This web page was produced as an assignment for Gen677, an undergraduate course at UW-Madison Spring 2009
To the Future and Beyond
Based on what we know so far, what is the next scientific breakthrough that will increase our knowledge of SORL1 and AD? To me, this answer is simple: gene expression. What controls it? How is it controlled? How can we manipulate gene expression? How does expression vary in different tissues (evidence indicates in AD, SORL1 expression is decreased in the neuron but not in the glial cells surrounding the neuron)? The answers to these questions may ultimately lead a therapeutic treatment for AD.
Another important avenue to investigate is the other players (in addition to SORL1) in AD. It is known that APOE plays a role, but can mutations in APP lead to AD? Do different isoforms of APP interact differently with SORL1 leading to more or less plaque buildup? Can we target BACE as a way to prevent APP from heading to the late endosomal pathway?
I think there is huge potential for a vast spread of microarray studies to fully understand how expression varies temporally, spatially, and in different tissues. Once we know more about the intronic regions that control expression, we can even do studies where we manipulate the intronic sequence and observe expression changes. This type of approach is ideally suited to the bioinformatics age we are entering where we can automate much of this process, running used t be multiple years worth of experiments in weeks or months.
Currently the mouse model of AD is ideally suited to investigate much of what I have mentioned. Due to the high degree of similarity between Human and Mouse SORL1 and the phenotypic similarity of the models, I suggest the mouse as the ideal model organism.
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Last Updated 5/13/09
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