Abstract: Provided are novel methods of inhibiting the propagation of pathological forms of tau between cells of the central nervous system by administration of an inhibitor of LRP1. LRP1 was discovered to facilitate the endocytosis of pathological forms of tau which enables the propagation of tau aggregates and resulting neurodegeneration. These methods enable the prevention and treatment of various tauopathies, such as Alzheimer's, chronic traumatic encephalopathy, corticobasal degeneration, and others.

Abstract: The invention is directed to the treatment of tauopathic neurodegenerative conditions and the underlying processes thereof. Based on the discovery that Rhes acts as a negative regulator of normal tau clearance, the compositions and methods of the invention may be applied to inhibit Rhes and reduce pathogenic tau aggregation. Rhes may be disrupted by disrupting RAS2D gene expression or reducing the abundance of Rhes protein in neurons. Additionally, post-translational modifications of Rhes may be targeted, including the disruption of Rhes farnesylation by the administration of farnesyltransferase inhibitors.

Abstract: The invention is directed to the treatment of tauopathic neurodegenerative conditions and the underlying processes thereof. Based on the discovery that Rhes acts as a negative regulator of normal tau clearance, the compositions and methods of the invention may be applied to inhibit Rhes and reduce pathogenic tau aggregation. Rhes may be disrupted by disrupting RAS2D gene expression or reducing the abundance of Rhes protein in neurons. Additionally, post-translational modifications of Rhes may be targeted, including the disruption of Rhes farnesylation by the administration of farnesyltransferase inhibitors.

Abstract: The invention is directed to the treatment of tauopathic neurodegenerative conditions and the underlying processes thereof. Based on the discovery that Rhes acts as a negative regulator of normal tau clearance, the compositions and methods of the invention may be applied to inhibit Rhes and reduce pathogenic tau aggregation. Rhes may be disrupted by disrupting RAS2D gene expression or reducing the abundance of Rhes protein in neurons. Additionally, post-translational modifications of Rhes may be targeted, including the disruption of Rhes farnesylation by the administration of farnesyltransferase inhibitors.

Abstract: The present invention relates to siRNA molecules derived from BACE1 and BACE2 genes. Accordingly, provided herein are siRNA molecules comprising a nucleotide sequence consisting essentially of a BACE1 or BACE2 gene. Also provided are methods for reducing the level of BACE1 protein in a cell. Further provided are methods for preparing a pharmaceutical composition comprising an siRNA with a pharmaceutically acceptable carrier.