Evidence map›Paper›PMID 33633188›Full record

ArticleScientific reports2021

Exploring the conservation of Alzheimer-related pathways between H. sapiens and C. elegans: a network alignment approach.

Avgi E Apostolakou, Xhuliana K Sula, Katerina C Nastou, Georgia I Nasi, Vassiliki A Iconomidou

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Studying the mechanisms of neurodegeneration:Frontiers in cellular neuroscience · 2025
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  12. AnFrontiers in molecular neuroscience · 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

5 authors at 2 institutions in 2 countries.

Avgi E Apostolakou *Section of Cell Biology and Biophysics, Department of Biology, National and Kapodistrian University of Athens, 15701, Panepistimiopolis, Athens, Greece.
Xhuliana K Sula *Section of Cell Biology and Biophysics, Department of Biology, National and Kapodistrian University of Athens, 15701, Panepistimiopolis, Athens, Greece.
Katerina C NastouSection of Cell Biology and Biophysics, Department of Biology, National and Kapodistrian University of Athens, 15701, Panepistimiopolis, Athens, Greece.
Georgia I NasiSection of Cell Biology and Biophysics, Department of Biology, National and Kapodistrian University of Athens, 15701, Panepistimiopolis, Athens, Greece.
Vassiliki A IconomidouSection of Cell Biology and Biophysics, Department of Biology, National and Kapodistrian University of Athens, 15701, Panepistimiopolis, Athens, Greece. veconom@biol.uoa.gr.
National and Kapodistrian University of Athens · GRNovo Nordisk Foundation · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer disease (AD) is a neurodegenerative disorder with an -as of yet- unclear etiology and pathogenesis. Research to unveil disease processes underlying AD often relies on the use of neurodegenerative disease model organisms, such as Caenorhabditis elegans. This study sought to identify biological pathways implicated in AD that are conserved in Homo sapiens and C. elegans. Protein-protein interaction networks were assembled for amyloid precursor protein (APP) and Tau in H. sapiens-two proteins whose aggregation is a hallmark in AD-and their orthologs APL-1 and PTL-1 for C. elegans. Global network alignment was used to compare these networks and determine similar, likely conserved, network regions. This comparison revealed that two prominent pathways, the APP-processing and the Tau-phosphorylation pathways, are highly conserved in both organisms. While the majority of interactions between proteins in those pathways are known to be associated with AD in human, they remain unexamined in C. elegans, signifying the need for their further investigation. In this work, we have highlighted conserved interactions related to AD in humans and have identified specific proteins that can act as targets for experimental studies in C. elegans, aiming to uncover the underlying mechanisms of AD.

Indexed as

BiomarkersSignal TransductionAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsComputational BiologyDisease Models, AnimalDisease SusceptibilityHumansMicrotubule-Associated ProteinsPhosphorylationProtein Interaction MappingProtein Interaction MapsProteomeAmyloid beta-Protein PrecursorBiomarkersCaenorhabditis elegans ProteinsMicrotubule-Associated ProteinsProteomePTL-1 protein, C eleganstau Proteins

Identifiers

PMID33633188
PMCPMC7907373
OpenAlexW3129658875

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Registered trials

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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.