|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
17
|
|
pubmed:dateCreated |
1998-2-17
|
|
pubmed:abstractText |
Mutations in presenilin-1 (PS-1) account for approximately half the cases of autosomal dominant early-onset Alzheimer's disease (AD). Recent data indicate that PS-1 mutations may render neurons vulnerable to apoptosis induced by various insults. We now report that 17beta-estradiol, which appears to reduce the risk of sporadic AD, protects cultured PC12 cells expressing mutant PS-1 against apoptosis induced by trophic factor withdrawal (TFW) and exposure to amyloid beta-peptide 25-35 (Abeta). Estriol also provided significant protection against apoptosis induced by TFW and Abeta, whereas corticosterone was ineffective. 17beta-Estradiol prevented decreases in mitochondrial transmembrane potential and energy charge/redox state following exposure of cells to TFW and Abeta in control cell lines and lines expressing mutant PS-1, suggesting an action in the apoptotic pathway upstream of mitochondrial alterations. Abeta caused an increase in mitochondrial reactive oxygen species which was enhanced by mutant PS-1, and suppressed by 17beta-estradiol. The ability of 17beta-estradiol to preserve mitochondrial function, suppress oxidative stress, and counteract the pro-apoptotic actions of mutant PS-1 suggests a generalized neuroprotective action of estrogens in both sporadic and inherited forms of AD.
|
|
pubmed:grant |
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Amyloid beta-Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/Corticosterone,
http://linkedlifedata.com/resource/pubmed/chemical/Estradiol,
http://linkedlifedata.com/resource/pubmed/chemical/Estriol,
http://linkedlifedata.com/resource/pubmed/chemical/Growth Substances,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/PSEN1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/Presenilin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Reactive Oxygen Species,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/amyloid beta-protein (25-35)
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Dec
|
|
pubmed:issn |
0959-4965
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:day |
1
|
|
pubmed:volume |
8
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
3817-21
|
|
pubmed:dateRevised |
2010-11-18
|
|
pubmed:meshHeading |
pubmed-meshheading:9427376-Amino Acid Substitution,
pubmed-meshheading:9427376-Amyloid beta-Peptides,
pubmed-meshheading:9427376-Animals,
pubmed-meshheading:9427376-Apoptosis,
pubmed-meshheading:9427376-Cell Differentiation,
pubmed-meshheading:9427376-Corticosterone,
pubmed-meshheading:9427376-Energy Metabolism,
pubmed-meshheading:9427376-Estradiol,
pubmed-meshheading:9427376-Estriol,
pubmed-meshheading:9427376-Growth Substances,
pubmed-meshheading:9427376-Humans,
pubmed-meshheading:9427376-Intracellular Membranes,
pubmed-meshheading:9427376-Membrane Potentials,
pubmed-meshheading:9427376-Membrane Proteins,
pubmed-meshheading:9427376-Mitochondria,
pubmed-meshheading:9427376-Oxidative Stress,
pubmed-meshheading:9427376-PC12 Cells,
pubmed-meshheading:9427376-Peptide Fragments,
pubmed-meshheading:9427376-Point Mutation,
pubmed-meshheading:9427376-Presenilin-1,
pubmed-meshheading:9427376-Rats,
pubmed-meshheading:9427376-Reactive Oxygen Species,
pubmed-meshheading:9427376-Recombinant Proteins,
pubmed-meshheading:9427376-Transfection
|
|
pubmed:year |
1997
|
|
pubmed:articleTitle |
Estrogens stabilize mitochondrial function and protect neural cells against the pro-apoptotic action of mutant presenilin-1.
|
|
pubmed:affiliation |
Sanders-Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington 40536, USA.
|
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
|
