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Finally, increasing levels of testosterone through a negative feedback loop act on the hypothalamus and pituitary to inhibit the release of GnRH and FSH/LH, respectively. In addition, the amount of testosterone produced by existing Leydig cells is under the control of LH, which regulates the expression of 17β-hydroxysteroid dehydrogenase. The number of Leydig cells in turn is regulated by luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Testosterone is also synthesized in far smaller total quantities in women by the adrenal glands, thecal cells of the ovaries, and, during pregnancy, by the placenta. Testosterone has been found to act as an antagonist of the TrkA and p75NTR, receptors for the neurotrophin nerve growth factor (NGF), with high affinity (around 5 nM). Testosterone treatment for reasons other than possible improvement of sexual dysfunction may not be recommended. Testosterone is used as a medication for the treatment of male hypogonadism, gender dysphoria, and certain types of breast cancer. As demonstrated by a meta-analysis, substitution therapy with testosterone results in a significant reduction of inflammatory markers. Attention, memory, and spatial ability are key cognitive functions affected by testosterone in humans. A study reviewing the effects of AR antagonism in presymptomatic SOD1- G93A male mice, noted an earlier onset of myofiber atrophy when compared with female mice. Therefore, studies have explored androgen antagonists as a potential therapeutic strategy to modify disease progression. SBMA is caused by CAG expansion at the first exon of the androgen receptor gene. Dose-dependent effects of testosterone and association with ischemic stroke have been established. The following section highlights our current understanding of the role of androgens in certain CNS disorders and their potential therapeutic role across neurological domains. A deeper understanding of the mechanisms involved in neuroplasticity could guide therapeutic interventions with androgens such as testosterone replacement therapy (TRT) in neurological recovery in neurodegenerative diseases. 17β-estradiol (E2) is a naturally occurring steroid hormone synthesized by the ovaries in females or produced through the aromatization of testosterone in males (Cooke et al., 2017; Hariri and Rehman, 2023). Functioning as a neuroactive steroid, it plays a crucial role in modulating neurotransmitter systems affecting neuronal circuits and brain functions including learning and memory, reward and sexual behaviors. For example, inhibition of 5α reductase, which converts testosterone to the more potent androgen DHT, has been proposed as a novel antipsychotic (Paba et al. 2011), while estrogen therapies have shown promise as adjunctives to antipsychotics (Kulkarni et al. 2002). Moderating the effects of stress on dopamine signaling in vulnerable individuals may therefore help reduce the risk of transition to psychosis around adolescence. The amygdala and other areas were selected as ROIs based either on significant clusters found in preliminary whole brain main effects analyses, or due to established links between these regions, hormones, and pain and threat inhibitory pathways (Schulkin et al. 1998). Peper et al. (2009b) tested the hypothesis that having a male co-twin would alter levels of testosterone exposure in utero, and that this would link to differences in brain volume at age 9. Two studies measured testosterone levels before birth, and linked these to brain volumes in childhood. There is some evidence to suggest that testosterone effects on brain volume are more pronounced in men than in women. Lentini et al. (2013) found that testosterone levels positively correlated with grey matter volume in the parahippocampus, amygdala, insular cortex, and the occipital lobes in male and female adults. These results are strengthened by another report, which indicates that progesterone therapy induces a switch of the microglia phenotype from pro-inflammatory to anti-inflammatory and suppresses inflammasome markers after cuprizone-induced demyelination in mice . The remyelinating effect of progesterone was PR-dependent, as it was absent in PR knockout mice . Using different models of demyelination with toxins such as LPC or cuprizone, progesterone has been shown to promote myelin repair and to modulate inflammatory responses 104,117,118.
