The Time to Change for Mental Health and Wellbeing via Virtual Professional Coaching: Longitudinal Observational Study.

BACKGROUND: Optimal mental health yields many benefits and reduced costs to employees and organizations; however, the workplace introduces challenges to building and maintaining mental health that affects wellbeing. While many organizations have introduced programming to aid employee mental health and wellbeing, the uptake and effectiveness of these efforts vary. One barrier to developing more effective interventions is a lack of understanding about how to improve wellbeing over time. The current study examined not only whether employer-provided coaching is an effective strategy to improve mental health and wellbeing in employees; but also how this intervention changes wellbeing in stages over time. OBJECTIVE: The goal of this study was to determine whether BetterUp, a longitudinal one-on-one virtual coaching intervention, improves components of mental health and psychological wellbeing and whether the magnitude of changes vary in stages over time. This is the first research study to evaluate the effectiveness of professional coaching through three repeated assessments, moving beyond a pre- to post-intervention design. The outcomes of this study will enable coaches and employers to design more targeted interventions by outlining when to expect maximal growth in specific outcomes throughout the coaching engagement. METHODS: Three identical assessments were completed by 391 users of BetterUp - prior to the start of coaching, after approximately 3-4 months of coaching, and again after 6-7 months of coaching. Three scales were used to evaluate psychological and behavioral dimensions that support management of mental health - stress management, resilience, and life satisfaction. Six additional scales assessed psychological wellbeing - emotional regulation, prospection ability, finding purpose and meaning, self-awareness, self-efficacy, and social connection. RESULTS: Using mixed effects modeling, varying rates of change were observed in several dimensions of mental health and psychological wellbeing. Initial rapid improvements in the first half of the intervention, followed by slower growth in the second half of the intervention, were found for prospection ability, self-awareness, self-efficacy, social connection, emotional regulation, and a reduction in stress (range of unstandardized ßs for each assessment: .10-.19). Life satisfaction improved continuously throughout the full intervention period (ß: .13). Finding purpose in meaning at work and building resilience both grew continuously throughout the coaching intervention, but larger gains were experienced in the second half of the intervention (ßs: .08-.18), requiring the full length of the intervention to realize maximal growth. CONCLUSIONS: The results demonstrate the effectiveness of the BetterUp virtual one-on-one coaching to improve psychological wellbeing, while mitigating threats to mental health such as excessive and prolonged stress, low resilience, and poor satisfaction with life. The improvements across the collection of outcomes were time-dependent and provide important insights to users and practitioners about how and when to expect maximal improvements in a range of interrelated personal and professional outcomes.

From student to steward: the Interdisciplinary Program in Neuroscience at Georgetown University as a case study in professional development during doctoral training.

A key facet of professional development is the formation of professional identity. At its most basic level, professional identity for a scientist centers on mastery of a discipline and the development of research skills during doctoral training. To develop a broader understanding of professional identity in the context of doctoral training, the Carnegie Initiative on the Doctorate (CID) ran a multi-institutional study from 2001 to 2005. A key outcome of the CID was the development of the concept of 'stewards of the discipline'. The Interdisciplinary Program in Neuroscience (IPN) at Georgetown University participated in CID from 2003 to 2005. Here, we describe the IPN and highlight the programmatic developments resulting from participation in the CID. In particular, we emphasize programmatic activities that are designed to promote professional skills in parallel with scientific development. We describe activities in the domains of leadership, communication, teaching, public outreach, ethics, collaboration, and mentorship. Finally, we provide data that demonstrate that traditional metrics of academic success are not adversely affected by the inclusion of professional development activities in the curricula. By incorporating these seven 'professional development' activities into the required coursework and dissertation research experience, the IPN motivates students to become stewards of the discipline.

Desipramine induced changes in the norepinephrine transporter, alpha- and gamma-synuclein in the hippocampus, amygdala and striatum.

The high incidence of depression in Parkinson's disease (PD) has been well documented in the clinic; however, the underlying molecular mechanisms of these overlapping pathologies remain elusive. Using a rodent model of depression, the Wistar-Kyoto (WKY) rat, we previously demonstrated that in the frontal cortex the altered expression and protein interactions of alpha- and gamma-synuclein (alpha-Syn, gamma-Syn) were associated with dysregulated trafficking of the norepinephrine transporter (NET). Chronic treatment with desipramine (DMI), a NET-selective antidepressant, caused a disappearance of depressive-like behavior that was accompanied by a change in alpha-Syn and gamma-Syn expression and their trafficking of NET. Using this same model, we examined the expression of NET, alpha-Syn and gamma-Syn in the hippocampus, amygdale, brainstem, and striatum, all regions implicated in the development or maintenance of depression or PD pathology. Following chronic treatment with DMI, we observed a significant decrease in NET in the hippocampus, amygdala, and brainstem; decrease in gamma-Syn in the hippocampus and amygdala; and, increase in alpha-Syn in the hippocampus and amygdala. Unexpectedly, we observed a significant decrease in alpha-Syn expression in the striatum of the WKY following chronic DMI treatment. The altered expression of NET, alpha-Syn and gamma-Syn in different brain suggest that DMI's ability to improve depressive-like behavior in a rodent is associated with region-specific changes in the regulation of NET by alpha- and gamma-Syn.

