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KMID : 0605720140200030173
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Journal of the Korean Society of Biological Therapies in Psychiatry
2014 Volume.20 No. 3 p.173 ~ p.186
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Amyloid Theory of Alzheimer’s Disease Revisited
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Kim Byung-Soo
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Abstract
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Alzheimer’s disease(AD) is one of the most common causes of degenerative dementia in the elderly, and is characterized by a progressive deterioration of memory and other higher cognitive functions. Amyloid plaque is observed in the brains of patients with AD and has received attention as a pathognomonic feature since the disease was first reported. The amyloid hypothesis proposes that the toxic accumulation of amyloid-β protein plays a dominant role in the development and progression of AD. Since this theory was first presented in the early 1990s, it has influenced the development of biomarkers for the earlier detection of AD and research to find new treatments. However, recent reports have shown that amyloid deposits are commonly observed in cognitively normal aged persons, and therapeutic agents that effectively reduce the concentration of amyloid-beta in the brains of AD patients have not been effective at improving either cognitive function or the activities of daily living. This suggests that we need to consider alternative theories for AD other than the amyloid hypothesis. This review focuses on the amyloid hypothesis, with details on the production, metabolism, and clearance of amyloid-beta, and on recent advances in the development of therapeutic agents based on this hypothesis.
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KEYWORD
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Alzheimer disease, Amyloid beta, Amyloid beta-protein precursor, Amyloid plaque, Amyloid precursor protein secretases
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