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Publication : Astroglial connexin immunoreactivity is specifically altered at β-amyloid plaques in β-amyloid precursor protein/presenilin1 mice.

First Author  Mei X Year  2010
Journal  Neuroscience Volume  171
Issue  1 Pages  92-105
PubMed ID  20813165 Mgi Jnum  J:169720
Mgi Id  MGI:4941694 Doi  10.1016/j.neuroscience.2010.08.001
Citation  Mei X, et al. (2010) Astroglial connexin immunoreactivity is specifically altered at beta-amyloid plaques in beta-amyloid precursor protein/presenilin1 mice. Neuroscience 171(1):92-105
abstractText  Activation of astrocytes surrounding amyloid plaques is a hallmark of Alzheimer disease (AD) with consequences yet poorly understood. Astrocytes are characterized by a high level of intercellular communication mediated by two gap-junction forming proteins, connexin-43 and connexin-30. As astroglial connexins (Cxs) are involved in neuronal dysfunctions and death, we have analyzed their expression pattern in two murine models of AD, that is two different beta-amyloid precursor protein (APP)/presenilin1(PS1) mice, using western blot and immunohistochemistry analyzed in confocal microscopy. In young mice at 2 months, before the emergence of beta-amyloid (Abeta) deposits, the distribution of both Cxs was similar to that of control mice. In older animals>/=4 months, local modifications in connexin immunostaining pattern were observed in the microenvironment of dense core Abeta plaques. In a majority of plaques, an elevated immunoreactivity was detected for both Cxs contributing to the overall increase in connexin expression detected in 18 month old APP/PS1 mice. Activated microglial cells did not contribute to the elevated connexin immunoreactivity that was concentrated in astroglial processes infiltrating the plaques. In a small proportion of plaques (</=15%) a depletion of immunoreactive connexin puncta was also found. As astroglial Cxs participate in neuroglial interactions, their remodeling may contribute to neuronal alterations observed at the periplaque area.
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