Journal
JOURNAL OF ALZHEIMERS DISEASE
Volume 34, Issue 3, Pages 563-588Publisher
IOS PRESS
DOI: 10.3233/JAD-121984
Keywords
Amyloid-beta 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
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Funding
- Maestro NCN grant [2011/02/A/NZ3/00144]
- EraNet Rus NCBiR grant
- Polish National Science Centre grant [NN401 596840]
- JPND grant [2/BIOMARKAPD/JPND/2012]
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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-beta 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.
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