Are transmembrane protein 106B levels a therapeutic target for frontotemporal dementia?

Takeaway

  • Loss of transmembrane protein 106B biological function leads to myelination deficits in a genetic mouse model of frontotemporal dementia.

Why this matters

    There is increasing interest in the feasibility of transmembrane protein 106B as a potential therapeutic target in frontotemporal dementia. These novel findings provide important information about the impact of lowering these protein levels in a unique mouse model.