Linked Life Data

18709343

Source:http://linkedlifedata.com/resource/pubmed/id/18709343

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2008-10-21
pubmed:abstractText
We recently provided evidence for a mitochondrial dysfunction in P301L tau transgenic mice, a strain modeling the tau pathology of Alzheimer's disease (AD) and frontotemporal dementia (FTD). In addition to tau aggregates, the AD brain is further characterized by A beta peptide-containing plaques. When we addressed the role of A beta, this indicated a synergistic action of tau and A beta pathology on the mitochondria. In the present study, we compared the toxicity of different A beta 42 conformations in light of recent studies suggesting that oligomeric rather than fibrillar A beta might be the actual toxic species. Interestingly, both oligomeric and fibrillar, but not disaggregated (mainly monomeric) A beta 42 caused a decreased mitochondrial membrane potential in cortical brain cells obtained from FTD P301L tau transgenic mice. This was not observed with cerebellar preparations indicating selective vulnerability of cortical neurons. Furthermore, we found reductions in state 3 respiration, the respiratory control ratio, and uncoupled respiration when incubating P301L tau mitochondria either with oligomeric or fibrillar preparations of A beta 42. Finally, we found that aging specifically increased the sensitivity of mitochondria to oligomeric A beta 42 damage indicating that oligomeric and fibrillar A beta 42 are both toxic, but exert different degrees of toxicity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0946-2716
pubmed:author
pubmed:issnType
Print
pubmed:volume
86
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1255-67
pubmed:dateRevised
2011-7-8
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Oligomeric and fibrillar species of beta-amyloid (A beta 42) both impair mitochondrial function in P301L tau transgenic mice.
pubmed:affiliation
Neurobiology Laboratory, Psychiatric University Clinic Basel, Wilhelm Klein-Strasse 27, 4025, Basel, Switzerland. anne.eckert@upkbs.ch
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't