Likewise, neurochemical and immunohistochemical studies conducted in recent years indicated that long-term caffeine intake in various animal models of Parkinson’s disease: (1) increased dopamine levels, (2) reversed the enhanced dopamine and noradrenalin levels in striatum, (3) improved the hippocampal neuronal viability, (4) increased tyrosine hydroxylase immunoreactivity in the striatum, (5) reduced the number of immunopositive cells for histone deacetylase, (6) decreased the level of pro-inflammatory cytokines, such as TNF-α and IL-1β [204,210,212,213,214,215]. This evidence concerns the gene IL1B and Parkinson disease.