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The pandemic highlighted the need for alternative, more accessible access to mental health interventions that can be readily administered remotely. The purpose of this pre-post-interventional study was to evaluate the effectiveness of a virtual mind-body medicine training course on stress, anxiety, and depression levels. University employees and members of the Las Vegas community were recruited via self-selection and snowball sampling and subjected to online mind-body practice sessions in December of 2020. Stress, anxiety, depression, and quality of life were assessed pre- and post-intervention using standardized psychometric valid tools. The paired t-test and related samples marginal homogeneity tests were used for continuous and categorical outcomes, respectively. Depression and stress scores were significantly decreased (p < 0.001). Mean scores of professional quality of life improved post-intervention compared to pre-intervention (p = 0.03). A significantly larger proportion of participants reported no depression or stress post-intervention compared with pre-intervention (p < 0.001, p = 0.003, respectively.) This study suggests that virtual mind-body practices had a pronounced impact on stress and depression levels during the pandemic. These findings support virtual, online-guided mind-body medicine training as an effective intervention that can be administered virtually to reduce stress and depression symptoms.
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Neuroinflammation, a core pathological feature observed in several neurodegenerative diseases, including Alzheimer's disease (AD), is rapidly gaining attention as a target in understanding the molecular underpinnings of these disorders. Glial cells, endothelial cells, peripheral immune cells, and astrocytes produce a variety of pro-inflammatory mediators that exacerbate the disease progression. Additionally, microglial cells play a complex role in AD, facilitating the clearance of pathological amyloid-beta peptide (Aß) plaques and aggregates of the tau protein. Tau proteins, traditionally associated with microtubule stabilization, have come under intense scrutiny for their perturbed roles in neurodegenerative conditions. In this narrative review, we focus on recent advances from molecular insights that have revealed aberrant tau post-translational modifications, such as phosphorylation and acetylation, serving as pathological hallmarks. These modifications also trigger the activation of CNS-resident immune cells, such as microglia and astrocytes substantially contributing to neuroinflammation. This intricate relationship between tau pathologies and neuroinflammation fosters a cascading impact on neural pathophysiology. Furthermore, understanding the molecular mechanisms underpinning tau's influence on neuroinflammation presents a frontier for the development of innovative immunotherapies. Neurodegenerative diseases have been relatively intractable to conventional pharmacology using small molecules. We further comprehensively document the many alternative approaches using immunotherapy targeting tau pathological epitopes and structures with a wide array of antibodies. Clinical trials are discussed using these therapeutic approaches, which have both promising and disappointing outcomes. Future directions for tau immunotherapies may include combining treatments with Aß immunotherapy, which may result in more significant clinical outcomes for neurodegenerative diseases.
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Ketamine is a promising alternative to traditional pharmacotherapies for major depressive disorder, treatment-resistant depression, and other psychiatric conditions that heavily contribute to the global disease burden. In contrast to the current standard of care medications for these disorders, ketamine offers rapid onset, enduring clinical efficacy, and unique therapeutic potential for use in acute, psychiatric emergencies. This narrative presents an alternative framework for understanding depression, as mounting evidence supports a neuronal atrophy and synaptic disconnection theory, rather than the prevailing monoamine depletion hypothesis. In this context, we describe ketamine, its enantiomers, and various metabolites in a range of mechanistic actions through multiple converging pathways, including N-methyl-D-aspartate receptor (NMDAR) inhibition and the enhancement of glutamatergic signaling. We describe the disinhibition hypothesis, which posits that ketamine's pharmacological action ultimately results in excitatory cortical disinhibition, causing the release of neurotrophic factors, the most important of which is brain-derived neurotrophic factor (BDNF). BDNF-mediated signaling along with vascular endothelial growth factor (VEGF) and insulin-like growth factor 1 (IGF-1) subsequently give rise to the repair of neuro-structural abnormalities in patients with depressive disorders. Ketamine's efficacious amelioration of treatment-resistant depression is revolutionizing psychiatric treatment and opening up fresh vistas for understanding the underlying causes of mental illness.
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Background: While several state-based studies have shown that children in foster care are more likely to be prescribed psychotropic medications and experience concomitant medication use both within and among medication class, these patterns have not been explored in the state of Nevada, which lacks state mandated oversight of psychotropic prescribing for foster care enrolled youth. Methods: Data from an electronic medical record system from a single institution were analyzed to examine the prevalence of psychotropic prescribing and concomitant medication use in children ages 2 to 19 who were enrolled and received psychotropic prescriptions between July 2019 to June 2022. Results: Out of 569 distinct psychotropic medication treatment episodes within this cohort, the most frequent psychotropic classes prescribed were non-stimulant ADHD medications (alpha-agonists and atomoxetine, 31.5%), atypical antipsychotics (22.1%), antidepressants (20.6%), and stimulants (16.0%). The use of stimulants and non-stimulant ADHD medications decreased in older age groups while the use of antidepressants and antipsychotics increased in older age groups. During the three-year period studied, 24.0% of psychotropic medications prescriptions increased in dosage. Treatments were prescribed for only one month in 43.8% of youth. In children prescribed psychotropic medications, concomitant medication use for at least 60 days occurred in 28.0% of children who had any psychotropic medication prescribed. Conclusion: Within the cohort of 273 foster care enrolled subjects aged 2 to 19 years old who received psychotropic medication prescriptions, non-stimulant ADHD medications (both alpha-agonists and atomoxetine) and atypical antipsychotics were more commonly co-prescribed additional psychotropic medication compared to other co-prescribed medication categories. This study illustrates prescribing patterns in a community mental health clinic focused on judicious prescribing of psychotropic medications in foster care enrolled youth. Despite this, 41% of the youth treated in this clinic received at least one prescription for psychotropic medication, and of those, 27.8% were prescribed more than one psychotropic medication at the same time. More studies are necessary to understand the underlying causes of high prevalence of concomitant medication use and prescribing practices of psychotropic medications use in foster care involved pediatric populations.
