Linked Life Data

11496136

Source:http://linkedlifedata.com/resource/pubmed/id/11496136

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2001-8-9
pubmed:abstractText
The beta-amyloid peptide (A beta) 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 A beta aggregation 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 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 A beta effects in a simple multicomponent system.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0959-4965
pubmed:author
pubmed:issnType
Print
pubmed:day
8
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2493-7
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
beta amyloid-induced disruption of ionic balance: studies on the isolated frog labyrinth.
pubmed:affiliation
Department of Cell and Molecular Physiological and Pharmacological Sciences, Via Forlanini 6, University of Pavia, 27100 Pavia, Italy.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't