Evidence map›Paper›PMID 27294139›Full record

ArticleBioMed research international2016

Deposition of BACE-1 Protein in the Brains of APP/PS1 Double Transgenic Mice.

Gang Luo, Hongxia Xu, Yinuo Huang, Dapeng Mo, Ligang Song, Baixue Jia, Bo Wang, Zhanqiang Jin, Zhongrong Miao

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.4field-weighted citation impact, top 33% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

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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

9 authors at 3 institutions in 1 country.

Gang LuoDepartment of Neurology, First Affiliated Hospital, Henan University, Kaifeng, Henan 475001, China; Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China.
Hongxia XuDepartment of Neurology, First Affiliated Hospital, Henan University, Kaifeng, Henan 475001, China.
Yinuo HuangDepartment of Neurology, First Affiliated Hospital, Henan University, Kaifeng, Henan 475001, China.
Dapeng MoDepartment of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China.
Ligang SongDepartment of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China.
Baixue JiaDepartment of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China.
Bo WangDepartment of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China.
Zhanqiang JinDepartment of Ultrasonic Imaging, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China.
Zhongrong MiaoDepartment of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China.
Capital Medical University · CNFirst Affiliated Hospital of Henan University · CNBeijing Tian Tan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The main causes of Alzheimer's disease remain elusive. Previous data have implicated the BACE-1 protein as a central player in the pathogenesis of Alzheimer's disease. However, many inhibitors of BACE-1 have failed during preclinical and clinical trials for AD treatment. Therefore, uncovering the exact role of BACE-1 in AD may have significant impact on the future development of therapeutic agents. Three- and six-month-old female APP/PS1 double transgenic mice were used to study abnormal accumulation of BACE-1 protein in brains of mice here. Immunofluorescence, immunohistochemistry, and western blot were performed to measure the distributing pattern and expression level of BACE-1. We found obvious BACE-1 protein accumulation in 3-month-old APP/PS1 mice, which had increased by the time of 6 months. Coimmunostaining results showed BACE-1 surrounded amyloid plaques in brain sections. The abnormal protein expression might not be attributable to the upregulation of BACE-1 protein, as no significant difference of protein expression was observed between wild-type and APP/PS1 mice. With antibodies against BACE-1 and CD31, we found a high immunoreactive density of BACE-1 protein on the outer layer of brain blood vessels. The aberrant distribution of BACE-1 in APP/PS1 mice suggests BACE-1 may be involved in the microvascular abnormality of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAnimalsAspartic Acid EndopeptidasesBrainDisease Models, AnimalFemaleHumansImmunohistochemistryMiceMice, Mutant StrainsMice, TransgenicMicrovesselsMutant ProteinsPlaque, AmyloidAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAPP protein, humanAspartic Acid EndopeptidasesBace1 protein, mouseMutant ProteinsPlatelet Endothelial Cell Adhesion Molecule-1Presenilin-1PSEN1 protein, humanRecombinant Proteins

Identifiers

PMID27294139
PMCPMC4887654
OpenAlexW2399847174

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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.