Zhu et al. (2024) investigated the anti-inflammatory potential of naringenin in AD, emphasizing its ability to reduce glial activation and cytokine production. In APP/PS1 transgenic mice, chronic administration of NRG significantly reduced the number of reactive microglia and astrocytes near Aβ plaques, as confirmed by immunohistochemical and molecular analyses. Naringenin treatment also led to a marked decline in the expression of pro-inflammatory markers such as TNF-α and IL-1β in brain regions commonly affected in AD. The gene discussed is TNF; the disease is Alzheimer disease.