Evidence map›Paper›PMID 27439903›Full record

ArticleAge (Dordrecht, Netherlands)2016

Characterization of AD-like phenotype in aged APPSwe/PS1dE9 mice.

Huang Huang, Sipei Nie, Min Cao, Charles Marshall, Junying Gao, Na Xiao, Gang Hu, Ming Xiao

Open access · greenAbstract read
In one paragraph

Article in Age (Dordrecht, Netherlands), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

44 citing papers in PubMed, 77 citations in OpenAlex.

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  19. The Microbiome-Gut-Brain Axis and Dementia: A Bibliometric Analysis.International journal of environmental research and public health · 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

8 authors at 2 institutions in 2 countries.

Huang HuangJiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, 101 Longmian Avenue, Jiangning District, Nanjing, Jiangsu, 211166, China.
Sipei NieJiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, 101 Longmian Avenue, Jiangning District, Nanjing, Jiangsu, 211166, China.
Min CaoJiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, 101 Longmian Avenue, Jiangning District, Nanjing, Jiangsu, 211166, China.
Charles MarshallJiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, 101 Longmian Avenue, Jiangning District, Nanjing, Jiangsu, 211166, China.
Junying GaoJiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, 101 Longmian Avenue, Jiangning District, Nanjing, Jiangsu, 211166, China.
Na XiaoJiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, 101 Longmian Avenue, Jiangning District, Nanjing, Jiangsu, 211166, China.
Gang HuJiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, 101 Longmian Avenue, Jiangning District, Nanjing, Jiangsu, 211166, China.
Ming XiaoJiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, 101 Longmian Avenue, Jiangning District, Nanjing, Jiangsu, 211166, China. mingx@njmu.edu.cn.
Nanjing Medical University · CNUniversity of Kentucky · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transgenic APPSwe/PS1dE9 (APP/PS1) mice that overproduce amyloid beta (Aβ) are extensively used in the studies of pathogenesis and experimental therapeutics and new drug screening for Alzheimer's disease (AD). However, most of the current literature uses young or adult APP/PS1 mice. In order to provide a broader view of AD-like phenotype of this animal model, in this study, we systematically analyzed behavioral and pathological profiles of 24-month-old male APP/PS1 mice. Aged APP/PS1 mice had reference memory deficits as well as anxiety, hyperactivity, and social interaction impairment. Consistently, there was obvious deposition of amyloid plaques in the dorsal hippocampus with decreased expression of insulin-degrading enzyme, a proteolytic enzyme responsible for degradation of intracellular Aβ. Furthermore, decreases in hippocampal volume, neuronal number and synaptophysin expression, and astrocyte atrophy were also observed in aged APP/PS1 mice. This finding suggests that aged APP/PS1 mice can well replicate cognitive and noncognitive behavioral abnormalities, hippocampal atrophy, and neuronal and astrocyte degeneration in AD patients, to enable more objective and refined preclinical evaluation of therapeutic drugs and strategies for AD treatment.

Indexed as

Disease Models, AnimalMiceAgingAlzheimer DiseaseAmyloid beta-PeptidesAnimalsAnxietyAstrocytesAtrophyCognitive DysfunctionHippocampusHumansInsulysinMaleMemory DisordersMice, TransgenicAmyloid beta-PeptidesInsulysinSynaptophysinAgedAlzheimer’s diseaseAPP/PS1 miceHippocampal atrophyNoncognitive abnormalitiesβ-amyloid

Identifiers

PMID27439903
PMCPMC5061676
OpenAlexW2479999044

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.