Abstract
Work on the biological as well as pathological functions of PS genes has contributed substantially to our knowledge of the molecular mechanisms causing AD as well as FAD. Again, the pivotal importance of Aβ42 is being emphasized, since FAD-associated PS mutations increase its production. Moreover, work in C. elegans provides the first biological assay to screen for further genes that might be involved in the prevention or enhancement of the molecular mechanisms causing AD. We now must identify proteins that interact with PS. Such knowledge might help elucidate the molecular interactions required for normal and abnormal function of PS as well as the mechanisms involved in pathological Aβ formation. Animal models exhibiting full AD pathology will certainly contribute to these upcoming challenges. Therefore, the community of AD researchers will be busy for the foreseeable future with the remaining mysteries of AD.
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