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Review
. 2009 Jul;30(2):106-18.
doi: 10.1016/j.yfrne.2009.04.016. Epub 2009 May 18.

Neuroprotective actions of brain aromatase

Colin J Saldanha  1 , Kelli A Duncan, Bradley J Walters
Affiliations
Review

Neuroprotective actions of brain aromatase

Colin J Saldanha et al. Front Neuroendocrinol. 2009 Jul.

Abstract

The steroidal regulation of vertebrate neuroanatomy and neurophysiology includes a seemingly unending list of brain areas, cellular structures and behaviors modulated by these hormones. Estrogens, in particular have emerged as potent neuromodulators, exerting a range of effects including neuroprotection and perhaps neural repair. In songbirds and mammals, the brain itself appears to be the site of injury-induced estrogen synthesis via the rapid transcription and translation of aromatase (estrogen synthase) in astroglia. This induction seems to occur regardless of the nature and location of primary brain damage. The induced expression of aromatase apparently elevates local estrogen levels enough to interfere with apoptotic pathways, thereby decreasing secondary degeneration and ultimately lessening the extent of damage. There is even evidence suggesting that aromatization may affect injury-induced cytogenesis. Thus, aromatization in the brain appears to confer neuroprotection by an array of mechanisms that involve the deceleration and acceleration of degeneration and repair, respectively. We are only beginning to understand the factors responsible for the injury-induced transcription of aromatase in astroglia. In contrast, much of the manner in which local and circulating estrogens may achieve their neuroprotective effects has been elucidated. However, gaps in our knowledge include issues about the cell-specific regulation of aromatase expression, steroidal influences of aromatization distinct from estrogen formation, and questions about the role of constitutive aromatase in neuroprotection. Here we describe the considerable consensus and some interesting differences in knowledge gained from studies conducted on diverse animal models, experimental paradigms and preparations towards understanding the neuroprotective actions of brain aromatase.

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Figures

Figure 1
Figure 1
This schematic represents the conceptual framework of this review. Brain damage results in an upregulation of aromatase transcription and translation in reactive astrocytes and radial glia (astroglia) in birds and mammals by mechanisms that are poorly understood. Components of the steroidogenic pathway including progestins and androgens themselves have some neuroprotective effects (gray arrows). However, it is often via their conversion to estrogens (black arrows) that these steroids may protect the brain from structural and functional degeneration. This influence is known to include, but is not limited to, actions on apoptotic and inflammatory pathways. Classical progesterone receptors (PR), androgen receptors (AR), and estrogen receptors (ER) have all been implicated in these effects, although some data do support estrogenic effects on neuroprotective mechanisms via ER-independent pathways.
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