Music‐Based Interventions for People Living with Dementia, targeting Behavioral and Psychological Symptoms: A scoping review

IntroductionDementia care is a major public health issue worldwide. The management of behavioral and psychological symptoms (BPSD) is one of the hardest challenges in this context. Non-pharmacological strategies, like music-based interventions (Mbi), seem promising options, being considered low-risk, widely available and inclusive. This scoping review aimed at mapping all Mbi used in dementia care, targeting BPSD, and debriefing its components, structure and rationale. Music therapy and other therapeutic music activities were included.MethodsThe Arksey and O'Malley framework, Cochrane recommendations and PRISMA checklist were followed. Embase, PubMed, PsycINFO, ASSIA and Humanities Index were searched from first records until the 31st of March 2020. Snowballing process and screening of relevant journals were also undertaken. A panel of experts critically guided the evidence synthesis.ResultsOverall, 103 studies (34 RCT; 12 NRT; 40 Before/After studies and 17 Case Studies) met inclusion criteria. Basic elements of the Mbi, the rationale supporting its development and hypothesis tested were mostly underreported, thus hampering cross-study comparisons and generalizations. Despite this, available evidence indicates that: it is feasible to deliver Mbi to PwD at very different stages and in different settings - from community to the acute setting - even for non-music therapists; positive or neutral effects in BPSD are often reported but not without exception; individualization seems a critical factor mediating Mbi effects.ConclusionsDetailed intervention and research reporting are essential to interpretation, replication and translation into practice. Ten years after the publication of specific reporting guidelines, this goal is not yet fully achieved in music in dementia care

Implementation of a quality improvement project on smoking cessation reduces smoking in a high risk trauma patient population

BACKGROUND: Cigarette smoking causes about one of every five deaths in the U.S. each year. In 2013 the prevalence of smoking in our institution’s trauma population was 26.7 %, well above the national adult average of 18.1 % according to the CDC website. As a quality improvement project we implemented a multimodality smoking cessation program in a high-risk trauma population. METHODS: All smokers with independent mental capacity admitted to our level I trauma center from 6/1/2014 until 3/31/2015 were counseled by a physician on the benefits of smoking cessation. Those who wished to quit smoking were given further counseling by a pulmonary rehabilitation nurse and offered nicotine replacement therapy (e.g. nicotine patch). A planned 30 day or later follow-up was performed to ascertain the primary endpoint of the total number of patients who quit smoking, with a secondary endpoint of reduction in the frequency of smoking, defined as at least a half pack per day reduction from their pre-intervention state. RESULTS: During the 9 month study period, 1066 trauma patients were admitted with 241 (22.6 %) identified as smokers. A total of 31 patients with a mean Injury Severity Score (ISS) of 14.2 (range 1–38), mean age of 47.6 (21–71) and mean years of smoking of 27.1 (2–55), wished to stop smoking. Seven of the 31 patients, (22.5 %, 95 % confidence interval [CI] of 10–41 %) achieved self-reported smoking cessation at or beyond 30 days post discharge. An additional eight patients (25.8 %, 95 % CI 12–45 %) reported significant reduction in smoking. CONCLUSIONS: Trauma patients represent a high risk smoking population. The implementation of a smoking cessation program led to a smoking cessation rate of 22.5 % and smoking reduction in 25.8 % of all identified smokers who participated in the program. This is a relatively simple, inexpensive intervention with potentially far reaching and beneficial long-term health implications. A larger, multi-center prospective study appears warranted. LEVEL OF EVIDENCE: Therapeutic Study, Level V evidence

Resting leukocyte telomerase activity is elevated in major depression and predicts treatment response

