Difference between revisions of "Team:Linkoping Sweden/Project"

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             <h4>Sources</h4>
 
             <h4>Sources</h4>
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<small>1. Alzheimerfonden. Alzheimers sjukdom [Internet]. Cited 2017-06-15.  
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<small>1. Alzheimerfonden. Alzheimers sjukdom [Internet]. Cited 2017-06-15. Available from: http://www.alzheimerfonden.se/om_demens/alzheimers_sjukdom [in swedish]  
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<br> Available from: http://www.alzheimerfonden.se/om_demens/alzheimers_sjukdom [in swedish]  
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           </small>  
 
           </small>  
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<small>2. Alzheimer´s Disease International. Dementia statistics [Internet]. Cited 2017-06-27.  
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<br><small>2. Alzheimer´s Disease International. Dementia statistics [Internet]. Cited 2017-06-27. Available from: https://www.alz.co.uk/research/statistics
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<br> Available from: https://www.alz.co.uk/research/statistics
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           </small>  
 
           </small>  
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<small>3. Alzheimerfonden. Lexikon för Alzheimers sjukdom och andra demenssjukdomar [Internet]. Cited 2017-06-15.  
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<br><small>3. Alzheimerfonden. Lexikon för Alzheimers sjukdom och andra demenssjukdomar [Internet]. Cited 2017-06-15. Available from: http://www.alzheimerfonden.se/om_demens/lexikon [in swedish]  
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<br> Available from: http://www.alzheimerfonden.se/om_demens/lexikon [in swedish]  
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           </small>  
 
           </small>  
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<small>4. Bloom GS. Amyloid-β and TauThe Trigger and Bullet in Alzheimer Disease Pathogenesis. JAMA Neurol. 2014;71(4):505-508. doi:10.1001/jamaneurol.2013.5847  
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<br><small>4. Bloom GS. Amyloid-β and TauThe Trigger and Bullet in Alzheimer Disease Pathogenesis. JAMA Neurol. 2014;71(4):505-508. doi:10.1001/jamaneurol.2013.5847  
 
           </small>  
 
           </small>  
 
            
 
            

Revision as of 14:07, 27 June 2017

Summary

Around 100,000 people in Sweden and a total of 46,8 million in the world suffer from Alzheimer's disease [1,2]. The cause of the disease is still largely unknown [1]. The proteins amyloid-beta and tau are two proteins known to be related to the development of the disease. The proteins are found in the brain in and around our neurons and in Alzheimer's disease, they accumulate to form plaques and tangles respectively [3, 4]. Because these proteins are prone to aggregate they are hard to study in a laboratory environment.

The aim of the project is to optimize the expression of the amyloid-beta and tau in Escherichia coli. Chaperones are proteins that can help other proteins to fold into their native three-dimensional shape, if Amyloid-beta and Tau are correctly folded they are less likely to aggregate. We will study four different chaperones to determine the optimal combination of chaperone system for expressing Amyloid-beta and Tau respectively.

With our project, we hope to make a new model for expressing these proteins without aggregation. We also see a future for our model to be used to express other difficult proteins.

Sources

1. Alzheimerfonden. Alzheimers sjukdom [Internet]. Cited 2017-06-15. Available from: http://www.alzheimerfonden.se/om_demens/alzheimers_sjukdom [in swedish]
2. Alzheimer´s Disease International. Dementia statistics [Internet]. Cited 2017-06-27. Available from: https://www.alz.co.uk/research/statistics
3. Alzheimerfonden. Lexikon för Alzheimers sjukdom och andra demenssjukdomar [Internet]. Cited 2017-06-15. Available from: http://www.alzheimerfonden.se/om_demens/lexikon [in swedish]
4. Bloom GS. Amyloid-β and TauThe Trigger and Bullet in Alzheimer Disease Pathogenesis. JAMA Neurol. 2014;71(4):505-508. doi:10.1001/jamaneurol.2013.5847