The other study, performed in humans and mouse models, demonstrated that in Alzheimer’s disease and other neurodegenerative diseases, such as frontotemporal dementia and dementia with Lewy bodies, the level of REST in neurons of the hippocampus and frontotemporal cortices does not increase in the nuclei, as observed in healthy aging humans, but remains in the cytoplasm, where it accumulates within autophagosomes together with misfolded proteins (Lu et al, 2014). Here, REST is linked to early-onset autosomal dominant Alzheimer disease.