TREM2 has recently been associated as an Alzheimer’s Disease risk gene. Little is known about TREM2, even in the context of Alzheimer’s Disease pathology. Unpublished data from Jay and colleagues suggests that TREM2 knockout mice may have a disruption of the synaptic pruning process in development. Because TREM2 is primarily expressed by microglia, which are the primary phagocytes in the central nervous system, the current study attempts to address how TREM2 affects synaptic pruning by microglia in development. Using immunohistochemistry, no differences in microglia morphology were found between TREM2 heterozygote and wild-type mice. These differences could be attributed to the lack of evidence in the current literature that shows no differences between TREM2 heterozygotes and wild-type littermates. To determine whether there are truly no differences between mice with a TREM2 deficiency and wild-type littermates, future studies with TREM2 knockout mice should follow up looking at a time point in between 21 days and 4 months of age.


Stavnezer, Amy Jo




Developmental Neuroscience | Molecular and Cellular Neuroscience | Molecular Genetics | Other Cell and Developmental Biology


microglia, TREM2, synaptic pruning, mouse, mice, immunohistochemistry, glia, glial cells, classical complement cascade, Fractalkine

Publication Date


Degree Granted

Bachelor of Arts

Document Type

Senior Independent Study Thesis



© Copyright 2016 William Walker V. Maghie