Testosterone depletion is a normal consequence of aging in men that is associated with senescent effects in androgen- responsive tissues. We discuss new evidence that one consequence of testosterone depletion in men is an increased risk for the development of Alzheimer's disease (AD). Furthermore, we discuss two candidate mechanisms by which testosterone may affect AD pathogenesis. First, testosterone has been identified as an endogenous regulator of beta-amyloid, a protein that abnormally accumulates in AD brain and is implicated as a causal factor in the disease. Second, findings from several different paradigms indicate that testosterone has both neurotrophic and neuroprotective functions. These new findings support the clinical evaluation of androgen-based therapies for the prevention and treatment of AD.