Mediation of estrogen actions by interactions with locally synthesized growth factors and their receptors, such as the neurotrophins in the brain, may represent a universal mechanism by which the effects of steroid hormones, such as estrogen, whose actions are widespread and varied, may exert local control and exhibit specificities at both tissue and developmental-stage levels. Cross-coupling of the ER and neurotrophin regulatory pathways may be relevant to understanding the mechanisms underlying not only the developmental actions of estrogen in the brain but also estrogen actions on neuronal survival, regeneration, repair and aging in brain regions that underlie learning, memory, and other cognitive functions. Estrogen and the neurotrophins may stimulate the synthesis of proteins required for neuronal differentiation, survival, and maintenance of function. In humans of both sexes, moreover, the natural decline in gonadal steroid levels, particularly in women, may contribute to the loss of neuronal systems vital to cognitive functions, whether this occurs to the extreme extent observed in Alzheimer's disease or follows the less traumatic path associated with the postmenopausal state and normal aging. Estrogen and neurotrophin interactions, latent since development, may be recruited, following loss of trophic support whether from injury or steroid deprivation, as occurs following the menopause, gonadectomy (especially ovariectomy), and anti-estrogen (tamoxifen) treatment for breast cancer, for example. Through their reciprocal interactions at transcrip-

tional, translational, and posttranslational levels, estrogen and the neurotrophins may have not only important and intertwined roles during brain development, but may also decrease the vulnerability of their target neurons to the consequences of neurodegenerative disease processes such as Alzheimer's disease.

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