Evidence map›Paper›PMID 28467789›Full record

ArticleOncotarget2017

Chronic diabetic states worsen Alzheimer neuropathology and cognitive deficits accompanying disruption of calcium signaling in leptin-deficient APP/PS1 mice.

Shuai Zhang, Rui Chai, Ying-Ying Yang, Shi-Qi Guo, Shan Wang, Tian Guo, Shuang-Feng Xu, Yan-Hui Zhang, Zhan-You Wang, Chuang Guo

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  6. The Brain Metabolome Is Modified by Obesity in a Sex-Dependent Manner.International journal of molecular sciences · 2024
    Article
  7. Article
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  10. Peripheral Aβ acts as a negative modulator of insulin secretion.Proceedings of the National Academy of Sciences of the United States of America · 2022
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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

10 authors at 1 institution in 1 country.

Shuai ZhangCollege of Life and Health Sciences, Northeastern University, Shenyang, China.
Rui ChaiCollege of Life and Health Sciences, Northeastern University, Shenyang, China.
Ying-Ying YangCollege of Life and Health Sciences, Northeastern University, Shenyang, China.
Shi-Qi GuoCollege of Life and Health Sciences, Northeastern University, Shenyang, China.
Shan WangCollege of Life and Health Sciences, Northeastern University, Shenyang, China.
Tian GuoCollege of Life and Health Sciences, Northeastern University, Shenyang, China.
Shuang-Feng XuCollege of Life and Health Sciences, Northeastern University, Shenyang, China.
Yan-Hui ZhangCollege of Life and Health Sciences, Northeastern University, Shenyang, China.
Zhan-You WangCollege of Life and Health Sciences, Northeastern University, Shenyang, China.
Chuang GuoCollege of Life and Health Sciences, Northeastern University, Shenyang, China.
Northeastern University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The coincidences between Alzheimer's disease (AD) and type 2 diabetes mellitus (T2DM) are so compelling that it is attractive to speculate that diabetic conditions might aggravate AD pathologies by calcium dysfunction, although the understanding of the molecular mechanisms involved remains elusive. The present work was undertaken to investigate whether calcium dyshomeostasis is associated with the exacerbated Alzheimer-like cognitive dysfunction observed in diabetic conditions in APP/PS1-ob/ob mice, which were generated by crossing ob/ob mice with APP/PS1 mice. We confirmed that the diabetic condition can aggravate not only Aβ deposition but also tau phosphorylation, synaptic loss, neuronal death, and inflammation, exacerbating cognitive impairment in AD mice. More importantly, we found that the diabetic condition dramatically elevated calcium levels in APP/PS1 mice, thereby stimulating the phosphorylation of the calcium-dependent kinases. Our findings suggest that controlling over-elevation of intracellular calcium may provide novel insights for approaching AD in diabetic patients and delaying AD progression.

Indexed as

Calcium SignalingCognitive DysfunctionAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainDiabetes Mellitus, Type 2Disease Models, AnimalHumansInflammationLeptinMaleMemory DisordersMiceMice, TransgenicPhosphorylationAmyloid beta-PeptidesLeptintau ProteinsAlzheimer’s diseasecalciumdiabetes mellitustauβ-amyloid

Identifiers

PMID28467789
PMCPMC5546429
OpenAlexW2606393184

What OpenQuestion holds

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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.