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Although clinicians frequently add a second medication to an ineffective antidepressant, randomized trials comparing augmentation medications are lacking. In this study, adult outpatients with nonpsychotic major depressive disorder who had not had a remission during citalopram therapy were assigned to sustained-release bupropion or buspirone and had similar remission rates on the basis of clinician and self-reports. Several important secondary measures favored citalopram plus bupropion over citalopram plus buspirone. Adult outpatients with nonpsychotic major depressive disorder who had not had a remission during citalopram therapy were assigned to bupropion or buspirone and had similar remission rates. Several important secondary measures favored citalopram plus bupropion over citalopram plus buspirone. Numerous studies, 1 – 7 including one by Rush et al. 8 reported elsewhere in this issue of the Journal, have shown that major depressive disorder often requires more than one step of treatment to elicit a remission of symptoms. Frequently, a second medication is added to augment the first. 4 , 6 Augmentations of an initial selective serotonin-reuptake inhibitor (SSRI) with sustained-release bupropion, buspirone, mirtazapine, or dopamine agonists (e.g., pramipexole, dextroamphetamine, and methylphenidate) have been evaluated largely in open case series conducted in symptomatic volunteers with few psychiatric or general medical coexisting illnesses. 9 No randomized, controlled, prospective trials have directly compared two or more . . .

This review provides the rationale and background for the development of diagnostic criteria for depression of Alzheimer disease (AD), including risk factors and neurobiological correlates, epidemiology, and clinical characteristics, along with course, assessment, treatment, economics, a description of the criteria, and future research directions. Overall, there is substantial research to suggest that the depression that may co-occur with AD is different from other depressive disorders. Further research is needed to better define core symptoms, clinical course, and efficacy of treatments.

The authors, a group of investigators with extensive research and clinical experience related to both late-life depression and Alzheimer disease (AD), propose provisional affective and behavioral inclusion and exclusion diagnostic criteria for Depression of AD.

This study compared the effectiveness of four second-generation antipsychotic agents (olanzapine, risperidone, quetiapine, and ziprasidone) with that of an older agent, perphenazine, in patients with chronic schizophrenia. Olanzapine was the most effective agent but was associated with greater weight gain and more adverse metabolic changes. Perphenazine was as effective as risperidone, quetiapine, and ziprasidone. This study compared the effectiveness of four second-generation antipsychotic agents (olanzapine, risperidone, quetiapine, and ziprasidone) with that of an older agent, perphenazine, in patients with chronic schizophrenia. Antipsychotic drugs have become the cornerstone of treatment for schizophrenia. The first-generation “conventional” antipsychotic drugs are high-affinity antagonists of dopamine D2 receptors that are most effective against psychotic symptoms but have high rates of neurologic side effects, such as extrapyramidal signs and tardive dyskinesia. 1 The introduction of second-generation, or “atypical,” antipsychotic drugs promised enhanced efficacy and safety. 2 The atypical agents differ pharmacologically from previous antipsychotic agents in their lower affinity for dopamine D2 receptors and greater affinities for other neuroreceptors, including those for serotonin (5-hydroxytryptamine 1A , 2A , 2C , 3 , 6 , and 7 ) and norepinephrine . . .

In this randomized trial of atypical antipsychotic medications in patients with Alzheimer's disease and psychosis, aggression, or agitation, effectiveness (as measured by the time to drug discontinuation) was similar for olanzapine, risperidone, quetiapine, and placebo. Patients were more likely to stop taking placebo because of lack of efficacy and were likely to stop taking antipsychotic medications because of intolerability. In this trial of atypical antipsychotic medications in patients with Alzheimer's disease, effectiveness was similar for olanzapine, risperidone, quetiapine, and placebo. Patients were more likely to stop taking placebo because of lack of efficacy and to stop taking antipsychotic medications because of intolerability. Delusions, hallucinations, aggression, and agitation affect more than half of patients with Alzheimer's disease and related dementias. 1 – 4 Antipsychotic drugs are used to treat these behaviors and symptoms and are among the most frequently used psychotropic drugs in Alzheimer's disease. 5 , 6 Second-generation (atypical) antipsychotic drugs have been considered to be at least as effective as conventional antipsychotic agents such as haloperidol, with a lower risk of most adverse effects, 7 and are used as first-line pharmacologic treatments for patients with dementia. 5 , 8 However, there is a dearth of placebo-controlled and active-drug–controlled, randomized trials and longer-term data from controlled trials regarding the . . .

