Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 2493-2497 |
| Number of pages | 5 |
| Journal | NeuroReport |
| Volume | 12 |
| Issue number | 11 |
| Publication status | Published - Aug 8 2001 |
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Keywords
- β-Amyloid
- Fibril
- Frog
- Semicircular canal
- Vestibular
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
β amyloid-induced disruption of ionic balance : Studies on the isolated frog labyrinth. / Botta, Laura; Valli, Paolo; Asti, Annalia; Perin, Paola; Zucca, Gianpiero; Racchi, Marco; Govoni, Stefano; Pascale, Alessia.
In: NeuroReport, Vol. 12, No. 11, 08.08.2001, p. 2493-2497.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - β amyloid-induced disruption of ionic balance
T2 - Studies on the isolated frog labyrinth
AU - Botta, Laura
AU - Valli, Paolo
AU - Asti, Annalia
AU - Perin, Paola
AU - Zucca, Gianpiero
AU - Racchi, Marco
AU - Govoni, Stefano
AU - Pascale, Alessia
PY - 2001/8/8
Y1 - 2001/8/8
N2 - 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.
AB - 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.
KW - β-Amyloid
KW - Fibril
KW - Frog
KW - Semicircular canal
KW - Vestibular
UR - http://www.scopus.com/inward/record.url?scp=0035828172&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0035828172&partnerID=8YFLogxK
M3 - Article
C2 - 11496136
AN - SCOPUS:0035828172
VL - 12
SP - 2493
EP - 2497
JO - NeuroReport
JF - NeuroReport
SN - 0959-4965
IS - 11
ER -