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International Journal of Alzheimer’s Disease
Volume 2010, Article ID 573138, 10 pages
Review Article

Modeling of Tau-Mediated Synaptic and Neuronal Degeneration in Alzheimer's Disease

1Experimental Genetics Group, Department of Human Genetics, KULeuven-Campus Gasthuisberg ON1-06.602, Herestraat 49, 3000 Leuven, Belgium
2Center of Molecular Physiology of the Brain (CMPB), Department of Neurology, University Medicine Göttingen, Waldweg 33, 37073 Göttingen, Germany

Received 18 May 2010; Accepted 9 July 2010

Academic Editor: Gemma Casadesus

Copyright © 2010 Tomasz Jaworski et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Patients suffering from Alzheimer's disease (AD) are typified and diagnosed postmortem by the combined accumulations of extracellular amyloid plaques and of intracellular tauopathy, consisting of neuropil treads and neurofibrillary tangles in the somata. Both hallmarks are inseparable and remain diagnostic as described by Alois Alzheimer more than a century ago. Nevertheless, these pathological features are largely abandoned as being the actual pathogenic or neurotoxic factors. The previous, almost exclusive experimental attention on amyloid has shifted over the last 10 years in two directions. Firstly, from the “concrete” deposits of amyloid plaques to less well-defined soluble or pseudosoluble oligomers of the amyloid peptides, ranging from dimers to dodecamers and even larger aggregates. A second shift in research focus is from amyloid to tauopathy, and to their mutual relation. The role of Tau in the pathogenesis and disease progression is appreciated as leading to synaptic and neuronal loss, causing cognitive deficits and dementia. Both trends are incorporated in a modified amyloid cascade hypothesis, briefly discussed in this paper that is mainly concerned with the second aspect, that is, protein Tau and its associated fundamental questions.