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Article type: Review Article
Authors: Wojda, Urszulaa; b; * | Kuznicki, Jaceka; c; *
Affiliations: [a] Laboratory of Neurodegeneration, International Institute of Molecular and Cell Biology, Warsaw, Poland | [b] Laboratory of Preclinical Testing of Higher Standards, Nencki Institute of Experimental Biology, Warsaw, Poland | [c] Laboratory of Calcium Binding Proteins, Nencki Institute of Experimental Biology, Warsaw, Poland
Correspondence: [*] Correspondence to: Urszula Wojda and Jacek Kuznicki, Laboratory of Neurodegeneration, International Institute of Molecular and Cell Biology, Trojdena 4, 02-109 Warsaw, Poland. Tel.: +48 22 5970 700; Fax.: +48 22 5970 715; E-mails: [email protected]; [email protected].
Abstract: Major breakthroughs are required to win the war against the increasing threat of Alzheimer's disease. Until now, however, despite enormous efforts and funds, effective therapies are lacking, and adequate models for drug validation are still unavailable. In this article, we review the available animal and cellular models of different features of human Alzheimer's disease and critically evaluate their usefulness for understanding the mechanisms of the disease. The majority of the presently used models are based on the amyloid-β and hyperphosphorylated tau hypothesis, which resembles features of familial Alzheimer's disease. Unfortunately, these models offer limited help for understanding the pathomechanisms of the early stages of sporadic Alzheimer's disease. Thus, new models are needed to discover ways to treat or delay the onset of Alzheimer's disease, and we discuss the prospects for such desperately needed models, including human induced pluripotent stem cells and in silico brain models.
Keywords: amyloid-β protein precursor, animal models, calcium homeostasis, cell cycle regulation, familial Alzheimer's disease, induced pluripotent stem cells, mitochondrial stress, presenilin 1, sporadic Alzheimer's disease, tau
DOI: 10.3233/JAD-121984
Journal: Journal of Alzheimer's Disease, vol. 34, no. 3, pp. 563-588, 2013
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