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Cellular and Molecular Life Sciences

, Volume 68, Issue 20, pp 3359–3375

First Online: 25 June 2011Received: 21 March 2011Revised: 01 June 2011Accepted: 06 June 2011DOI: 10.1007-s00018-011-0750-2

Cite this article as: Götz, J., Eckert, A., Matamales, M. et al. Cell. Mol. Life Sci. 2011 68: 3359. doi:10.1007-s00018-011-0750-2


Alzheimer’s disease AD is reaching epidemic proportions, yet a cure is not yet available. While the genetic causes of the rare familial inherited forms of AD are understood, the causes of the sporadic forms of the disease are not. Histopathologically, these two forms of AD are indistinguishable: they are characterized by amyloid-β Aβ peptide-containing amyloid plaques and tau-containing neurofibrillary tangles. In this review we compare AD to frontotemporal dementia FTD, a subset of which is characterized by tau deposition in the absence of overt plaques. A host of transgenic animal AD models have been established through the expression of human proteins with pathogenic mutations previously identified in familial AD and FTD. Determining how these mutant proteins cause disease in vivo should contribute to an understanding of the causes of the more frequent sporadic forms. We discuss the insight transgenic animal models have provided into Aβ and tau toxicity, also with regards to mitochondrial function and the crucial role tau plays in mediating Aβ toxicity. We also discuss the role of miRNAs in mediating the toxic effects of the Aβ peptide.

KeywordsAlzheimer Amyloid Frontotemporal dementia Fyn miRNA Mitochondria Oligomer Proteomic Tau Transgenic  Download fulltext PDF

Autor: Jürgen Götz - Anne Eckert - Miriam Matamales - Lars M. Ittner - Xin Liu


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