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Onset of motor deficits, but not their severity, is augmented by TREM2 reduction in P301S tau transgenic mice

Alzheimer’s disease (AD) is characterised by extracellular amyloid‐β plaques and intracellular neurofibrillary tangles composed of the hyperphosphorylated microtubule associated protein tau. These two pathological hallmarks have been explored for decades however it remains not fully understood how they interact with each other and how they trigger disease onset and progression. Recently, in genome wide association studies other genetic risk factors have been identified. One of them being polymorphisms of the triggering receptor expressed on myeloid cells 2 (TREM2). The effects of TREM2 on disease and especially in the context of tau pathology remain poorly understood and the current literature is conflicting.