Furthermore, treatment with DMF alleviated tauopathy, decreased GSK-3β activity, and promoted neuronal viability by increasing brain-derived neurotrophic factor (BDNF) expression and reduced inflammatory processes in the hippocampus of Nrf2 −/− mice that stereotaxically expressed the human TAUP301L gene, which is a tau modification responsible for frontotemporal dementia [73]. Here, BDNF is linked to frontotemporal dementia.