Medical Research Council G0800509Medical Research Council G0801418NIA NIH HHS K01 AG046374NIA NIH HHS P50 AG005681NIA NIH HHS R01 AG035083NIA NIH HHS U01 AG032438Wellcome Trust 503147Wellcome Trust G0801418
6 · The paper itself

Abstract

We review the genetic risk factors for late-onset Alzheimer's disease (AD) and their role in AD pathogenesis. More recent advances in understanding of the human genome-technologic advances in methods to analyze millions of polymorphisms in thousands of subjects-have revealed new genes associated with AD risk, including ABCA7, BIN1, CASS4, CD33, CD2AP, CELF1, CLU, CR1, DSG2, EPHA1, FERMT2, HLA-DRB5-DBR1, INPP5D, MS4A, MEF2C, NME8, PICALM, PTK2B, SLC24H4-RIN3, SORL1, and ZCWPW1. Emerging technologies to analyze the entire genome in large data sets have also revealed coding variants that increase AD risk: PLD3 and TREM2. We review the relationship between these AD risk genes and the cellular and neuropathologic features of AD. Understanding the mechanisms underlying the association of these genes with risk for disease will provide the most meaningful targets for therapeutic development to date.

Indexed as

Genetic Predisposition to DiseaseAlzheimer DiseaseAmyloid beta-Protein PrecursorCholesterolEndocytosisGenome-Wide Association StudyHumansPhenotypePresenilin-1Presenilin-2Risk FactorsAmyloid beta-Protein PrecursorCholesterolPresenilin-1Presenilin-2PSEN1 protein, humanPSEN2 protein, humanAlzheimer’s DiseaseAmyloid Precursor ProteinCholesterol MetabolismEndocytosisGenome-Wide Association StudiesImmune Response

Identifiers

PMID24951455
PMCPMC4234692
OpenAlexW1999794509

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.