Telomeres are DNA-protein complexes that cap linear DNA strands, protecting DNA from damage. When telomeres critically shorten, cells become susceptible to senescence and apoptosis. Telomerase, a cellular ribonucleoprotein enzyme, rebuilds the length of telomeres and promotes cellular viability. Leukocyte telomeres are reportedly shortened in major depression, but telomerase activity in depression has not been previously reported. Further, there are no published reports of the effects of antidepressants on telomerase activity or on the relationship between telomerase activity and antidepressant response. Peripheral blood mononuclear cell (PBMC) telomerase activity was assessed in 20 medication-free depressed individuals and 18 controls. In total, 16 of the depressed individuals were then treated with sertraline in an open-label manner for 8 weeks, and PBMC telomerase activity was reassessed in 15 of these individuals after treatment. Pre- and post-treatment symptom severity was rated with the Hamilton Depression Rating Scale. All analyses were corrected for age and sex. Pretreatment telomerase activity was significantly elevated in the depressed individuals compared with the controls (P = 0.007) and was directly correlated with depression ratings (P< 0.05) across all subjects. In the depressed group, individuals with relatively lower pretreatment telomerase activity and with relatively greater increase in telomerase activity during treatment, showed superior antidepressant responses (P < 0.05 and P < 0.005, respectively). This is the first report characterizing telomerase activity in depressed individuals. PBMC telomerase activity might reflect a novel aspect of depressive pathophysiology and might represent a novel biomarker of antidepressant responsiveness

Alterations in leukocyte transcriptional control pathway activity associated with major depressive disorder and antidepressant treatment.

Major depressive disorder (MDD) is associated with a significantly elevated risk of developing serious medical illnesses such as cardiovascular disease, immune impairments, infection, dementia and premature death. Previous work has demonstrated immune dysregulation in subjects with MDD. Using genome-wide transcriptional profiling and promoter-based bioinformatic strategies, we assessed leukocyte transcription factor (TF) activity in leukocytes from 20 unmedicated MDD subjects versus 20 age-, sex- and ethnicity-matched healthy controls, before initiation of antidepressant therapy, and in 17 of the MDD subjects after 8 weeks of sertraline treatment. In leukocytes from unmedicated MDD subjects, bioinformatic analysis of transcription control pathway activity indicated an increased transcriptional activity of cAMP response element-binding/activating TF (CREB/ATF) and increased activity of TFs associated with cellular responses to oxidative stress (nuclear factor erythroid-derived 2-like 2, NFE2l2 or NRF2). Eight weeks of antidepressant therapy was associated with significant reductions in Hamilton Depression Rating Scale scores and reduced activity of NRF2, but not in CREB/ATF activity. Several other transcriptional regulation pathways, including the glucocorticoid receptor (GR), nuclear factor kappa-B cells (NF-κB), early growth response proteins 1-4 (EGR1-4) and interferon-responsive TFs, showed either no significant differences as a function of disease or treatment, or activities that were opposite to those previously hypothesized to be involved in the etiology of MDD or effective treatment. Our results suggest that CREB/ATF and NRF2 signaling may contribute to MDD by activating immune cell transcriptome dynamics that ultimately influence central nervous system (CNS) motivational and affective processes via circulating mediators

PBMC telomerase activity, but not leukocyte telomere length, correlates with hippocampal volume in major depression

Accelerated cell aging, indexed in peripheral leukocytes by telomere shortness and in peripheral blood mononuclear cells (PBMCs) by telomerase activity, has been reported in several studies of major depressive disorder (MDD). However, the relevance of these peripheral measures for brain indices that are presumably more directly related to MDD pathophysiology is unknown. In this study, we explored the relationship between PBMC telomerase activity and leukocyte telomere length and magnetic resonance imaging-estimated hippocampal volume in un-medicated depressed individuals and healthy controls. We predicted that, to the extent peripheral and central telomerase activity are directly related, PBMC telomerase activity would be positively correlated with hippocampal volume, perhaps due to hippocampal telomerase-associated neurogenesis, neuroprotection or neurotrophic facilitation, and that this effect would be clearer in individuals with increased PBMC telomerase activity, as previously reported in un-medicated MDD. We did not have specific hypotheses regarding the relationship between leukocyte telomere length and hippocampal volume, due to conflicting reports in the published literature. We found, in 25 un-medicated MDD subjects, that PBMC telomerase activity was significantly positively correlated with hippocampal volume; this relationship was not observed in 18 healthy controls. Leukocyte telomere length was not significantly related to hippocampal volume in either group (19 unmedicated MDD subjects and 17 healthy controls). Although the nature of the relationship between peripheral telomerase activity and telomere length and the hippocampus is unclear, these preliminary data are consistent with the possibility that PBMC telomerase activity indexes, and may provide a novel window into, hippocampal neuroprotection and/or neurogenesis in MDD