Abstract: The present invention is based, at least in part on the discovery of therapeutic agents capable of preventing, inhibiting or modulating abnormal processing, misfolding or aggregation of protein. The therapeutic agents of the invention may prevent, inhibit or modulate the formation of inclusions. The therapeutic agents of the invention may also be capable of facilitating clearance and/or blocking the cellular toxicity of inclusions to treat or ameliorate disorders characterized by protein aggregation. Compounds which bind to structural motifs commonly found in protein aggregates, such as ?-sheets, would represent strong candidates for such compounds and are therefore desirable.

Abstract: The present invention provides nucleic acids encoding the Doppel (“Dpl”) protein, Dpl peptides, and assays utilizing the Dpl nucleic acids and/or peptides. In related aspects the invention features expression vectors and host cells comprising nucleic acids that encode a human Dpl polypeptide. The present invention also relates to antibodies that bind specifically to a human Dpl polypeptide, methods for producing human Dpl polypeptides, methods for identifying cells expressing Dpl, methods for using the Dpl gene and the Dpl polypeptide to alter cellular function and prion infectivity in culture or in vivo, and identification of individuals at risk for prion disorders by detecting alteration in Dpl coding and regulatory sequences and Dpl expression levels.

Abstract: The present invention provides nucleic acids encoding the Doppel (“Dpl”) protein, Dpl peptides, and assays utilizing the Dpl nucleic acids and/or peptides. In related aspects the invention features expression vectors and host cells comprising nucleic acids that encode a human Dpl polypeptide. The present invention also relates to antibodies that bind specifically to a human Dpl polypeptide, methods for producing human Dpl polypeptides, methods for identifying cells expressing Dpl, methods for using the Dpl gene and the Dpl polypeptide to alter cellular function and prion infectivity in culture or in vivo, and identification of individuals at risk for prion disorders by detecting alteration in Dpl coding and regulatory sequences and Dpl expression levels.