During the past several years, we have achieved a deeper understanding of the etiology/pathophysiology of major depressive disorder (MDD). However, this improved understanding has not translated to improved treatment outcome. Treatment often results in symptomatic improvement, but not full recovery. Clinical approaches are largely trial-and-error, and when the first treatment does not result in recovery for the patient, there is little proven scientific basis for choosing the next. One approach to enhancing treatment outcomes in MDD has been the use of standardized sequential treatment algorithms and measurement-based care. Such treatment algorithms stand in contrast to the personalized medicine approach, in which biomarkers would guide decision making. Incorporation of biomarker measurements into treatment algorithms could speed recovery from MDD by shortening or eliminating lengthy and ineffective trials. Recent research results suggest several classes of physiologic biomarkers may be useful for predicting response. These include brain structural or functional findings, as well as genomic, proteomic, and metabolomic measures. Recent data indicate that such measures, at baseline or early in the course of treatment, may constitute useful predictors of treatment outcome. Once such biomarkers are validated, they could form the basis of new paradigms for antidepressant treatment selection.

The objective of the present study was to examine the relationship between serum folate, vitamin B12, and homocysteine levels and the timing of clinical improvement to fluoxetine in major depressive disorder (MDD) patients. A total of 110 outpatients with MDD who responded to an 8-wk trial of fluoxetine had serum folate, B12, and homocysteine measurements at baseline (prior to fluoxetine initiation). Onset of clinical improvement was defined as a 30% decrease in Hamilton Depression Scale scores that led to a 50% decrease by week 8. Patients with low folate levels ([les ]2.5 ng/ml) were more likely to experience a later onset of clinical improvement than eufolatemic patients (p=0.0028). B12 and homocysteine level status did not predict time to clinical improvement (p>0.05). In conclusion, low serum folate levels were found to be associated with a delayed onset of clinical improvement during treatment with fluoxetine in MDD by, on average, 1.5 wk.

In a web-based survey asking adults diagnosed with bipolar disorder about illness management, we obtain frequency of self-reported usage and perceived helpfulness of 27 self-management strategies. We correlated the strategy use and perceived helpfulness with demographic and clinical characteristics, along with the Illness Intrusiveness Scale total score. Completed surveys were obtained from 1,024 individuals. Perceived helpfulness of 18 of 27 strategies was correlated negatively with illness intrusiveness at the P  < 0.001 level. Given limitations of web-based surveys, our study underscores the substantial negative impact of bipolar disorder, along with the potential of the Internet to enhance the use of self-management strategies.

Objective: There is a critical need for new researchers in psychiatry, including subspecialties such as geriatric psychiatry. Many existing research training programs focus on post-doctoral-level trainees and involve several years of hands-on research with experienced mentors at major universities. Although valuable, such programs have some limitations in expanding the pool of investigators in specific areas. In this article, the authors describe several successful short-term research training programs. Method: The authors, at the University of California, San Diego, coordinate three federally funded programs that take place during the summer and include trainees at different levels from across the United States. These programs are 1) Summer Training on Aging Research Topics-Mental Health (START-MH) for undergraduate, graduate, and medical students; 2) Stein Institute for Research on Aging (SIRA) Medical Student Training In Aging Research (MSTAR); and 3) Summer Research Institute (SRI) in Geriatric Psychiatry for postdoctoral fellows and junior faculty. The authors compare salient characteristics of these programs, illustrating similarities as well as differences. Results: The authors' experience to date suggests that these initiatives have been highly successful in attracting talented trainees at various levels, and the participants have found these experiences useful. The available follow-up suggests positive effects on research career development of the trainees, at least in the shorter run. Conclusions: There are several possible models that seem to have considerable promise for expanding the pool of scientists in a given field. Limitations of this approach as well as plans for the future are discussed.