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Vol. 8, No. 5, 2011
Issue release date: June 2011
Section title: Original Paper
Neurodegenerative Dis 2011;8:352–363
(DOI:10.1159/000323871)

Characterization of the Brain β-Amyloid Isoform Pattern at Different Ages of Tg2576 Mice

Mustafiz T. · Portelius E. · Gustavsson M.K. · Hölttä M. · Zetterberg H. · Blennow K. · Nordberg A. · Unger Lithner C.
aDivision of Alzheimer Neurobiology, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Karolinska University Hospital, bDepartment of Geriatric Medicine, Karolinska University Hospital, Huddinge, and cDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 10/29/2010
Accepted: 12/22/2010
Published online: 2/23/2011

Number of Print Pages: 12
Number of Figures: 6
Number of Tables: 1

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

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

Abstract

Background: Although genetic and biochemical studies have suggested a cardinal role for β-amyloid (Aβ) in Alzheimer’s disease, the underlying mechanism(s) of how Aβ induces neurodegeneration is still unclear. Our objective was to investigate the consequences of Aβ, especially on tau phosphorylation at specific epitopes important for Alzheimer’s disease. Methods: We used cortices from Tg2576 mice at 7 days to 15 months of age. Results: MALDI-TOF MS revealed an age-dependent shift in the Aβ isoform pattern. Young animals displayed high cortical levels of the shorter Aβ isoforms (Aβ1–16 and Aβ1–17) compared to 15-month-old Tg2576 mice which mainly expressed Aβ1–40 and Aβ1–42. The Aβ1–42 showed an age-dependent increase, whereas total Aβ1–40 levels remained constant. The highest levels of TBS-soluble Aβ oligomers were found at 90 days of age. Brain Aβ build-up did not affect the phosphorylation of tau at the epitopes investigated. Conclusions: This study provides new information about age-dependent Aβ isoforms and oligomers as well as their effect on site-specific tau phosphorylation in this transgenic mouse model. Our observations suggest that the different human Aβ isoforms do not directly cause increased tau phosphorylation and that the cognitive deficits seen in this mouse model are only related to the Aβ overexpression.


  

Author Contacts

Christina Unger Lithner
Division of Alzheimer Neurobiology, Department of Neurobiology,
Care Sciences and Society, Karolinska Institutet, Karolinska University Hospital
Novum, 4th floor, Huddinge, SE–141 86 Stockholm (Sweden)
Tel. +46 8 585 836 15, E-Mail Christina.Unger@ki.

  

Article Information

Received: October 29, 2010
Accepted after revision: December 23, 2010
Published online: February 23, 2011
Number of Print Pages : 12
Number of Figures : 6, Number of Tables : 1, Number of References : 41

  

Publication Details

Neurodegenerative Diseases

Vol. 8, No. 5, Year 2011 (Cover Date: June 2011)

Journal Editor: Nitsch R.M. (Zürich), Hock C. (Zürich)
ISSN: 1660-2854 (Print), eISSN: 1660-2862 (Online)

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


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 10/29/2010
Accepted: 12/22/2010
Published online: 2/23/2011

Number of Print Pages: 12
Number of Figures: 6
Number of Tables: 1

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

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


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