Evidence map›Paper›PMID 30692199›Full record

ArticleThe Journal of biological chemistry2019

Reduction of the expression of the late-onset Alzheimer's disease (AD) risk-factor

Robert J Andrew, Pierre De Rossi, Phuong Nguyen, Haley R Kowalski, Aleksandra J Recupero, Thomas Guerbette, Sofia V Krause, Richard C Rice, Lisa Laury-Kleintop, Steven L Wagner and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

29 citing papers in PubMed, 69 citations in OpenAlex.

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  8. Cell type-specific functions of Alzheimer's disease endocytic risk genes.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
    Review
  9. BIN1Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    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

11 authors at 3 institutions in 1 country.

Robert J AndrewFrom the Department of Neurobiology, The University of Chicago, Chicago, Illinois, 60637.
Pierre De RossiFrom the Department of Neurobiology, The University of Chicago, Chicago, Illinois, 60637.
Phuong NguyenDepartment of Neurosciences, University of California, San Diego, La Jolla, California, 92093.
Haley R KowalskiFrom the Department of Neurobiology, The University of Chicago, Chicago, Illinois, 60637.
Aleksandra J RecuperoFrom the Department of Neurobiology, The University of Chicago, Chicago, Illinois, 60637.
Thomas GuerbetteFrom the Department of Neurobiology, The University of Chicago, Chicago, Illinois, 60637.
Sofia V KrauseFrom the Department of Neurobiology, The University of Chicago, Chicago, Illinois, 60637.
Richard C RiceFrom the Department of Neurobiology, The University of Chicago, Chicago, Illinois, 60637.
Lisa Laury-KleintopLankenau Institute for Medical Research, Wynnewood, Pennsylvania, 19096.
Steven L WagnerDepartment of Neurosciences, University of California, San Diego, La Jolla, California, 92093.
Gopal ThinakaranFrom the Department of Neurobiology, The University of Chicago, Chicago, Illinois, 60637, gopal@uchicago.edu.ORCID 0000-0001-5523-6780
University of Chicago · USUniversity of California San Diego · USLankenau Institute for Medical Research · US

Funding

The role of elevated BIN1 expression in Alzheimer's diseaseRF1AG056061 · NIA · UNIVERSITY OF SOUTH FLORIDA · PI THINAKARAN, GOPAL · 2018 to 2018
$3.7M
Cell autonomous and non-cell autonomous roles of the GWAS risk factor BIN1 in Alzheimer's disease neuropathologyRF1AG054223 · NIA · UNIVERSITY OF SOUTH FLORIDA · PI THINAKARAN, GOPAL · 2016 to 2016
$2.9M
Multi-purpose Superresolution Microscope for Core FacilityS10OD010649 · OD · UNIVERSITY OF CHICAGO · PI THINAKARAN, GOPAL · 2012 to 2012
$511k
NIA NIH HHS RF1 AG054223NIA NIH HHS RF1 AG056061NIH HHS S10 OD010649
6 · The paper itself

Abstract

Alzheimer's disease (AD) is pathologically characterized by the deposition of the β-amyloid (Aβ) peptide in senile plaques in the brain, leading to neuronal dysfunction and eventual decline in cognitive function. Genome-wide association studies have identified the

Indexed as

Genetic Predisposition to DiseaseAdaptor Proteins, Signal TransducingAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAnimalsAspartic Acid EndopeptidasesBrainDisease Models, AnimalEndocytosisEndosomesFemaleHumansMaleMiceAdaptor Proteins, Signal TransducingAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesBace1 protein, mouseBin1 protein, mouseNerve Tissue ProteinsTumor Suppressor Proteins5XFADAlzheimer diseaseamphiphysinamyloidamyloid precursor protein (APP)APPBACE1beta-amyloid (AB)beta-secretase 1 (BACE1)BIN1endocytosisGWASneurodegenerationpathogenesissecretase

Identifiers

PMID30692199
PMCPMC6433054
OpenAlexW2914475876

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.