FIG. 4. Proposed multicellular mechanism of estrogen neuroprotection.
Estrogen neuroprotection is proposed to be mediated by genomic, nongenomic and anti-inflammatory mechanisms. Both direct effects on neurons and indirect effects mediated via astrocytes, endothelial cells and microglia are suggested to contribute to the overall protective actions of estrogen in the brain. E2 = 17β-Estradiol, ER = estrogen receptor, ERK = extracellular signal regulated kinase, JNK = Jun NH(2)-terminal kinase, (?) = unknown mediators. See text for further detailed description.