| Alzheimer's Disease (AD) is a leading cause of death and disability in elderly populations. There is currently no way to treat AD, and diagnosis can still only be definitively achieved post-mortem. Recently identified coding alterations in Triggering Receptor Expressed on Myeloid Cells-2 (TREM2) have been identified which substantially increase risk of developing late-onset AD (LOAD). In the current thesis, we examine the role of TREM2 in regulating AD related tau pathology and determine that TREM2 plays overall protective roles in regulating intraneuronal MAPT pathology. In addition, we characterize TREM2 expression in human peripheral blood monocytes, and determine that AD patients exhibit increased levels of inflammatory TREM2 positive monocytes. Our studies identify a novel target which may be utilized for the development of future AD therapeutics. |
