Abstract: Methods are provided for treating dementia and or impaired cognition, as well as assays useful for identifying novel anti-dementia agents. Compounds and compositions for treating dementia and or impaired cognition are also provided.

Abstract: Provided are non-human mammals comprising a knock-in nucleic acid sequence capable of causing an alteration of expression of wild-type Bri2 in the mammal or a knockout of wild-type Bri2. Also provided are the non-human mammals as a model for Alzheimer's disease.

Abstract: Provided are non-human mammals comprising a transgenic nucleic acid sequence capable of causing an alteration of expression of Bri2 or Bri3 in the mammal. Also provided are non-human mammals comprising a Bri2 or Bri3 gene under the control of the native Bri2 or Bri3 promoter. Additionally provided are non-human mammals genetically engineered to lack expression of a Bri2 or Bri3 gene. Further, non-human mammals comprising a transgene encoding a Bri2 or Bri3 protein under the control of the ?CaMKII promoter are provided. Non-human mammals comprising a transgene encoding a furin protein are additionally provided. Embryonic stem cells of any of the above-described non-human mammals are further provided. Methods of screening a compound for treatment of a disease characterized by cerebral amyloidosis are additionally provided. Also provided are methods of making transgenic non-human mammals.

Abstract: Provided are methods for reducing inhibiting or preventing A? and/or AID production by a cell and methods of treating a subject having Alzheimer's disease. Also provided are methods of determining whether a compound is a mimic of a BRI2 or a BRI3. Additionally provided are pharmaceutical compositions of BRI2, BRI3 or furin, or vectors encoding those proteins.