TY - JOUR
T1 - Laser-induced propagation and destruction of amyloid β fibrils
AU - Yagi, Hisashi
AU - Ozawa, Daisaku
AU - Sakurai, Kazumasa
AU - Kawakami, Toru
AU - Kuyama, Hiroki
AU - Nishimura, Osamu
AU - Shimanouchi, Toshinori
AU - Kuboi, Ryoichi
AU - Naiki, Hironobu
AU - Goto, Yuji
PY - 2010/6/18
Y1 - 2010/6/18
N2 - The amyloid deposition of amyloid β(Aβ) peptides is a critical pathological event in Alzheimer disease (AD). Preventing the formation of amyloid deposits and removing preformed fibrils in tissues are important therapeutic strategies against AD. Previously, we reported the destruction of amyloid fibrils of β2-microglobulin K3 fragments by laser irradiation coupled with the binding of amyloid-specific thioflavin T. Here, we studied the effects of a laser beam on Aβ fibrils. As was the case for K3 fibrils, extensive irradiation destroyed the preformed Aβ fibrils. However, irradiation during spontaneous fibril formation resulted in only the partial destruction of growing fibrils and a subsequent explosive propagation of fibrils. The explosive propagation was caused by an increase in the number of active ends due to breakage. The results not only reveal a case of fragmentation-induced propagation of fibrils but also provide insights into therapeutic strategies for AD.
AB - The amyloid deposition of amyloid β(Aβ) peptides is a critical pathological event in Alzheimer disease (AD). Preventing the formation of amyloid deposits and removing preformed fibrils in tissues are important therapeutic strategies against AD. Previously, we reported the destruction of amyloid fibrils of β2-microglobulin K3 fragments by laser irradiation coupled with the binding of amyloid-specific thioflavin T. Here, we studied the effects of a laser beam on Aβ fibrils. As was the case for K3 fibrils, extensive irradiation destroyed the preformed Aβ fibrils. However, irradiation during spontaneous fibril formation resulted in only the partial destruction of growing fibrils and a subsequent explosive propagation of fibrils. The explosive propagation was caused by an increase in the number of active ends due to breakage. The results not only reveal a case of fragmentation-induced propagation of fibrils but also provide insights into therapeutic strategies for AD.
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U2 - 10.1074/jbc.M109.076505
DO - 10.1074/jbc.M109.076505
M3 - Article
C2 - 20406822
AN - SCOPUS:77953495098
SN - 0021-9258
VL - 285
SP - 19660
EP - 19667
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
IS - 25
ER -