Several possible mechanisms between estrogen and anti-PD have been studied, including anti-aggregation and fibril destabilization properties in α-synuclein, decreased inflammatory cytokines, decreased microglia activation, decreased leukocyte CNS entry, decreased apoptosis of neurons, increased dopamine synthesis, and increased expression of neurotrophic factors, such as glial cell line-derived neurotrophic factor (GDNF) and brain-derived neurotrophic factor (BDNF) [41–45]. This evidence concerns the gene GDNF and Parkinson disease.