Associate Professor of Neuroscience, Mayo Clinic Arizona
Dr. Fryer’s lab is focused on understanding the cellular and molecular mechanisms of Alzheimer’s disease (AD) pathogenesis. During his graduate studies in the lab of Dr. David M. Holtzman, MD at Washington University in St. Louis, he elucidated the role of apolipoprotein E (apoE) in the formation of amyloid in the cerebrovasculature, termed cerebral amyloid angiopathy, a pathology that occurs in the majority of Alzheimer’s cases and can lead to fatal hemorrhages. For his postdoctoral work, Dr. Fryer joined the lab of Dr. Huda Y. Zoghbi, MD at Baylor College of Medicine (Houston, TX), where he studied detailed molecular mechanisms of underlying spinocerebellar ataxia type 1, a severe neurodegenerative disease due to a polyglutamine repeat expansion. Upon his recruitment to Mayo Clinic in 2011, he returned to the Alzheimer’s field and has focused on studying the role of the immune system in Alzheimer’s disease pathogenesis as well as the role of other AD genes such as Clusterin (CLU), also known as apolipoprotein J (apoJ). His lab published an unexpected role of CLU in the formation of cerebral amyloid angiopathy, but his recent work indicates that CLU also plays a role tau pathology. ApoE was recently shown to play a role in not only amyloid but also tau pathology, and CLU also seems to be another apolipoprotein that plays a role in this process. He continues to use mouse models and human tissue samples to study how CLU is impacting AD and hopes this understanding will lead to new therapeutic approaches to halt or slow the progression of AD pathology.