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Experimental Genetics Group
Biochim Biophys Acta. 2004 Dec 6;1742(1-3):161-8. Boom A1, Pochet R1*, Authelet M1, Pradier L2, Borghgraef P3, Van Leuven F3, Heizmann CW4, Brion JP1. 1Laboratory of Histology, Neuroanatomy and Neuropathology, School of Medicine, Université Libre de Bruxelles, Brussels, Belgium. 2Neurodegerative Disease Group, Aventis Pharma, Vitry-sur-Seine, France. 3Experimental Genetics Group, EGG Department Human Genetics, K.U.Leuven, Leuven, Belgium. 4Department of Pediatrics, Division of Clinical Chemistry and Biochemistry, University of Zürich, Zürich, Switzerland. Astrocytes recruitment and activation are a hallmark of many neurodegenerative diseases including Alzheimer's disease (AD). We have previously observed an overexpression for S100A6 protein, a Ca(2+)/Zn(2+) binding protein presenting more affinity for zinc than for calcium, in amyotrophic lateral sclerosis (ALS). Here we demonstrated in AD patients but also in two different AD mouse models, that astrocytic S100A6 protein was homogeneously up-regulated within the white matter. However, within the grey matter, almost all S100A6 immunoreactivity was concentrated in astrocytes surrounding the Abeta amyloid deposits of senile plaques. These S100A6 neocortex labelled astrocytes were also positive for the glial fibrillary acidic protein (GFAP) and S100B protein. Contrasting with S100A6, the distribution for S100B and GFA astrocytic labelled cells was not restricted to the Abeta amyloid deposit in grey matter, but widely distributed throughout the neocortex. Coupling the knowledge that biometals such as zinc are highly concentrated in the amyloid deposits in AD and S100A6 having a high affinity for Zn(2+) may suggest that S100A6 plays a role in AD neuropathology.  FULL TEXT |
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