Abstract
Drug development for the treatment of Alzheimer's disease (AD) has been for a long time focused on agents that were expected to support endogenous β-amyloid (Aβ) in a monomeric state and destroy soluble Aβ oligomers and insoluble Aβ aggregates. However, this strategy has failed over the last 20 years and was eventually abandoned. In this review, we propose a new approach to the anti-amyloid AD therapy based on the latest achievements in understanding molecular causes of cerebral amyloidosis in AD animal models.
MeSH terms
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Alzheimer Disease / drug therapy*
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Alzheimer Disease / pathology
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Amyloid beta-Peptides / antagonists & inhibitors
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Amyloid beta-Peptides / immunology
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Amyloid beta-Peptides / metabolism*
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Animals
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Antibodies, Monoclonal / immunology
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Antibodies, Monoclonal / therapeutic use*
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Cholinesterase Inhibitors / metabolism
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Cholinesterase Inhibitors / therapeutic use
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Humans
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Peptides / chemistry
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Peptides / metabolism
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Peptides / therapeutic use
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Receptors, Nicotinic / chemistry
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Zinc / chemistry
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Zinc / metabolism
Substances
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Amyloid beta-Peptides
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Antibodies, Monoclonal
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Cholinesterase Inhibitors
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Peptides
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Receptors, Nicotinic
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nicotinic acetylcholine receptor alpha4 subunit
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Zinc