Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Science 24 August 2001:
Vol. 293. no. 5534, pp. 1446 - 1447
DOI: 10.1126/science.1064684

Perspectives

Also see the archival list of Science's Compass: Enhanced Perspectives

BIOMEDICINE:
Enhanced: Tauists and baptists United--Well Almost!

Virginia M.-Y. Lee

Controversy still rages over which of the two hallmark pathologies of Alzheimer's disease (AD), amyloid plaques and tau tangles, is the primary cause of neurodegeneration in the brain. As many suspected and as Lee points out in her Perspective, the two pathologies are not separate processes. New work (Lewis et al., Götz et al.) in transgenic mice shows that amyloid-b deposits influence the formation of tau tangles in areas of the brain known to be affected in AD.


The author is at the Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-4283, USA. E-mail: vmylee{at}mail.med.upenn.edu

Read the Full Text



THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Phosphorylation of actin-depolymerizing factor/cofilin by LIM-kinase mediates amyloid beta-induced degeneration: a potential mechanism of neuronal dystrophy in Alzheimer's disease..
L. Heredia, P. Helguera, S. de Olmos, G. Kedikian, F. Sola Vigo, F. LaFerla, M. Staufenbiel, J. de Olmos, J. Busciglio, A. Caceres, et al. (2006)
J. Neurosci. 26, 6533-6542
   Abstract »    Full Text »    PDF »
From the Cover: Abeta and tau form soluble complexes that may promote self aggregation of both into the insoluble forms observed in Alzheimer's disease.
J.-P. Guo, T. Arai, J. Miklossy, and P. L. McGeer (2006)
PNAS 103, 1953-1958
   Abstract »    Full Text »    PDF »
Learning and Memory Deficits Upon TAU Accumulation in Drosophila Mushroom Body Neurons.
A. Mershin, E. Pavlopoulos, O. Fitch, B. C. Braden, D. V. Nanopoulos, and E. M.C. Skoulakis (2004)
Learn. Mem. 11, 277-287
   Abstract »    Full Text »    PDF »
Detangling Alzheimer's Disease.
L. Helmuth (2003)
Sci. Aging Knowl. Environ. 2003, oa2-2
   Abstract »    Full Text »    PDF »
{alpha}7 Nicotinic Acetylcholine Receptors Mediate {beta}-Amyloid Peptide-induced Tau Protein Phosphorylation.
H.-Y. Wang, W. Li, N. J. Benedetti, and D. H. S. Lee (2003)
J. Biol. Chem. 278, 31547-31553
   Abstract »    Full Text »    PDF »
Amyloid Precursor Protein, Presenilins, and alpha -Synuclein: Molecular Pathogenesis and Pharmacological Applications in Alzheimer's Disease.
Y.-H. Suh and F. Checler (2002)
Pharmacol. Rev. 54, 469-525
   Abstract »    Full Text »    PDF »
Alzheimer Disease.
J. L. Cummings and G. Cole (2002)
JAMA 287, 2335-2338
   Full Text »    PDF »
Chronic Overexpression of the Calcineurin Inhibitory Gene DSCR1 (Adapt78) Is Associated with Alzheimer's Disease.
G. Ermak, T. E. Morgan, and K. J. A. Davies (2001)
J. Biol. Chem. 276, 38787-38794
   Abstract »    Full Text »    PDF »
Tau and Amyloid-{beta} Peptide: Linking the Molecular Markers of Alzheimer's Disease.
(2001)
Journal Watch (General) 2001, 8
   Full Text »



To Advertise     Find Products


Science. ISSN 0036-8075 (print), 1095-9203 (online)