We examine the role of physiologically derived androgens and androgenic supplements in neurodevelopment and neuroplasticity and delve into the involvement of androgen pathways in the pathogenesis of various neurological disorders. These exploratory findings suggest that testosterone treatment is safe and well tolerated and has potential protective effects and improved cognition in MS patients. Moreover, it could be hypothesized that the later age of onset of MS in men, relative to women, may result from the age-related decline in protective testosterone levels . In this study, we reported the unexpected observation that myelin is already sexually differentiated in early postnatal life.
Overall, the sexual brain is a complex and fascinating area of study that continues to yield new insights into human sexuality and behaviour. The neurotransmitters dopamine, serotonin, and norepinephrine are also important in sexual function, as they affect mood, motivation, and arousal . Other areas of the brain, such as the amygdala, prefrontal cortex, and insula, are also involved in processing sexual stimuli and generating sexual responses . Overall, this comprehensive review provides a valuable synthesis of current knowledge on the sexual brain, offering insights into the neurobiological mechanisms underlying human sexual response. Finally, the review acknowledges the importance of societal and cultural factors in shaping sexual behaviour and the brain’s response to sexual stimuli. Moreover, the review examines the influence of sexual orientation on the neural processing of sexual stimuli, emphasizing the differentiation between romantic love and sexual desire in the brain.
In the sciatic nerve of streptozotocin (STZ)-treated animals (i.e., an experimental model of diabetes inducing peripheral neuropathy), the levels of PREG, T, DHT and 3α-diol were significantly decreased in males but not in females, while those of PROG, THP and isopregnanolone were decreased only in females . P0 and PMP22 play an important role for the maintenance of the multilamellar structure of PNS myelin . In further support of a classic genomic mechanism, steroid receptor coactivator (SRC)-1, a member of the p160 family of nuclear receptor coactivators , is involved in the control of P0 expression . Another myelin protein, the peripheral myelin protein 22 (PMP22) is under the control of THP and 3α-diol 11,16,53,54. Therefore, neuroactive steroids may regulate PNS physiology through different signaling pathways. Thus, PNS express steroidogenic capability as well as the presence of consistent in situ amounts of neuroactive steroids.
Glial cells in the demyelinating lesions appear to be the primary site of expression of steroidogenic enzymes and steroid receptors 85,87. These neuroactive steroids (S) either derived from the systemic circulation or produced locally in the brain, bind and dissociate nuclear receptors (SR) from HSPs (heat shock proteins). The term "neuroactive steroid" corresponds to a functional concept and refers to natural hormonal steroids, produced by the nervous system or the peripheral glands, and to synthetic steroids, that modify the activity of neural cells.
These conditions can affect the brain and nervous system, leading to changes in sexual desire, arousal, and performance. In addition to these specific disorders, other conditions such as depression, anxiety, and stress can significantly impact sexual function. Some studies suggest that HSDD may be linked to changes in brain chemistry, particularly in the neurotransmitters dopamine and serotonin, which regulate mood and motivation . Other factors, such as social and cultural influences, genetic factors, and individual experiences, also play a role in developing sexual orientation. However, it is essential to note that sexual orientation is complex and multifaceted and cannot be reduced to differences in brain structure alone. LeVay compared the brains of homosexual and heterosexual men and found differences in the size of the anterior hypothalamus .
A study of the effects of pubertal induction with monthly testosterone injections in young boys aged 12 to 17 years receiving glucocorticoids demonstrated no effects on bone density or bone age advancement but improved muscle strength. 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. It is hypothesized that loss of function of ARs located at spinal motor neurons, skeletal muscles, and certain cranial nerves increases axonal vulnerability to various insults, contributing to disease pathogenesis . SBMA is caused by CAG expansion at the first exon of the androgen receptor gene. Spinal and bulbar muscular atrophy (SBMA), also known as Kennedy disease, is an X-linked neuromuscular disease characterized by loss of lower motor neurons located in the brainstem and spinal cord. One study highlighted an association between decreased free testosterone levels and an increased risk of aneurysmal subarachnoid hemorrhage (SAH) in women .
Mutations in the AR can lead to several diseases in humans such as cancer, Kennedy’s disease (spinal and bulbar muscular atrophy) and complete androgen insensitivity syndrome (CAIS) 128,129,130. Interestingly, treatment with 5a-DHP, a progesterone metabolite, has been shown to increase the expression of MBP in the spinal cord of streptozotocin (STZ)-induced diabetic rats . 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. In this model, progesterone also promoted the differentiation of proliferating OPCs into mature oligodendrocytes and exerted myelinating, neuroprotective and anti-inflammatory actions 111,114. Furthermore, it decreased the number of astrocytes and microglial cells and down-regulated mRNA expression of inflammatory factors such as interleukin-1β, tumor necrosis factor α, interleukin-6, inducible nitric oxide synthase and cyclooxygenase-2 111,112,113. Axons of Purkinje cells are labelled with Calbindin marker, in red and myelin is labelled with MBP marker, in green. Then, slices were demyelinated by lysolecithin (LPC) and treated for 5 days with vehicle (middle panel), progestins (progesterone or nestorone; right panel).

Gender : Male