Evidence map›Paper›PMID 32696288›Full record

ArticleCellular and molecular neurobiology2021

The Interplay of Tau Protein and β-Amyloid: While Tauopathy Spreads More Profoundly Than Amyloidopathy, Both Processes Are Almost Equally Pathogenic.

Mahsa Pourhamzeh, Mohammad Taghi Joghataei, Soraya Mehrabi, Reza Ahadi, Seyed Mohammad Massood Hojjati, Nasrin Fazli, Seyed Massood Nabavi, Hossein Pakdaman, Koorosh Shahpasand

RetractedOpen access · greenAbstract readRetracted Publication
In one paragraph

Article in Cellular and molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

7 citing papers in PubMed, 17 citations in OpenAlex.

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  7. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 1 country.

Mahsa PourhamzehDepartment of Anatomy, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Mohammad Taghi JoghataeiDepartment of Anatomy, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran. joghataei.mt@iums.ac.ir.
Soraya MehrabiDepartment of Physiology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Reza AhadiDepartment of Anatomy, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Seyed Mohammad Massood HojjatiDepartment of Neurology, Babol University of Medical Sciences, Babol, Iran.
Nasrin FazliDepartment of Brain and Cognitive Sciences, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran.
Seyed Massood NabaviDepartment of Brain and Cognitive Sciences, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran.
Hossein PakdamanBrain Mapping Research Center, Department of Neurology, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Koorosh ShahpasandDepartment of Brain and Cognitive Sciences, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran. shahpasand@royaninstitute.org.ORCID http://orcid.org/0000-0003-2153-0564
Iran University of Medical Sciences · IRRoyan Institute · IRBabol University of Medical Sciences · IRShahid Beheshti University of Medical Sciences · IR

Funding

Iran University of Medical Sciences (IR) 443Royan Institute 97000115
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder, in which amyloid precursor protein (APP) misprocessing and tau protein hyperphosphorylation are well-established pathogenic cascades. Despite extensive considerations, the central mediator of neuronal cell death upon AD remains under debate. Therefore, we examined the direct interplay between tauopathy and amyloidopathy processes. We employed primary culture neurons and examined pathogenic P-tau and Aβ oligomers upon hypoxia treatment by immunofluorescence and immunoblotting. We observed both tauopathy and amyloidopathy processes upon the hypoxia condition. We also applied Aβ

Indexed as

Amyloid beta-PeptidesAnimalsCell Line, TumorCells, CulturedCerebral Amyloid AngiopathyFemaleHumansMaleMiceMicroinjectionsPeptide FragmentsRatsRats, WistarTauopathiestau ProteinsAmyloid beta-Peptidesamyloid beta-protein (1-42)Mapt protein, mousePeptide Fragmentstau ProteinsAlzheimer’s diseaseOxidative stressP-tauβ-Amyloid

Identifiers

PMID32696288
PMCPMC11448628
OpenAlexW3043965514

What OpenQuestion holds

Textmetadata
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.