Evidence map›Paper›PMID 33279620›Full record

ArticleFree radical biology & medicine2021

Pharmacological intervention in a transgenic mouse model improves Alzheimer's-associated pathological phenotype: Involvement of proteasome activation.

Aleksandra N Mladenovic Djordjevic, Marianna Kapetanou, Natasa Loncarevic-Vasiljkovic, Smilja Todorovic, Sofia Athanasopoulou, Milena Jovic, Milica Prvulovic, Era Taoufik, Rebecca Matsas, Selma Kanazir and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Free radical biology & medicine, 2021. 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
1.7field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

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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

11 authors at 4 institutions in 3 countries.

Aleksandra N Mladenovic DjordjevicDepartment for Neurobiology, Institute for Biological Research "Sinisa Stankovic", National Institute of Republic of Serbia, University of Belgrade, Boulevard Despota Stefana, 142, 11000, Belgrade, Serbia. Electronic address: anamikos@ibiss.bg.ac.rs.
Marianna KapetanouInstitute of Chemical Biology, National Hellenic Research Foundation, 48 Vassileos Constantinou Ave., 11635, Athens, Greece.
Natasa Loncarevic-VasiljkovicDepartment for Neurobiology, Institute for Biological Research "Sinisa Stankovic", National Institute of Republic of Serbia, University of Belgrade, Boulevard Despota Stefana, 142, 11000, Belgrade, Serbia; Molecular Nutrition and Health Lab, CEDOC - Centro de Estudos de Doenças Crónicas, NOVA Medical School / Faculdade de Ciências Médicas, Universidade Nova de Lisboa, Edifício CEDOC II, Rua Câmara Pestana 6, 1150-082, Lisboa, Portugal.
Smilja TodorovicDepartment for Neurobiology, Institute for Biological Research "Sinisa Stankovic", National Institute of Republic of Serbia, University of Belgrade, Boulevard Despota Stefana, 142, 11000, Belgrade, Serbia.
Sofia AthanasopoulouInstitute of Chemical Biology, National Hellenic Research Foundation, 48 Vassileos Constantinou Ave., 11635, Athens, Greece; Department of Biology, Faculty of Medicine, University of Thessaly, Biopolis, 41500, Larissa, Greece.
Milena JovicDepartment for Neurobiology, Institute for Biological Research "Sinisa Stankovic", National Institute of Republic of Serbia, University of Belgrade, Boulevard Despota Stefana, 142, 11000, Belgrade, Serbia.
Milica PrvulovicDepartment for Neurobiology, Institute for Biological Research "Sinisa Stankovic", National Institute of Republic of Serbia, University of Belgrade, Boulevard Despota Stefana, 142, 11000, Belgrade, Serbia.
Era TaoufikLaboratory of Cellular and Molecular Neurobiology-Stem Cells, Department of Neurobiology, Hellenic Pasteur Institute, 127 Vasilissis Sofias Avenue, 11521, Athens, Greece.
Rebecca MatsasLaboratory of Cellular and Molecular Neurobiology-Stem Cells, Department of Neurobiology, Hellenic Pasteur Institute, 127 Vasilissis Sofias Avenue, 11521, Athens, Greece.
Selma KanazirDepartment for Neurobiology, Institute for Biological Research "Sinisa Stankovic", National Institute of Republic of Serbia, University of Belgrade, Boulevard Despota Stefana, 142, 11000, Belgrade, Serbia.
Efstathios S GonosInstitute of Chemical Biology, National Hellenic Research Foundation, 48 Vassileos Constantinou Ave., 11635, Athens, Greece. Electronic address: sgonos@eie.gr.
University of Belgrade · RSNational Hellenic Research Foundation · GRPasteur Hellenic Institute · GRUniversity of Thessaly · GR

Funding

Caloric restriction and Alzheimers ABeta clearance pathwayR03AG046216 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ZLOKOVIC, BERISLAV V · 2013 to 2015
$193k
NIA NIH HHS R03 AG046216
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common form of dementia worldwide, characterized by a progressive decline in a variety of cognitive and non-cognitive functions. The amyloid beta protein cascade hypothesis places the formation of amyloid beta protein aggregates on the first position in the complex pathological cascade leading to neurodegeneration, and therefore AD might be considered to be a protein-misfolding disease. The Ubiquitin Proteasome System (UPS), being the primary protein degradation mechanism with a fundamental role in the maintenance of proteostasis, has been identified as a putative therapeutic target to delay and/or to decelerate the progression of neurodegenerative disorders that are characterized by accumulated/aggregated proteins. The purpose of this study was to test if the activation of proteasome in vivo can alleviate AD pathology. Specifically by using two compounds with complementary modes of proteasome activation and documented antioxidant and redox regulating properties in the 5xFAD transgenic mice model of AD, we ameliorated a number of AD related deficits. Shortly after proteasome activation we detected significantly reduced amyloid-beta load correlated with improved motor functions, reduced anxiety and frailty level. Essentially, to our knowledge this is the first report to demonstrate a dual activation of the proteasome and its downstream effects. In conclusion, these findings open up new directions for future therapeutic potential of proteasome-mediated proteolysis enhancement.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsDisease Models, AnimalMiceMice, TransgenicPhenotypeProteasome Endopeptidase ComplexAmyloid beta-PeptidesProteasome Endopeptidase ComplexAlzheimer's diseaseBehaviorFrailtyProteasomeTherapeutic

Identifiers

PMID33279620
PMCPMC7889698
OpenAlexW3110370007

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.