Evidence map›Paper›PMID 29222348›Full record

ArticleBioscience reports2018

Insulin degrading enzyme contributes to the pathology in a mixed model of Type 2 diabetes and Alzheimer's disease: possible mechanisms of IDE in T2D and AD.

Huajie Li, Jian Wu, Linfeng Zhu, Luolin Sha, Song Yang, Jiang Wei, Lei Ji, Xiaochun Tang, Keshi Mao, Liping Cao and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Bioscience reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

41 citing papers in PubMed, 65 citations in OpenAlex.

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  6. Associations Between Diabetes Mellitus and Neurodegenerative Diseases.International journal of molecular sciences · 2025
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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

13 authors at 1 institution in 1 country.

Huajie LiDepartment of Neurology, the First People's Hospital of Changzhou, Jiangsu, China lihuajie0589@sohu.com.
Jian WuDepartment of Neurology, the First People's Hospital of Changzhou, Jiangsu, China.
Linfeng ZhuDepartment of Neurology, the First People's Hospital of Changzhou, Jiangsu, China.
Luolin ShaDepartment of Neurology, the First People's Hospital of Changzhou, Jiangsu, China.
Song YangDepartment of Neurology, the First People's Hospital of Changzhou, Jiangsu, China.
Jiang WeiDepartment of General Laboratory, the First People's Hospital of Changzhou, Jiangsu, China.
Lei JiDepartment of Neurology, the First People's Hospital of Changzhou, Jiangsu, China.
Xiaochun TangDepartment of Neurology, the First People's Hospital of Changzhou, Jiangsu, China.
Keshi MaoDepartment of Neurology, the First People's Hospital of Changzhou, Jiangsu, China.
Liping CaoDepartment of Neurology, the First People's Hospital of Changzhou, Jiangsu, China.
Ning WeiDepartment of Neurology, the First People's Hospital of Changzhou, Jiangsu, China.
Wei XieDepartment of Neurology, the First People's Hospital of Changzhou, Jiangsu, China.
Zhilong YangDepartment of Neurology, the First People's Hospital of Changzhou, Jiangsu, China.
The First People's Hospital of Changzhou · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin degrading enzyme (IDE) is believed to act as a junction point of Type 2 diabetes (T2D) and Alzheimer's disease (AD); however, the underlying mechanism was not completely clear yet. Transgenic APPSwe/PS1 mice were used as the AD model and were treated with streptozocin/streptozotocin (STZ) to develop a mixed mice model presenting both AD and T2D. Morris Water Maze (MWM) and recognition task were performed to trace the cognitive function. The detection of fasting plasma glucose (FPG) and plasma insulin concentration, and oral glucose tolerance test (OGTT) were used to trace the metabolism evolution. Aβ40 and Aβ42 were quantified by colorimetric ELISA kits. The mRNA or protein expression levels were determined by quantitative real-time RT-PCR and Western blotting analysis respectively. T2D contributes to the AD progress by accelerating and worsening spatial learning and recognition impairments. Metabolic parameters and glucose tolerance were significantly changed in the presence of the AD and T2D. The expression levels of IDE, PPARγ, and AMPK were down-regulated in mice with AD and T2D. PPARγ activator rosiglitazone (RSZ) or AMPK activator AICAR increased the expression level of IDE and decreased Aβ levels in mice with AD and T2D. RSZ or AICAR treatment also alleviated the spatial learning and recognition impairments in AD and T2D mice. Our results found that, in the mice with T2D and AD, the activators of PPARγ/AMPK signaling pathway significantly increased the expression level of IDE, and decreased the accumulation of Aβ40 and Aβ42, as well as alleviated the spatial learning and recognition impairments.

Indexed as

Alzheimer DiseaseAminoimidazole CarboxamideAMP-Activated Protein KinasesAmyloid beta-PeptidesAnimalsBlood GlucoseDiabetes Mellitus, Type 2Disease Models, AnimalFastingGene Expression RegulationGlucose Tolerance TestHumansInsulinInsulysinLearningMiceAICA ribonucleotideAminoimidazole CarboxamideAMP-Activated Protein KinasesAmyloid beta-PeptidesBlood GlucoseInsulinInsulysinPPAR gammaPrkaa1 protein, mouseRibonucleotidesRosiglitazoneStreptozocinThiazolidinedionesAlzheimer's diseaseInsulin degrading enzymetype 2 diabetes

Identifiers

PMID29222348
PMCPMC6435468
OpenAlexW2773229684

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.