Evidence map›Paper›PMID 28402338›Full record

ArticleScientific reports2017

Insulin deprivation induces PP2A inhibition and tau hyperphosphorylation in hTau mice, a model of Alzheimer's disease-like tau pathology.

Maud Gratuze, Jacinthe Julien, Franck R Petry, Françoise Morin, Emmanuel Planel

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 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 64 citations in OpenAlex.

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  13. Ser/Thr phosphatases: One of the key regulators of insulin signaling.Reviews in endocrine & metabolic disorders · 2022
    Review
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  15. Passive immunization against phosphorylated tau improves features of Huntington's disease pathology.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  16. Frontotemporal Dementia and Glucose Metabolism.Frontiers in neuroscience · 2022
    Review
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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 2 institutions in 1 country.

Maud GratuzeUniversité Laval, Faculté de médecine, Département de Psychiatrie et Neurosciences, Québec, QC, Canada.
Jacinthe JulienCentre de Recherche du CHU de Québec, Axe Neurosciences, Québec, QC, Canada.
Franck R PetryUniversité Laval, Faculté de médecine, Département de Psychiatrie et Neurosciences, Québec, QC, Canada.
Françoise MorinCentre de Recherche du CHU de Québec, Axe Neurosciences, Québec, QC, Canada.
Emmanuel PlanelUniversité Laval, Faculté de médecine, Département de Psychiatrie et Neurosciences, Québec, QC, Canada.
Centre hospitalier universitaire de Québec · CAUniversité Laval · CA

Funding

CIHR MOP-106423
6 · The paper itself

Abstract

Abnormally hyperphosphorylated tau aggregated as intraneuronal neurofibrillary tangles is one of the two neuropathological hallmarks of Alzheimer's disease (AD). The majority of AD cases are sporadic with numerous environmental, biological and genetic risks factors. Interestingly, insulin dysfunction and hyperglycaemia are both risk factors for sporadic AD. However, how hyperglycaemia and insulin dysfunction affect tau pathology, is not well understood. In this study, we examined the effects of insulin deficiency on tau pathology in transgenic hTau mice by injecting different doses of streptozotocin (STZ), a toxin that destroys insulin-producing cells in the pancreas. One high dose of STZ resulted in marked diabetes, and five low doses led to a milder diabetes. Both groups exhibited brain tau hyperphosphorylation but no increased aggregation. Tau hyperphosphorylation correlated with inhibition of Protein Phosphatase 2A (PP2A), the main tau phosphatase. Interestingly, insulin injection 30 minutes before sacrifice partially restored tau phosphorylation to control levels in both STZ-injected groups. Our results confirm a link between insulin homeostasis and tau phosphorylation, which could explain, at least in part, a higher incidence of AD in diabetic patients.

Indexed as

Alzheimer DiseaseAnimalsBrainDiabetes Mellitus, ExperimentalDisease Models, AnimalMiceMice, TransgenicNeurofibrillary TanglesPhosphorylationProtein Phosphatase 2Tauopathiestau ProteinsProtein Phosphatase 2tau Proteins

Identifiers

PMID28402338
PMCPMC5389355
OpenAlexW2606704562

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.