| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Stroke. 1997;28:1948-1950.)
© 1997 American Heart Association, Inc.
Articles |
From the Department of Neurology, Tokyo (Japan) Medical and Dental University (T.U.), and Department of Neuropathology, Tokyo Institute of Psychiatry (T.U., H.A., H.K., K.I.).
Correspondence to T. Uchihara, MD, PhD, Department of Neurology, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113 Japan. E-mail t-uchihara.nuro{at}med.tmd.ac.jp
Background and Purpose Microglial cells are present in the center of senile plaques (SPs) in Alzheimer's disease (AD) brain. Such a localization of microglial cells suggests that they are involved in the deposition or the clearance of amyloid-ß protein (Aß) in the brain. We examined their association with another type of parenchymal Aß deposit, which is termed the perivascular deposits of Aß (PAß).
Methods Thick sections from AD brain were stained with a three-color immunofluorescence method that labeled Aß, activated microglial cells, and vascular endothelial cells simultaneously.
Results Three-dimensional observation under a laser scanning microscope confirmed that perivascular aggregates of activated microglial cells were colocalized with PAß.
Conclusions Microglia occur in association with both SPs and PAß, suggesting that they play important roles in the metabolism of Aß in AD brain.
Key Words: Alzheimer's disease microscopy, confocal microglia
This article has been cited by other articles:
![]() |
B. Liu, S. Rasool, Z. Yang, C. G. Glabe, S. S. Schreiber, J. Ge, and Z. Tan Amyloid-Peptide Vaccinations Reduce {beta}-Amyloid Plaques but Exacerbate Vascular Deposition and Inflammation in the Retina of Alzheimer's Transgenic Mice Am. J. Pathol., November 1, 2009; 175(5): 2099 - 2110. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. K. Giri, V. Rajagopal, S. Shahi, B. V. Zlokovic, and V. K. Kalra Mechanism of amyloid peptide induced CCR5 expression in monocytes and its inhibition by siRNA for Egr-1 Am J Physiol Cell Physiol, August 1, 2005; 289(2): C264 - C276. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. J. Scolding, F. Joseph, P. A. Kirby, I. Mazanti, F. Gray, J. Mikol, D. Ellison, D. A. Hilton, T. L. Williams, J. M. MacKenzie, et al. A{beta}-related angiitis: primary angiitis of the central nervous system associated with cerebral amyloid angiopathy Brain, March 1, 2005; 128(3): 500 - 515. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. K. Giri, S. K. Selvaraj, and V. K. Kalra Amyloid Peptide-Induced Cytokine and Chemokine Expression in THP-1 Monocytes Is Blocked by Small Inhibitory RNA Duplexes for Early Growth Response-1 Messenger RNA J. Immunol., May 15, 2003; 170(10): 5281 - 5294. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Giri, S. Selvaraj, C. A. Miller, F. Hofman, S. D. Yan, D. Stern, B. V. Zlokovic, and V. K. Kalra Effect of endothelial cell polarity on beta -amyloid-induced migration of monocytes across normal and AD endothelium Am J Physiol Cell Physiol, September 1, 2002; 283(3): C895 - C904. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Giri, Y. Shen, M. Stins, S. Du Yan, A. M. Schmidt, D. Stern, K.-S. Kim, B. Zlokovic, and V. K. Kalra beta -Amyloid-induced migration of monocytes across human brain endothelial cells involves RAGE and PECAM-1 Am J Physiol Cell Physiol, December 1, 2000; 279(6): C1772 - C1781. [Abstract] [Full Text] [PDF] |
||||
![]() |
F. Nourhashemi, S. Gillette-Guyonnet, S. Andrieu, A. Ghisolfi, P. J. Ousset, H. Grandjean, A. Grand, J. Pous, B. Vellas, and J.-L. Albarede Alzheimer disease: protective factors1 Am. J. Clinical Nutrition, February 1, 2000; 71(2): 643s - 649s. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Tan, T. Town, D. Paris, T. Mori, Z. Suo, F. Crawford, M. P. Mattson, R. A. Flavell, and M. Mullan Microglial Activation Resulting from CD40-CD40L Interaction After -Amyloid Stimulation Science, December 17, 1999; 286(5448): 2352 - 2355. [Abstract] [Full Text] |
||||
![]() |
J. Robertson, J.-M. Beaulieu, M. M. Doroudchi, H. D. Durham, J.-P. Julien, and W. E. Mushynski Apoptotic death of neurons exhibiting peripherin aggregates is mediated by the proinflammatory cytokine tumor necrosis factor-{alpha} J. Cell Biol., October 15, 2001; 155(2): 217 - 226. [Abstract] [Full Text] [PDF] |
||||
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1997 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |