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Medicina is published by MDPI from Volume 54 Issue 1 (2018). Articles in this Issue were published by another publisher in Open Access under a CC-BY (or CC-BY-NC-ND) licence. Articles are hosted by MDPI on as a courtesy and upon agreement with Lithuanian Medical Association, Lithuanian University of Health Sciences, and Vilnius University.
Open AccessArticle

Alzheimer’s disease: a molecular mechanism, new hypotheses, and therapeutic strategies

Laboratory of Immunology and Cell Biology, Institute of Biotechnology, Lithuania
Medicina 2010, 46(1), 70;
Received: 15 July 2008 / Accepted: 4 January 2010 / Published: 9 January 2010
Human diseases involving protein misfolding and aggregation have received increasing attention in recent years. Alzheimer’s disease and other diseases associated with aging are sweeping the developed countries whose populations are rapidly aging. Recent progress has improved our knowledge about molecular and cellular pathogenesis of these diseases. For more than 20 years, multiple diseases such as Alzheimer’s and Parkinson’s diseases have been associated with accumulation of abnormal protein fibrils. These self-assembling fibrils, referred as “amyloid,” have been considered the pathogenic molecules that cause cellular degeneration. Accumulation of fibrillar Aβ in plaques underlies the theory for Alzheimer’s disease. Recent experiments have provided evidence that fibrils are not the only neurotoxins. Soluble oligomers and protofibrils play a crucial role in causing cellular dysfunction and death. These oligomers, the missing links in the original amyloid cascade hypothesis, have been incorporated into an updated amyloid cascade. Despite new information gained, there is no disease-modifying treatment. New insights into disease mechanisms and new therapeutic strategies give hope for change.
Keywords: Alzheimer’s disease; protein folding; amyloid protein; fibrils; oligomers Alzheimer’s disease; protein folding; amyloid protein; fibrils; oligomers
MDPI and ACS Style

Plečkaitytė, M. Alzheimer’s disease: a molecular mechanism, new hypotheses, and therapeutic strategies. Medicina 2010, 46, 70.

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