Desipramine modulation of alpha-, gamma-synuclein, and the norepinephrine transporter in an animal model of depression.

The mechanisms underlying depression remain elusive. We previously determined that alpha-synuclein (alpha-Syn) modulates the activity and trafficking of the norepinephrine transporter (NET) in a manner that is dependent on its interactions with microtubules (MTs). Here we sought to determine if alpha-Syn, or the other synuclein family members, beta-synuclein (beta-Syn) and gamma-synuclein (gamma-Syn), modulate NET activity in an animal model of depression, the Wistar-Kyoto (WKY) rat. The NET-selective antidepressant desipramine (DMI) was chronically administered for 14 days to WKY rats and the strain from which it was outbred that does not show depressive-like behavior, the Wistar rat. This drug regimen induced significant behavioral improvements in the WKY, but not the Wistar rat, in the forced swim test. In WKY rats there was an overexpression of gamma-Syn which was reduced following DMI treatment. In parallel, DMI caused an increase in both alpha-Syn and NET in the frontal cortex. Frontal cortex synaptosomes from WKY rats were not sensitive to nocodazole, a compound that promotes MT destabilization. However, in WKYs treated with DMI, nocodazole induced an increase in [(3)H]-NE uptake. This trend was reversed in Wistars. Underlying these DMI-induced changes were alterations in the protein interactions between the synucleins and NET with the tubulins. These results are the first to implicate alpha-Syn or gamma-Syn in the pathophysiology of depression and suggest that targeting synucleins may provide a new therapeutic option for depression.

Regulated interactions of the norepineprhine transporter by the actin and microtubule cytoskeletons.

One role of the actin cytoskeleton is to maintain the structural morphology and activity of the pre-synaptic terminal. We sought to determine if the actin cytoskeleton plays a role in regulating interactions between the norepinephrine transporter (NET) and alpha-Synuclein (alpha-Syn), two proteins expressed in the pre-synaptic terminal. In cells transfected with either 0.5 microg/mL or 3 microg/mL of alpha-Syn and 1 microg/mL of NET DNA, treatment with cytochalasin D, an actin depolymerizing agent, caused a dose-dependent decrease and increase, respectively, in [3H]-NE uptake. Protein interactions between NET, beta-actin, and alpha-Syn were modified, along with levels of surface transporters. Treatment of primary brainstem neurons and frontal cortex synaptosomes with cytochalasin D caused a 115% and 28% increase, respectively, in NET activity. Depolymerization of both actin and microtubules did not alter NET activity in cells with 0.5 microg/mL alpha-Syn, but caused an increase in [3H]-NE uptake in cells transfected with 3 microg/mL of alpha-Syn and primary neurons. This is the first direct demonstration of NET activity being regulated via actin and modulated by interactions with alpha-Syn.

Regulation of the norepinephrine transporter by alpha-synuclein-mediated interactions with microtubules.

alpha-Synuclein (alpha-Syn) regulates catecholaminergic neurotransmission. We demonstrate that alpha-Syn regulates the activity and surface expression of the norepinephrine transporter (NET), depending on its expression levels. In cells co-transfected with NET and low amounts of alpha-Syn, NET activity and cell surface expression were increased and protein interactions with alpha-Syn decreased, compared with cells transfected with NET alone. Converse effects were observed at higher levels of alpha-Syn expression. Treatment with nocodazole and other microtubule (MT) destabilizers abolished the expression-dependent bimodal regulation of NET by alpha-Syn. At low alpha-Syn levels, nocodazole had no effect on NET surface expression or protein interactions, while inducing increases in these measures at higher levels. Cells that were transfected with NET alone displayed no sensitivity to nocodazole, indicating that alpha-Syn expression was necessary for the MT-dependent changes in NET activity. MT destabilizers also caused a significant increase in [(3)H]-NE uptake in brainstem primary neurons and synaptosomes from the frontal cortex, but not striatal synaptosomes. These findings suggest that the surface localization and activity of NET is modulated by alpha-Syn in a manner that is both dependent on interactions with the MT cytoskeleton and varies across brain regions.