| Autor: |
Fröhlich C; Neurodegeneration Research Lab (NRL), Department of Neurology, University of Magdeburg, Leipziger Str. 44, 39120 Magdeburg, Germany., Paarmann K, Steffen J, Stenzel J, Krohn M, Heinze HJ, Pahnke J |
| Jazyk: |
angličtina |
| Zdroj: |
European journal of microbiology & immunology [Eur J Microbiol Immunol (Bp)] 2013 Mar 01; Vol. 3 (1), pp. 21-27. |
| DOI: |
10.1556/EuJMI.3.2013.1.3 |
| Abstrakt: |
Alzheimer's disease (AD) is by far the most common neurodegenerative disease. AD is histologically characterized not only by extracellular senile plaques and vascular deposits consisting of β-amyloid (Aβ) but also by accompanying neuroinflammatory processes involving the brain's microglia. The importance of the microglia is still in controversial discussion, which currently favors a protective function in disease progression. Recent findings by different research groups highlighted the importance of strain-specific and mitochondria-specific genomic variations in mouse models of cerebral β-amyloidosis. Here, we want to summarize our previously presented data and add new results that draw attention towards the consideration of strain-specific genomic alterations in the setting of APP transgenes. We present data from APP-transgenic mice in commonly used C57Bl/6J and FVB/N genomic backgrounds and show a direct influence on the kinetics of Aβ deposition and the activity of resident microglia. Plaque size, plaque deposition rate and the total amount of Aβ are highest in C57Bl/6J mice as compared to the FVB/N genomic background, which can be explained at least partially by a reduced microglia activity towards amyloid deposits in the C57BL/6J strain. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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