Evidence map›Paper›PMID 28733667›Full record

ArticleScientific reports2017

RTN1 and RTN3 protein are differentially associated with senile plaques in Alzheimer's brains.

Qi Shi, Yingying Ge, Wanxia He, Xiangyou Hu, Riqiang Yan

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
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  16. The dense-core plaques of Alzheimer's disease are granulomas.The Journal of experimental medicine · 2022
    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

5 authors at 1 institution in 1 country.

Qi ShiDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.
Yingying GeDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.
Wanxia HeDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.
Xiangyou HuDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.
Riqiang YanDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA. yanr@ccf.org.
Cleveland Clinic Lerner College of Medicine · US

Funding

Roles of reticulon proteins in neurodegenerative disordersR01AG025493 · NIA · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI YAN, RIQIANG · 2005 to 2024
$5.9M
Supplement for BACE1 in neurodegeneration and neuronal dysfunctionR01NS074256 · NINDS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI RIQIANG YAN · 2011 to 2026
$5.8M
Inhibition of BACE1 for benefiting Alzheimer's patientsR01AG046929 · NIA · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI RIQIANG YAN · 2013 to 2026
$3.9M
Inhibition of BACE1 for benefiting Alzheimer's patientsRF1AG046929 · NIA · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI YAN, RIQIANG · 2018 to 2018
$3.3M
Roles of reticulon proteins in neurodegenerative disordersRF1AG025493 · NIA · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI YAN, RIQIANG · 2020 to 2020
$3.0M
BACE1 in neurodegeneration and neurological dysfunctionRF1NS074256 · NINDS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI YAN, RIQIANG · 2021 to 2021
$2.1M
NIA NIH HHS R01 AG025493NIA NIH HHS R01 AG046929NIA NIH HHS RF1 AG025493NIA NIH HHS RF1 AG046929NINDS NIH HHS R01 NS074256NINDS NIH HHS RF1 NS074256
6 · The paper itself

Abstract

Reticulon proteins (RTNs), consisting of RTN1 to RTN4, were previously shown to interact with BACE1 by negatively modulating its secretase activity. In RTN3-null mice, RTN1 expression was slightly elevated. To understand the in vivo role of RTN1, we generated RTN1-null mice and compared the effects of RTN1 and RTN3 on BACE1 modulation. We show that RTN1 is mostly expressed by neurons and not by glial cells under normal conditions, similar to the expression of RTN3. However, RTN1 is more localized in dendrites and is an excellent marker for dendrites of Purkinje cells, while RTN3 expression is less evident in dendrites. This differential localization also correlates with their associations with amyloid plaques in Alzheimer's brains: RTN3, but not RTN1, is abundantly enriched in dystrophic neurites. RTN3 deficiency causes elevation of BACE1 protein levels, while RTN1 deficiency shows no obvious effects on BACE1 activity due to compensation by RTN3, as RTN1 deficiency causes elevation of RTN3 expression. Hence, expression of RTN1 and RTN3 is tightly regulated in mouse brains. Together, our data show that RTN1 and RTN3 have differential effects on the formation of senile plaques in Alzheimer's brains and that RTN3 has a more prominent role in Alzheimer's pathogenesis.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAnimalsAspartic Acid EndopeptidasesCarrier ProteinsDendritesDisease Models, AnimalGene Expression RegulationHEK293 CellsHumansMembrane ProteinsMiceNerve Tissue ProteinsNeuronsPlaque, AmyloidAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesBACE1 protein, humanCarrier ProteinsMembrane ProteinsNerve Tissue ProteinsRTN1 protein, humanRTN3 protein, human

Identifiers

PMID28733667
PMCPMC5522448
OpenAlexW2734511985

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Registered trials

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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.