Abstract
Originalsprog | Engelsk |
---|---|
Tidsskrift | Glia |
Vol/bind | 41 |
Udgave nummer | 2 |
Sider (fra-til) | 169-79 |
Antal sider | 10 |
ISSN | 0894-1491 |
DOI | |
Status | Udgivet - 2003 |
Bibliografisk note
Copyright 2003 Wiley-Liss, Inc.Adgang til dokumentet
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Astrocytic expression of the Alzheimer's disease beta-secretase (BACE1) is stimulus-dependent. / Hartlage-Rübsamen, Maike; Zeitschel, Ulrike; Apelt, Jenny; Gärtner, Ulrich; Franke, Heike; Stahl, Tobias; Günther, Albrecht; Schliebs, Reinhard; Penkowa, Milena; Bigl, Volker; Rossner, Steffen.
I: Glia, Bind 41, Nr. 2, 2003, s. 169-79.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
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TY - JOUR
T1 - Astrocytic expression of the Alzheimer's disease beta-secretase (BACE1) is stimulus-dependent
AU - Hartlage-Rübsamen, Maike
AU - Zeitschel, Ulrike
AU - Apelt, Jenny
AU - Gärtner, Ulrich
AU - Franke, Heike
AU - Stahl, Tobias
AU - Günther, Albrecht
AU - Schliebs, Reinhard
AU - Penkowa, Milena
AU - Bigl, Volker
AU - Rossner, Steffen
N1 - Keywords: Aging; Alzheimer Disease; Amyloid Precursor Protein Secretases; Amyloid beta-Protein; Amyloid beta-Protein Precursor; Animals; Animals, Newborn; Aspartic Endopeptidases; Astrocytes; Brain; Brain Ischemia; Cells, Cultured; Disease Models, Animal; Encephalomyelitis, Autoimmune, Experimental; Endopeptidases; Female; Gliosis; Humans; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Rats; Rats, Inbred Lew; Rats, Inbred SHR
PY - 2003
Y1 - 2003
N2 - The beta-site APP-cleaving enzyme (BACE1) is a prerequisite for the generation of beta-amyloid peptides, which give rise to cerebrovascular and parenchymal beta-amyloid deposits in the brain of Alzheimer's disease patients. BACE1 is neuronally expressed in the brains of humans and experimental animals such as mice and rats. In addition, we have recently shown that BACE1 protein is expressed by reactive astrocytes in close proximity to beta-amyloid plaques in the brains of aged transgenic Tg2576 mice that overexpress human amyloid precursor protein carrying the double mutation K670N-M671L. To address the question whether astrocytic BACE1 expression is an event specifically triggered by beta-amyloid plaques or whether glial cell activation by other mechanisms also induces BACE1 expression, we used six different experimental strategies to activate brain glial cells acutely or chronically. Brain sections were processed for the expression of BACE1 and glial markers by double immunofluorescence labeling and evaluated by confocal laser scanning microscopy. There was no detectable expression of BACE1 protein by activated microglial cells of the ameboid or ramified phenotype in any of the lesion paradigms studied. In contrast, BACE1 expression by reactive astrocytes was evident in chronic but not in acute models of gliosis. Additionally, we observed BACE1-immunoreactive astrocytes in proximity to beta-amyloid plaques in the brains of aged Tg2576 mice and Alzheimer's disease patients.
AB - The beta-site APP-cleaving enzyme (BACE1) is a prerequisite for the generation of beta-amyloid peptides, which give rise to cerebrovascular and parenchymal beta-amyloid deposits in the brain of Alzheimer's disease patients. BACE1 is neuronally expressed in the brains of humans and experimental animals such as mice and rats. In addition, we have recently shown that BACE1 protein is expressed by reactive astrocytes in close proximity to beta-amyloid plaques in the brains of aged transgenic Tg2576 mice that overexpress human amyloid precursor protein carrying the double mutation K670N-M671L. To address the question whether astrocytic BACE1 expression is an event specifically triggered by beta-amyloid plaques or whether glial cell activation by other mechanisms also induces BACE1 expression, we used six different experimental strategies to activate brain glial cells acutely or chronically. Brain sections were processed for the expression of BACE1 and glial markers by double immunofluorescence labeling and evaluated by confocal laser scanning microscopy. There was no detectable expression of BACE1 protein by activated microglial cells of the ameboid or ramified phenotype in any of the lesion paradigms studied. In contrast, BACE1 expression by reactive astrocytes was evident in chronic but not in acute models of gliosis. Additionally, we observed BACE1-immunoreactive astrocytes in proximity to beta-amyloid plaques in the brains of aged Tg2576 mice and Alzheimer's disease patients.
U2 - 10.1002/glia.10178
DO - 10.1002/glia.10178
M3 - Journal article
C2 - 12509807
VL - 41
SP - 169
EP - 179
JO - GLIA
JF - GLIA
SN - 0894-1491
IS - 2
ER -