Transgenic mice for screening for inhibitors of protein aggregation and methods for making and using them
The methodologies of the present invention demonstrate that a critical balance between pro- and anti-amyloidogenic molecules exists that regulates amyloid formation and cell death in Alzheimer\'s disease and Parkinson\'s disease. .beta.-Synuclein, the non-amyloidogenic homologue of .alpha.-synuclein, is a negative modulator of .alpha.-synuclein and A.beta. aggregation, having neuroprotective properties against .alpha.-synuclein and A.beta. neurotoxicity and that .beta.-synuclein and therapeutic agents derived therefrom block amyloidogenesis and neurodegeneration in vivo. The method of the present invention establishes that .beta.-synuclein blocks A.beta. aggregation either by direct inhibition of A.beta. amyloidogenesis or indirectly via either .alpha.-synuclein or its 35 a.a. NAC region, inferring neuroprotective characteristics within the effected cells. The generation of a transgenic mouse line and a cell system overexpressing .alpha.-synuclein characterizes the mechanisms by which .beta.-synuclein blocks .alpha.-synuclein and A.beta. aggregation and that this mechanism offers protection to the cell against amyloid formation as seen in the pathologies of Alzheimer\'s disease and Parkinson\'s disease.
Masliah; Eliezer (San Diego, CA), Rockenstein; Edward (Chula Vista, CA), Hashimoto; Makoto (La Jolla, CA)
The Regents of the University of California (Oakland, CA)
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