부산대학교 도서관

Highlights from the article: We have previously described the discovery and development of GAIM (general amyloid interaction motif)-Ig (immunoglobulin) fusions as therapeutic candidates for neurodegenerative indications [[1]]. In addition, we show that GAIM-Ig fusions co-localize with amyloid deposits in mouse models for LC amyloidosis, and that GAIM-Ig can mediate the disruption of an amyloidoma consisting of human patient derived LC fibres. In the studies described here, we have confirmed and extended GAIM's ability to recognize canonical amyloid structures found in peripheral amyloid diseases, such as TTR and AL amyloidosis.