The beta -amyloid pepticle (A beta) is a key player in the pathogenesis of
Alzheimer's disease. Although its mechanisms of action are not fully elucid
ated, a disruption of ionic homeostasis has been suggested, and A beta aggr
egation in fibrils seems correlated to its toxic potential. In the present
work, we studied the effects of different A beta fragments on the activity
of frog ampullar nerve fibers. Our results show that A beta fragments are a
ble to reduce ampullar nerve responses, with a potency correlated to their
fibrillogenic capability. This study may have clinical implications, since
vestibular problems are often reported in Alzheimer patients, and provide a
model for the dissection of AP effects in a simple multicomponent system.
NeuroReport 12:2493-2497 (C) 2001 Lippincott Williams & Wilkins.