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For the effects of androgens on sexual functioning, aromatization of T is probably not required; but for other effects on the brain the evidence is much stronger, and it seems recommendable that androgen-de cient men, including the androgende cient aging male, should receive an aromatizable androgen preparation It is of note that almost all the above studies are observational and in need of replication Placebocontrolled studies proving the bene ts of (aromatizable) androgens on cognitive functioning, and prevention or slowing of dementia, are lacking Therefore, it is too early to recommend androgens to improve the age-related decline of cognition in men

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With regard to Alzheimer disease, men are relatively protected in comparison to women One intriguing possibility is the putative neuroprotective effect of estrogens in preventing or retarding this condition [147] Estrogens increase choline acetyltransferase, the enzyme needed to synthesize acetylcholine [148] The assumption that postmenopausal women enjoy protection from Alzheimer disease when they receive estrogen replacement therapy has been challenged by the recently discontinued Women s Health Initiative (WHI) study The WHI Memory Study showed that the combination of conjugated equine estrogens and progestagens increased the risk of probable dementia in postmenopausal women aged 65 years or over [149] This could be due to the antagonistic effects of medroxyprogesterone acetate on the positive effects of estrogens on cognitive functions [150], and not to estrogenic effects per se There is evidence that androgens confer protection from Alzheimer disease in their own right [151] So there may be an advantage in supplementing androgens in aging men whose T levels have fallen below a certain limit, thereby in fact substituting both androgens and estrogens Not all studies in aging men are in agreement, however A recent study [152] found only a link between cognition and estrogens in women but not in men, whereas Yaffe et al found a correlation between cognitive functioning and BT, but not E2 [153] Estrogens contribute to explicit (or declarative) memory function through their action on hippocampal neurons The implication of this estrogen effect is improved (conscious) recall of facts, events, and autobiographic memories [153,154] Explicit memory is considered the cognitive function that is most vulnerable to loss of estrogen Women receiving estrogen replacement, and men whose estrogen levels are above those of postmenopausal women, score better on explicit memory tasks [155]

Aging is the most robust risk factor predicting erectile dif culties It is obvious that aging per se is associated with a deterioration of the biologic functions mediating erectile function: hormonal, vascular, and neural processes This is often aggravated by intercurrent disease in old age, such as diabetes mellitus, cardiovascular disease, and use of medical drugs T is only one of the elements which may explain sexual dysfunction with aging It has been repeatedly shown in hypogonadal patients (with a wide age range) that sexual functions only require androgen levels below or at the lower end of reference values of T [8 10] The relative androgen-independence of erections in response to erotic stimuli in the rst studies [33], since then challenged in many others [156], and the relatively low androgen levels required, suggest that T was not a useful treatment for men with erectile dif culties whose T levels were usually only marginally low This was reinforced with the advent of intracorporal smooth muscle relaxants (papaverine, prostaglandin E1), later superseded by the PDE5i, hailed as the ultimate successful treatment of ED As already detailed in p 231, T therapyreplacement alone may not suf ce to restore erectile potency in every case since ED is often multifactorial in aging patients It is a matter of clinical judgment what type of treatment should be tried rst, PDE5i or T, but it is important to remember that insuf cient success of one type of treatment might require

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