liu.seSearch for publications in DiVA
Change search
ReferencesLink to record
Permanent link

Direct link
Endogenous murine A beta increases amyloid deposition in APP23 but not in APPPS1 transgenic mice
University of Tubingen, Germany; German Centre Neurodegenerat Disease, Germany; University of Tubingen, Germany.
Nathan S Kline Institute Psychiat Research, NY 10962 USA; NYU, NY USA.
University of Tubingen, Germany; German Centre Neurodegenerat Disease, Germany; University of Tubingen, Germany.
University of Tubingen, Germany; German Centre Neurodegenerat Disease, Germany.
Show others and affiliations
2015 (English)In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 36, no 7, 2241-2247 p.Article in journal (Refereed) Published
Abstract [en]

Endogenous murine amyloid-beta peptide (A beta) is expressed in most A beta precursor protein (APP) transgenic mouse models of Alzheimers disease but its contribution to beta-amyloidosis remains unclear. We demonstrate similar to 35% increased cerebral A beta load in APP23 transgenic mice compared with age-matched APP23 mice on an App-null background. No such difference was found for the much faster A beta-depositing APPPS1 transgenic mouse model between animals with or without the murine App gene. Nevertheless, both APP23 and APPPS1 mice codeposited murine A beta, and immunoelectron microscopy revealed a tight association of murine A beta with human A beta fibrils. Deposition of murine A beta was considerably less efficient compared with the deposition of human A beta indicating a lower amyloidogenic potential of murine A beta in vivo. The amyloid dyes Pittsburgh Compound-B and pentamer formyl thiophene acetic acid did not differentiate between amyloid deposits consisting of human A beta and deposits of mixed human-murine A beta. Our data demonstrate a differential effect of murine A beta on human A beta deposition in different APP transgenic mice. The mechanistically complex interaction of human and mouse A beta may affect pathogenesis of the models and should be considered when models are used for translational preclinical studies.

Place, publisher, year, edition, pages
Elsevier , 2015. Vol. 36, no 7, 2241-2247 p.
Keyword [en]
Alzheimers disease; APP transgenic mouse models; Murine APP knockout; Murine amyloid-beta (A beta); Beta-amyloid; Mixed amyloid-beta (A beta) fibrils
National Category
Chemical Sciences
Identifiers
URN: urn:nbn:se:liu:diva-119786DOI: 10.1016/j.neurobiolaging.2015.03.011ISI: 000355378700003PubMedID: 25911278OAI: oai:DiVA.org:liu-119786DiVA: diva2:827279
Note

Funding Agencies|German Network in Degenerative Dementias [BMBF-01G10705]; NIA [AG017617]; Hertie Foundation, Frankfurt, Germany; ERC Starting Independent Researcher Grant (Project: MUMID) from the European Research Council

Available from: 2015-06-26 Created: 2015-06-26 Last updated: 2015-06-26

Open Access in DiVA

No full text

Other links

Publisher's full textPubMed

Search in DiVA

By author/editor
Nilsson, Peter
By organisation
ChemistryFaculty of Science & Engineering
In the same journal
Neurobiology of Aging
Chemical Sciences

Search outside of DiVA

GoogleGoogle Scholar
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

Altmetric score

Total: 58 hits
ReferencesLink to record
Permanent link

Direct link