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Original Paper

Influence of Lentiviral β-Synuclein Overexpression in the Hippocampus of a Transgenic Mouse Model of Alzheimer's Disease on Amyloid Precursor Protein Metabolism and Pathology

Krassnig S.a · Schweinzer C.c · Taub N.c · Havas D.c · Auer E.c · Flunkert S.c · Schreibmayer W.a · Hutter-Paier B.c · Windisch M.b

Author affiliations

aInstitute of Biophysics, Medical University Graz, and bNeuroScios GmbH, Graz, and cQPS Austria, Grambach, Austria

Related Articles for ""

Neurodegener Dis 2015;15:243-257

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: September 28, 2014
Accepted: April 26, 2015
Published online: June 25, 2015
Issue release date: July 2015

Number of Print Pages: 15
Number of Figures: 6
Number of Tables: 0

ISSN: 1660-2854 (Print)
eISSN: 1660-2862 (Online)

For additional information: http://www.karger.com/NDD

Abstract

Background: β-Synuclein (β-Syn) is a member of the highly homologous synuclein protein family. The most prominent family member, α-synuclein (α-Syn), abnormally accumulates in so-called Lewy bodies, one of the major pathological hallmarks of α-synucleinopathies. Notably, parts of the peptide backbone, called the nonamyloid component, are also found in amyloid plaques. However, β-Syn seems to have beneficial effects by reducing α-Syn aggregation, and amyloid antiaggregatory activity has been described. Objective: The aim of the study was to analyze if wild-type β-Syn can counteract functional and pathological changes in a murine Alzheimer model over different time periods. Methods: At the onset of pathology, lentiviral particles expressing human β-Syn were injected into the hippocampus of transgenic mice overexpressing human amyloid precursor protein with Swedish and London mutations (APPSL). An empty vector served as the control. Behavioral analyses were performed 1, 3 and 6 months after injection followed by biochemical and histological examinations of brain samples. Results: β-Syn expression was locally concentrated and rather modest, but nevertheless changed its effect on APP expression and plaque load in a time- and concentration-dependent manner. Interestingly, the phosphorylation of glycogen synthase kinase 3 beta was enhanced in APPSL mice expressing human β-Syn, but an inverse trend was observed in wild-type animals. Conclusion: The initially reported beneficial effects of β-Syn could be partially reproduced, but locally elevated levels of β-Syn might also cause neurodegeneration. To enlighten the controversial pathological mechanism of β-Syn, further examinations considering the relationship between concentration and exposure time of β-Syn are needed.

© 2015 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: September 28, 2014
Accepted: April 26, 2015
Published online: June 25, 2015
Issue release date: July 2015

Number of Print Pages: 15
Number of Figures: 6
Number of Tables: 0

ISSN: 1660-2854 (Print)
eISSN: 1660-2862 (Online)

For additional information: http://www.karger.com/NDD


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