Monitoring low molecular weight oligomeric forms of amyloid beta in the early stages of aggregation using X-ray footprinting mass spectrometry

Abstract

The aggregation-prone Amyloid Beta (Aβ) peptide has been the target of the majority of efforts to develop Alzheimer’s Disease therapeutics, most of which have failed or have shown mixed results. Although clinical trials are ongoing, the failure of many efforts to slow or block pathogenesis by targeting Aβ over the past two decades calls for an urgent development of novel therapeutic concepts. In particular, the role of amyloid aggregation has come into question as it relates to Alzheimer's disease progression and it is no longer widely believed that buildup of amyloid fibrils in brain tissue is a causal factor in cognitive decline associated with the disease.