Research 

Alzheimer’s disease (AD), the most common cause of dementia in the elderly, is now the fourth major cause of death in the developed world after heart disease, cancer, and stroke. Epidemiological studies have demonstrated that AD is a complex disorder with many proposed genetic and environmental etiologies.

 The fact that AD is a late-onset neurodegenerative disease with no accurate diagnostic markers makes the identification of the genetic, environmental, and therapeutic factors that modify risk for AD exceedingly difficult. Thus my laboratory has turned to the mouse as a genetically defined and tractable model to study AD phenotypes.

Over the past several years, we have focused on developing and characterizing genomic-based mouse models of AD through the introduction of complete copies of human AD genes into the germline of mice.

In particular, we have developed mutant amyloid precursor protein (APP) yeast artificial chromosome transgenic mice, which exhibit numerous biochemical, neuropathological, ultrastructural, and behavioral characteristics similar to those seen in human AD patients.

The current studies in my laboratory focus on using genomic-based transgenic mouse models of AD to identify and characterize modifiers of AD phenotypes in the mouse based on biochemistry, human genetics, mouse genetics, and environment.