Alzheimer病の治療：現状と展望

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Alzheimer's disease (AD), the most common neurodegenerative disorder in the aged, is characterized by the cerebral deposition of fibrils formed by the amyloid β–protein (Aβ), a 40–42 amino acid peptide. The folding of Aβ into neurotoxic oligomeric, protofibrillar, and fibrillar assemblies is hypothesized to be the key pathologic event in AD (Amyloid hypothesis). These facts support the relevance of therapeutic strategies targeting Aβ aggregation. Currently, no disease–modifying therapeutic agents (DMT) are available for AD patients. We summarize here recent efforts to produce DMT targeting Aβ. Conventionally, it has been thought that fibers accumulating as cerebral amyloid exert neurotoxicity, but recently it was reported that dimers extracted from brains of AD patients are the smallest toxic unit of amyloid aggregates, focusing on the study of soluble oligomers (Oligomer hypothesis), AD is called “Oligomeropathy”.