We previously reported that deficits in white matter function and pathology following chronic cerebral hypoperfusion was associated with increased density of microglia/macrophages [14, 15] Similarly, Nrf2−/− mice have been reported to have an increased number of microglia at baseline [47] and an exacerbated microglial response in disease models such as Parkinson’s disease [47] and Alzheimer’s disease [39–41]. The gene discussed is NFE2L2; the disease is early-onset autosomal dominant Alzheimer disease.