The β-amyloid peptide (Aβ) is a key player in the pathogenesis of Alzheimer's disease. Although its mechanisms of action are not fully elucidated, a disruption of ionic homeostasis has been suggested, and Aβ aggregation in fibrils seems correlated to its toxic potential. In the present work, we studied the effects of different Aβ fragments on the activity of frog ampullar nerve fibers. Our results show that Aβ fragments are able 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 Aβ effects in a simple multicomponent system.
|Number of pages||5|
|Publication status||Published - Aug 8 2001|
- Semicircular canal
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