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some evidence suggests a high number of CAG repeats may be associated with cognitive aging

androgens (like other steroid hormones) promote or repress the expression of genes specifying an array of cellular proteins

diurnal variation in testosterone levels

salivary testosterone correlated negatively with participant age and positively with CAG length variation in the AR gene

CAG repeat number varied inversely with reactivity of the ventral amygdala to facial expressions of negative affect

higher salivary testosterone was likewise associated with a greater number of AR CAG repeats

relative androgen insensitivity in ARs with a larger number of CAG repeats

Because circulating testosterone is regulated via negative feedback through the hypothalamic-pituitary-gonadal axis, diminished androgen sensitivity at higher CAG repeat lengths may reduce feedback suppression of luteinizing hormone (LH). LH would then be maintained at higher levels, in turn promoting higher testosterone production

Testosterone up-regulates AVP expression in the amygdala

Oxytocin exerts an inhibitory influence on AVP expression in the central amygdala, and the synthesis of oxytocin is mediated by estrogen and estrogen receptors

There is considerable evidence of modest cardiac and metabolic benefits that are shown to reduce cardiovascular risk plus sexual, mood, and quality of life changes associated with restoring testosterone levels

This study demonstrates that testosterone treatment either before or after EAE disease induction partially restores deficits in synaptic transmission, preserves presynaptic and postsynaptic integrity, and prevents hippocampal pathology.

treatment with a pregnancy estrogen, estriol, can prevent deficits in excitatory synaptic transmission in the hippocampus during EAE

testosterone is important to the maintenance of normal synaptic spine density in the hippocampus

estriol treatment was also capable of preserving levels of synaptic proteins that are known to orchestrate functional synaptic transmission within the hippocampus.

Estriol is a therapeutic candidate in MS because it has widespread effects on the immune system and the CNS

MS patients have significantly decreased relapse rates during the third trimester of pregnancy, when estriol levels are most elevated, and relapse rates rebound during the postpartum period coinciding with an abrupt decline in serum estriol levels

In nonpregnant MS patients, estriol treatment has been shown to significantly reduce gadolinium-enhancing lesion number and volumes measured by MRI

Different members of neurotrophins are expressed during cancer progression, suggesting their involvement in cell proliferation, anoikis protection, and malignancy

Regulation of the apoptotic machinery in prostate and colon cancer cells by testosterone occurs rapidly and is initiated at the plasma membrane level through specific membrane-binding sites not involving the classical cytoplasmic AR

testosterone exerts potent regulatory effects on prostate and colon cancer cell apoptosis

Testosterone increased cell death in a dose-dependent manner

testosterone antagonizes the prosurvival effects of DHEA in neuronal cells, blocking its binding to NGF receptors

treatment of cells with DHEA exerted a strong antiapoptotic effect,

Androgens hold a central role in prostate and colon cancer biology

elevated levels of DHEA or its sulfate ester DHEA-sulfate in young adults are associated to low incidence of androgen-dependent tumors

DHEA may play a protective role in young prostate

The decline of DHEA with aging may contribute to prostate cancer progression associated with advanced age

DHEA is an effective antiapoptotic factor, reversing the serum deprivation-induced apoptosis in prostate cancer cells (DU145 and LNCaP cell lines) as well as in colon cancer cells

NGF appears to exert similar antiapoptotic actions in both prostate and color cancer cells

exposure of prostate DU145 and colon Caco2 cancer cells to testosterone totally blocked the protective effects of both DHEA and NGF. These findings suggest that testosterone acts as an antagonist of DHEA and NGF

These findings support the hypothesis that testosterone may inhibit cancer cell growth by antagonizing the proliferative, antiapoptotic effects of endogenous factors, such as DHEA or NGF, in the case of prostate and colon cancer cells

intratumor hormonal microenvironment may play a critical role in tumor progression.

The paracrine interactions of androgens with locally produced NGF may define tumor cell fate

Bioavailable and free testosterone are known to correlate better than total testosterone with clinical sequelae of androgenization such as bone mineral density and muscle strength

peak levels seen in the morning following sleep, which can be maintained into the seventh decade

Samples should always be taken in the morning before 11 am

The reliable measurement of serum free testosterone requires equilibrium dialysis. This is not appropriate for clinical use as it is very time consuming and therefore expensive.

With increasing age, a greater number of men have total testosterone levels just below the normal range or in the low-normal range. In these patients total testosterone can be an unreliable indicator of hypogonadal status.

It is advised that at least two serum testosterone measurements, taken before 11 am on different mornings, are necessary to confirm the diagnosis.

Patients with serum total testosterone consistently below 8 nmol/l invariably demonstrate the clinical syndrome of hypogonadism and are likely to benefit from treatment. Patients with serum total testosterone in the range 8–12 nmol/l often have symptoms attributable to hypogonadism and it may be decided to offer either a clinical trial of testosterone treatment or to make further efforts to define serum bioavailable or free testosterone and then reconsider treatment. Patients with serum total testosterone persistently above 12 nmol/l do not have hypogonadism and symptoms are likely to be due to other disease states or ageing per se so testosterone treatment is not indicated.

Total testosterone levels fall at an average of 1.6% per year whilst free and bioavailable levels fall by 2%–3% per year.

With advancing age there is also a reduction in androgen receptor concentration in some target tissues and this may contribute to the clinical syndrome of LOH

Metabolic clearance declines with age

Gonadotrophin levels rise during aging (Feldman et al 2002) and testicular secretory responses to recombinant human chorionic gonadotrophin (hCG) are reduced

There are changes in the lutenising hormone (LH) production which consist of decreased LH pulse frequency and amplitude, (Veldhuis et al 1992; Pincus et al 1997) although pituitary production of LH in response to pharmacological stimulation with exogenous GnRH analogues is preserved

the decreases in testosterone levels with aging seem to reflect changes at all levels of the hypothalamic-pituitary-testicular axis