TMEM106B is a key genetic risk factor in frontotemporal dementia (FTD). This gene encodes for the lysosomal transmembrane protein TMEM106B and often forms polymorphic dimers with itself (“homodimers”), with high levels protecting against the disease and lower levels leading to increased risk of FTD. For this project, I am conducting wet lab experiments at the Gitler Lab using a HEK293T (human embryonic kidney) cell model to determine how TMEM106B’s protein interaction partners differ between TMEM106B monomers and dimers. Specifically, I am using transfection to introduce these plasmid constructs into cells and immunoprecipitation to pull out my desired proteins, then sending them to a mass spectrometry facility in Australia and analyzing my results via bioinformatics tools. This research will provide new molecular insights into whether the monomerization of TMEM106B may affect its protein interaction partners and further elucidate mechanisms underpinning FTD.