Abstract
The 'amyloid hypothesis', initially put forward in 1992, posits that amyloid β protein (Aβ) contributes to neurodegeneration through aberrant aggregation. In the process of this aberrant aggregation, Aβ forms oligomers, protofibrils, and mature fibrils, ultimately developing plaques. These mature fibrils and plaques were believed to be the culprits behind the neurotoxicity and neurodegeneration seen in Alzheimer's disease (AD). However, growing evidence in recent years has led to the 'Aβ oligomer hypothesis', which suggests that the intermediate forms of aggregates, such as oligomers and protofibrils, exhibit stronger neurotoxicity than the mature forms. Consequently, efforts have been made to develop anti-Aβ antibody drugs that specifically target these intermediate aggregates. Such interventions hold promise as disease-modifying treatments for AD.
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