Object's details: The role of the Amyloid Precursor Protein mutations and PERK-dependent signaling pathways in the pathogenesis of Alzheimer’s disease

Provider:Repozytorium Uniwersytetu Łódzkiego

Description

Title:
The role of the Amyloid Precursor Protein mutations and PERK-dependent signaling pathways in the pathogenesis of Alzheimer’s disease
Creator:
Rozpędek, Wioletta;
Nowak, Alicja;
Pytel, Dariusz;
Lewko, Dawid;
Diehl, J. Alan;
Majsterek, Ireneusz
Contributor:
Rozpędek, Wioletta - 1. Department of Clinical Chemistry and Biochemistry, Military-Medical Faculty, Medical University of Lodz, Hallera 1, 90-647 Lodz, Poland;
Nowak, Alicja - 1. Department of Clinical Chemistry and Biochemistry, Military-Medical Faculty, Medical University of Lodz, Hallera 1, 90-647 Lodz, Poland;
Pytel, Dariusz - 2. Department of Biochemistry and Molecular Biology, Hollings Cancer Center, Medical University of South Carolina, 86 Jonathan Lucas Street, Charleston, SC 29425, United States of America;
Lewko, Dawid - 1. Department of Clinical Chemistry and Biochemistry, Military-Medical Faculty, Medical University of Lodz, Hallera 1, 90-647 Lodz, Poland;
Diehl, J. Alan - 2. Department of Biochemistry and Molecular Biology, Hollings Cancer Center, Medical University of South Carolina, 86 Jonathan Lucas Street, Charleston, SC 29425, United States of America;
Majsterek, Ireneusz - 1. Department of Clinical Chemistry and Biochemistry, Military-Medical Faculty, Medical University of Lodz, Hallera 1, 90-647 Lodz, Poland;
Majsterek, Ireneusz - ireneusz.majsterek@umed.lodz.pl
Description:
Alzheimer’s disease (AD) is a highly complex, progressive, age-related neurodegenerative human disease entity. The genetic basis of AD is strictly connected with occurrence of mutations in Amyloid Precursor (APP) gene on chromosome 21. Molecular mechanism that leads to AD development still remains unclear. Recent data reported that it is closely correlated with Endoplasmic Reticulum (ER) stress conditions, which subsequently activate Unfolded Protein Response (UPR) signaling pathways, via the induction of protein kinase RNA-like endoplasmic reticulum kinase (PERK), as a self-protective, adaptive response to adverse stress conditions. That results in the attenuation of global protein synthesis and, on the contrary, selective translation of Activating Transcriptor Factor 4 (ATF4) and secretase β. Interestingly, under prolonged, severe ER stress UPR may switch its signal into apoptotic cell death. That ensues by ATF4-CHOP-mediated activation of a range of pro-apoptotic genes and, on the other hand, downregulation of the expression of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) genes. Current investigations suggest that inhibitions of PERK activity may contribute to the attenuation of the deposition of toxic senile plaques in the brain tissue and, as a result, prevent degeneration of neurons and decline in cognitive abilities.
Object availability:
free access
Rights:
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.;
http://creativecommons.org/licenses/by-nc-nd/3.0
Date:
2017.03.07;
2017.02.07
Format:
application/pdf
Publisher:
Wydawnictwo Uniwersytetu Łódzkiego
Relation:
Folia Biologica et Oecologica;12
Subject:
Amyloid β;
Endoplasmic Reticulum stress;
Unfolded Protein Response;
eIF2α;
CHOP
Identifier:
1730-2366;
http://hdl.handle.net/11089/20775 ;
10.1515/fobio-2016-0005
Data provider:
Repozytorium Uniwersytetu Łódzkiego

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Object's details: The role of the Amyloid Precursor Protein mutations and PERK-dependent signaling pathways in the pathogenesis of Alzheimer’s disease

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