Serum levels of brain-derived neurotrophic factor in remission, but not the acute phase, may predict the development from depression to dementia.

OBJECTIVES: Depression may be a risk factor or a prodromal symptom of dementia, and decreased serum levels of brain-derived neurotrophic factor (BDNF) have been observed in both depression and dementia. The aim of the present study was to determine whether serum levels of BDNF in the remitted or acute phase of depression predicted the transition from depression to dementia. METHODS: Serum levels of BDNF were measured in the acute phase of depression (n = 204) and after remission (n = 117), and we followed (mean: 24.3 months) the participants to assess the subsequent onset of dementia or mild cognitive impairment (MCI). RESULTS: Serum levels of BDNF after remission, but not those in the acute depressive phase, predicted the future development of dementia or MCI. CONCLUSIONS: Patients with low serum BDNF levels, even after depression remission, might have an increased risk of developing dementia. These findings suggest a potential association between residual low serum BDNF levels after remission and the prodromal state of dementia, or the involvement of BDNF in the transition from depression to dementia. However, given that this study is low-powered and preliminary, interpretation of the results should be approached with caution.

Clinical course and serum amyloid ß levels in elderly patients with major depressive disorder.

BACKGROUND: Depression is known to be a risk factor for Alzheimer's disease (AD). Changes in amyloid ß protein (Aß) metabolism have been speculated as a factor contributing to the transition from depression to AD. The aim of this study is to reveal the time course and state-dependency of Aß metabolism. METHODS: Serum Aß levels in 277 elderly (≥60 years) patients with depression (both early- and late-onset) were measured at admission, immediately after remission, and 1 year after remission, and compared them with 178 healthy subjects. RESULTS: The analysis revealed decreased Aß42 levels and increased Aß42/40 ratios in elderly patients with depression at admission compared with healthy subjects. These changes in the acute phase of depression were not normalized immediately after remission; however, they recovered to healthy levels 1 year after remission. LIMITATIONS: There is a possibility that the results may be influenced by antidepressants. CONCLUSIONS: These results suggest that altered Aß metabolism caused by depression may ameliorate, although after a lengthy period of time after remission. Our findings also suggest that the AD-related pathological changes caused or increased by depression can be reduced by maintaining remission for an extended period of time.