Evidence map›Paper›PMID 32547392›Full record

ArticleFrontiers in pharmacology2020

Insulin and Exendin-4 Reduced Mutated Huntingtin Accumulation in Neuronal Cells.

Silvia Rea, David Della-Morte, Francesca Pacifici, Barbara Capuani, Donatella Pastore, Andrea Coppola, Roberto Arriga, Aikaterini Andreadi, Giulia Donadel, Nicola Di Daniele and 2 more

Abstract read
In one paragraph

Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Non-Cell Autonomous and Epigenetic Mechanisms of Huntington's Disease.International journal of molecular sciences · 2021
    Review
  14. PARP overactivation in neurological disorders.Molecular biology reports · 2021
    Review
  15. Review
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

12 authors.

Silvia ReaDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.
David Della-MorteDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.
Francesca PacificiDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.
Barbara CapuaniDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.
Donatella PastoreDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.
Andrea CoppolaDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.
Roberto ArrigaDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.
Aikaterini AndreadiDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.
Giulia DonadelDepartment of Clinical Sciences and Translational Medicine, University of Rome Tor Vergata, Rome, Italy.
Nicola Di DanieleDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.
Alfonso BelliaDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.
Davide LauroDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with diabetes mellitus (DM) are more prone to develop cognitive decline and neurodegenerative diseases. A pathological association between an autosomal dominant neurological disorder caused by brain accumulation in mutated huntingtin (mHTT), known as Huntington disease (HD), and DM, has been reported. By using a diabetic mouse model, we previously suggested a central role of the metabolic pathways of HTT, further suggesting the relevance of this protein in the pathology of DM. Furthermore, it has also been reported that intranasal insulin (Ins) administration improved cognitive function in patients with neurodegenerative disorders such as Alzheimer disease, and that exendin-4 (Ex-4) enhanced lifespan and ameliorated glucose homeostasis in a mouse model of HD. Although antioxidant properties have been proposed, the underlying molecular mechanisms are still missing. Therefore, the aim of the present study was to investigate the intracellular pathways leading to neuroprotective effect of Ins and Ex-4 hypoglycemic drugs by using an

Indexed as

exendin-4Huntington diseaseinsulinmutated huntingtinneuronal survival

Identifiers

PMID32547392
PMCPMC7270204

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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.