Aβ immunotherapy for Alzheimer’s disease: where are we?
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Alzheimer's disease (AD) was implicated in most of the estimated 46.8 million worldwide dementia cases in 2015, with projections set to almost triple by 2050 [1]. Because current therapies are focused on ameliorating AD symptoms instead of targeting the underlying causes of the disease, it is necessary to develop disease-modifying therapies. In accordance with the amyloid cascade hypothesis, AD is caused by the progressive aggregation of the Aβ peptide into oligomers, fibrils and amyloid plaques, which results on synaptic loss, neuronal dysfunction and cell death [2]. Accumulation of the Aβ peptide is thought to start more than a decade before...