Both mAbs showed marked reductionof Aβ plaques by positron emission tomography in patients whomet the clinical criteria of Alzheimer’s disease.90,91 However, given the complexity of protein aggregation processes,an attractive therapeutic strategy is to stabilize the native stateof aggregation-prone proteins.92,93 Here, our data areconsistent with a model whereby interdomain contacts, mediated byspecific RNA sequences, stabilize the native state of TDP-43 and preventaggregation. Here, TARDBP is linked to Alzheimer disease.