Evidence map›Paper›PMID 31427921›Full record

ArticleFrontiers in neuroscience2019

Insulin-Mediated Changes in Tau Hyperphosphorylation and Autophagy in a

Shreyasi Chatterjee, Suren S Ambegaokar, George R Jackson, Amritpal Mudher

Open access · goldAbstract read
In one paragraph

Article in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

21 citing papers in PubMed, 33 citations in OpenAlex.

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  13. Frontiers in neuroscience · 2023
    Review
  14. Protein modification regulated autophagy inFrontiers in physiology · 2023
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  17. Article
  18. Autophagy and Tau Protein.International journal of molecular sciences · 2021
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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

4 authors at 3 institutions in 2 countries.

Shreyasi ChatterjeeDepartment of Neurology, Mitchell Center for Neurodegenerative Diseases, The University of Texas Medical Branch at Galveston, Galveston, TX, United States.
Suren S AmbegaokarDepartment of Neurology, Mitchell Center for Neurodegenerative Diseases, The University of Texas Medical Branch at Galveston, Galveston, TX, United States.
George R JacksonDepartment of Neurology, Mitchell Center for Neurodegenerative Diseases, The University of Texas Medical Branch at Galveston, Galveston, TX, United States.
Amritpal MudherDepartment of Biological Sciences, University of Southampton, Southampton, United Kingdom.
The University of Texas Medical Branch at Galveston · USMichael E. DeBakey VA Medical Center · USUniversity of Southampton · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Almost 50 million people in the world are affected by dementia; the most prevalent form of which is Alzheimer's disease (AD). Although aging is considered to be the main risk factor for AD, growing evidence from epidemiological studies suggests that type 2 diabetes mellitus (T2DM) increases the risk of dementia including AD. Defective brain insulin signaling has been suggested as an early event in AD and other tauopathies but the mechanisms that link these diseases are largely unknown. Tau hyperphosphorylation is a hallmark of neurofibrillary pathology and insulin resistance increases the number of neuritic plaques particularly in AD. Utilizing a combination of our

Indexed as

Alzheimer’s diseaseautophagytau aggregationtau hyper-phosphorylationtype 2 diabetes

Identifiers

PMID31427921
PMCPMC6688711
OpenAlexW2957115895

What Socratic 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 Socratic graph.