Evidence map›Paper›PMID 32657227›Full record

ArticleUpsala journal of medical sciences2020

Distinctive alteration in the expression of autophagy genes in Drosophila models of amyloidopathy and tauopathy.

Mehrnaz Haghi, Raheleh Masoudi, Seyed Morteza Najibi

Open access · diamondAbstract read
In one paragraph

Article in Upsala journal of medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Molecular mechanism on autophagy associated cardiovascular dysfunction inFrontiers in cell and developmental biology · 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

3 authors at 2 institutions in 2 countries.

Mehrnaz HaghiDepartment of Biology, College of Sciences, Shiraz University, Shiraz, Iran.
Raheleh MasoudiDepartment of Biology, College of Sciences, Shiraz University, Shiraz, Iran.
Seyed Morteza NajibiCenter for Molecular Protein Science, Lund University, Lund, Sweden.
Shiraz University · IRLund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is one the most common types of dementia. Plaques of amyloid beta and neurofibrillary tangles of tau are two major hallmarks of AD. Metabolism of these two proteins, in part, depends on autophagy pathways. Autophagy dysfunction and protein aggregation in AD may be involved in a vicious circle. The aim of this study was to investigate whether tau or amyloid beta 42 (Aβ42) could affect expression of autophagy genes, and whether they exert their effects in the same way or not.

methodsExpression levels of some autophagy genes,

resultsWe found that

conclusionWe conclude that both Aβ42 and Tau R406W may affect autophagy through dysregulation of autophagy genes. Interestingly, it seems that these pathological proteins exert their toxic effects on autophagy through different pathways and independently.

Indexed as

AutophagyGene Expression RegulationAlzheimer DiseaseAmyloidAmyloid beta-PeptidesAnimalsAnimals, Genetically ModifiedBayes TheoremBeclin-1BrainDisease Models, AnimalDrosophila melanogasterDrosophila ProteinsFemaleMalePhosphorylationAmyloidAmyloid beta-PeptidesAtg6 protein, DrosophilaBeclin-1Drosophila Proteinstau ProteinsAlzheimer’s diseaseamyloid betaautophagy genesDrosophila melanogastertau

Identifiers

PMID32657227
PMCPMC7594860
OpenAlexW3041360755

What OpenQuestion holds

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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.