Recent studies have suggested that depression may both contribute to the cause and also be the effect of brain abnormalities in patients with Alzheimer’s disease. Lifetime duration of depression was found to correlate with hippocampal volume reduction, although some disagreement exists (5). Gray matter atrophy has been documented in the subgenual prefrontal cortex of some depressed patients, and glial cell loss has been found in several prefrontal regions, the amygdala, and the hippocampus of depressed patients (5). Excessive secretion of glucocorticoids and other stress-related hormones reduce neurotrophic factors, inhibit neurogenesis, and may promote amyloid neurotoxicity, thus accelerating the pathological cascade of Alzheimer’s disease. Conversely, degenerative changes in brainstem aminergic nuclei occurring during Alzheimer’s disease have been thought to contribute to depression (6). Therefore, once depression develops as part of the brain changes of Alzheimer’s disease, it may further accelerate the progression of Alzheimer’s neuropathological changes. These observations suggest that antidepressants may confer benefits beyond decreasing depressive symptoms. Several antidepressants elevate brain-derived neurotrophic factor in the rat hippocampus, an action perhaps mediated by the 5-HT2A and the β-adrenoreceptor subtypes. Through this action, antidepressants may prevent stress-induced inhibition of neurogenesis and increase dendritic branching (7). It remains to be seen whether antidepressants delay the onset and slow down the progress of Alzheimer’s disease in patients with depressive symptoms.