N-Terminally Truncated Aβ Peptide Variants in Alzheimer’s Disease

摘要: ABSTRACT The accumulation and aggregation of amyloid-β (Aβ) peptides in the brain is believed to be initial trigger molecular pathology Alzheimer’s disease (AD). In addition widely studied full-length Aβ (mainly Aβ1–40 Aβ1–42), a variety amino-terminally truncated (N-truncated) peptides, such as AβpE3-x Aβ4-x, have been detected high abundance autopsy samples from sporadic familial AD patients. N-truncated species adopt specific physicochemical properties resulting higher propensity increased peptide stability, which likely account for their neurotoxic potential. The presence transgenic mouse models selective overexpression variants murine facilitated investigation relevant vivo settings. this chapter, we address pathological relevance summarize current knowledge about enzymatic activities that might involved generation.