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Förslaget inkom 2003-11-14

Effects of three key Alzheimer´s Disease proteins (amyloid beta-peptide, apolipoprotein E and presenilin-1) on the thioredoxin/glutaredoxin antioxidant systems

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Alzheimer´s disease (AD) is a complex neurodegenerative disorder that causes dementia. Four different genes have been associated with an inherited susceptibility to AD. Mutations in 3 genes, the presenilin 1 (PS1), the presenilin 2 (PS2) and the amyloid precursor protein gene, are highly penetrant, but represent only few of all AD cases. The apoE gene on chromosome 19 is a susceptibility factor that accounts for half of late onset AD. The human apoE gene shows polymorphism, with three different
alleles, e2, e3 and e4. ApoE4 carriers have a higher risk for AD. The mechanisms underlying the pathology of AD are not fully understood although overproduction of beta amyloid (Ab), oxidative stress and apoptotic processes play important roles. Cells have a wide array of antioxidant mechanisms including enzymes such as thioredoxin (TRX) and glutaredoxin (GRX).
We will investigate the effects of Ab, apoE isoforms, and PSmutations on the integrity of both the TRX and GRX systems. Experiments will be performed in vitro using cells transfected with wild type PS1 and several PS1 mutations, as well as untransfected cells. We will use immunoblotting, immunocytochemistry and ELISA techniques to study the expression, subcellular localization and the activity of TRX and GRX under normal, apoptotic and oxidative conditions. Characterising the role of TRX and GRX in AD will determine if these molecules could provide valid candidates for treatment.


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