Residual memory dysfunction in recurrent major depressive disorder-A longitudinal study from Juntendo University Mood Disorder Project
Department of Psychiatry, Juntendo University, School of Medicine, Tokyo, Japan. Journal of Affective Disorders
(Impact Factor: 3.38).
07/2012; 143(1-3). DOI: 10.1016/j.jad.2012.05.033
BACKGROUND: Depression may increase the risk of developing Alzheimer's disease. Large cohort studies have shown that recurrent depression is associated with a risk of developing dementia. Other studies have documented smaller hippocampal volume in patients with recurrent depression. It is speculative that a greater risk of developing dementia may result from a higher number of previous depressive episodes. This study compared patients with recurrent and single-episode depression in the remitted stage, and healthy controls to elucidate the impact of the number of depressive episodes on memory. METHODS: Logical memory and visual reproduction subtests of the Wechsler Memory Scale-Revised were given to 68 patients with major depressive disorder (MDD) (30 patients with a single episode and residual 38 patients with recurrent multiple episodes) and 57 healthy controls. The patients with MDD received memory assessment at the time of initial remission and at the follow-up period 3 years after remission. RESULTS: At the time of initial remission, scores of both logical memory and visual reproduction subtests were significantly lower in both patient groups compared with healthy controls. At follow-up, memory dysfunction of the single-episode group disappeared, whereas scores in the recurrent group remained significantly lower than those of the single-episode group and controls. LIMITATIONS: All patients in the present study were on antidepressant medications. CONCLUSIONS: Patients with recurrent MDD with multiple depressive episodes showed residual memory dysfunction even after 3 years of remission. Persistence of memory deficits in the recurrent depression may be a risk factor for developing dementia.
Available from: Tonita E Wroolie
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ABSTRACT: The objective of this study was to examine the effects of estrogen-based hormone therapy (HT) on regional cerebral metabolism in postmenopausal women (mean age = 58, SD = 5) at risk for development of dementia. The prospective clinical trial design included pre- and post-intervention neuroimaging of women randomized to continue (HT+) or discontinue (HT-) therapy following an average of 10 years of use. The primary outcome measure was change in brain metabolism during the subsequent two years, as assessed with fluorodeoxyglucose-18 positron emission tomography (FDG-PET). Longitudinal FDG-PET data were available for 45 study completers. Results showed that women randomized to continue HT experienced relative preservation of frontal and parietal cortical metabolism, compared with women randomized to discontinue HT. Women who discontinued 17-β estradiol (17βE)-based HT, as well as women who continued conjugated equine estrogen (CEE)-based HT, exhibited significant decline in metabolism of the precuneus/posterior cingulate cortical (PCC) area. Significant decline in PCC metabolism was additionally seen in women taking concurrent progestins (with either 17βE or CEE). Together, these findings suggest that among postmenopausal subjects at risk for developing dementia, regional cerebral cortical metabolism is relatively preserved for at least two years in women randomized to continue HT, compared with women randomized to discontinue HT. In addition, continuing unopposed 17βE therapy is associated specifically with preservation of metabolism in PCC, known to undergo the most significant decline in the earliest stages of Alzheimer's disease.
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ABSTRACT: Patients with major depressive disorder (MDD) are known to present with cognitive deficits; however, the presence of these deficits in the remitted state have been inconsistent. One of the most important factors potentially contributing to inconsistencies between studies may be the influence of medications. To explore the influence of antidepressants on cognitive performance in remitted MDD, we evaluated memory and executive functions using Wechsler Memory Scale-Revised and Stroop Color and Word Test, and compared performance among 50 medicated (29 treated with tricyclic antidepressants [TCA], 21 treated with selective serotonin reuptake inhibitors or serotonin noradrenalin reuptake inhibitors) and 19 medication-free MDD patients and 31 controls. The results showed that all 3 MDD groups had significantly lower performance for verbal memory compared with controls. Both medicated groups showed significantly lower performance for visual memory compared with controls; however, the medication-free group did not differ from controls. For the executive function, only the TCA group showed a significantly lower performance compared with controls. These results suggest that cognitive impairment remained even in remitted patients with MDD, however, part of this impairment may be influenced by class-specific antidepressant side effects.
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Older patients may be more vulnerable to the deleterious effect of depressive episodes on delayed narrative memory, a cognitive task which reflects hippocampal activity. We aimed to disentangle which factors could explain such increased vulnerability in the elderly, including the poorer response to treatment, a longer lifetime exposure to past depressive episodes, and lower baseline memory skills.
From an initial sample of 8,229 depressed outpatients, we focused on the 2,424 treatment responders, and compared older (65 years old and over, N = 233) to younger (N = 2,191) ones. These patients were included through general practitioners' assessment and tested for the Wechsler delayed paragraph recall index, a valid and sensitive test assessing verbal declarative memory (and a marker of the hippocampal function), at baseline and after six weeks of treatment.
As expected, older patients after response to antidepressants showed decreased narrative memory abilities compared to younger ones. As baseline memory performance and residual depressive symptoms were also found in excess in this sample, they could act as confounders. Indeed, after controlling for these two factors, the role of age in memory performance after treatment response was ruled out.
The potential "toxicity" of a depressive episode to cognitive functions related to the hippocampus may not be more critical in older patients compared to younger ones. Limiting remaining depressive symptoms in older depressed patients might be a way to counteract the observed worsening of memory functions in depressed patients.
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