Estrogens, Conjugated Synthetic B(Teva Pharmaceutical Industries Ltd.)

Baseline differences in sex hormone levels between males and females influence tissues including the brain and eye. To investigate the effects of estrogens and androgens on ocular physiology and glaucoma, we review the current literature on the influence of primary sex hormones on ocular function, glaucoma incidence and related parameters like intraocular pressure (IOP) at physiologic levels and related to hormone therapies in men and women. These articles reveal activity of estrogen, testosterone, and progesterone within ocular tissues including the retinal pigment epithelium and ciliary epithelium where they likely influence glaucoma pathophysiology through effects on ocular blood flow and aqueous outflow. A growing body of evidence demonstrates a protective role of estrogen in glaucoma. With fluctuations across a woman's lifetime through menstrual phases, pregnancy, and menopause, the general association seen is a lower risk of glaucoma and lower IOP with higher estrogen. Exogenous hormones in the form of oral contraceptive pills and hormone replacement therapy also appear to affect glaucoma risk, although published findings are inconsistent. Few studies have reported a positive association between IOP and serum testosterone, and men treated with androgen deprivation therapy have shown a reduced risk of glaucoma while masculinizing hormone therapies at supra-physiologic testosterone levels have significantly increased IOP. Sex hormone perturbations affect components of glaucoma pathogenesis including IOP and ocular blood flow and overlap with known risk factors like age and sex. Standardized studies are needed to further elucidate the roles of estrogen and testosterone in glaucoma risk and progression.

Chronic stress profoundly affects the structure and function of the prefrontal cortex (PFC), a brain region critical for executive functions and emotional regulation. This review synthesizes current knowledge on stress-induced PFC plasticity, encompassing structural, functional, and molecular changes. We examine how chronic stress leads to dendritic atrophy, spine loss, and alterations in neuronal connectivity within the PFC, particularly affecting the medial PFC. These structural changes are accompanied by disruptions in neurotransmitter systems, most notably glutamatergic and GABAergic signaling, and alterations in synaptic plasticity mechanisms. At the molecular level, we discuss the intricate interplay between stress hormones, neurotrophic factors, and epigenetic modifications that underlie these changes. The review highlights the significant behavioral and cognitive consequences of stress-induced PFC plasticity, including impairments in working memory, decision-making, and emotional regulation, which may contribute to the development of stress-related psychiatric disorders. We also explore individual differences in stress susceptibility, focusing on sex-specific effects and age-dependent variations in stress responses. The role of estrogens in conferring stress resilience in females and the unique vulnerabilities of the developing and aging PFC are discussed. Finally, we consider potential pharmacological and non-pharmacological interventions that may mitigate or reverse stress-induced changes in the PFC. The review concludes by identifying key areas for future research, including the need for more studies on the reversibility of stress effects and the potential of emerging technologies in unraveling the complexities of PFC plasticity. This comprehensive overview underscores the critical importance of understanding stress-induced PFC plasticity for developing more effective strategies to prevent and treat stress-related mental health disorders.