Abstract:Background:A significant proportion of amyloid-beta (Ab) peptides in Alzheimer's disease (AD) is truncated at the N-terminus. Among these, accumulation of pGlu-modified amyloid (pGlu-Ab3-40/42) has been shown to correlate with disease progression and tau pathology. Therapeutic strategies targeting pGlu-Ab, e.g. inhibitors of glutaminyl cyclase (QC) that catalyzes pGlu-formation, are currently in clinical assessment. However, it is still unclear, which enzyme(s) might be responsible for N-truncation of Ab and t… Show more
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