Different Classes Of Antidepressants Research Articles

Evaluating Fluoxetine's Growth-Inhibitory Impact on Clinical Isolates of Enteric Bacteria: Harnessing Repurposing Potential

The over-the-counter use and imprudent utilization of antibiotics in recent times have led to the emergence of microbial resistance. This has given rise to an alarming situation, prompting researchers to explore novel strategies for managing infections induced by antibiotic-resistant species. However, the process of drug discovery is time-consuming and expensive, which makes it a challenging endeavor. In recent years, drug repurposing has gained significant attention as an alternative strategy. Notably, several antidepressants have piqued interest as potential candidates for repositioning as antibiotics. Thus, the present study was aimed at investigating the anti-bacterial potential of different classes of antidepressants i.e., fluoxetine, venlafaxine, and phenelzine in clinical isolates of Escherichia coli, Enterobacter aerogenes, Enterococcus faecalis, Klebsiella pneumonia, Pseudomonas aeruginosa, Proteus mirabilis, Salmonella typhi, Shigella dysenteriae, and Staphylococcus aureus. The strains were cultivated on Mueller Hinton agar, with the aforementioned antidepressants or conventional antibiotics. Following a 24-hour incubation period, the extent of growth inhibition was assessed by measuring the zone of inhibition, serving as an indicator of their inhibitory potential. The findings showed that fluoxetine arrested the growth of almost all isolates with maximal effect against Pseudomonas aeruginosa. The impact of venlafaxine was exclusively observed in Enterobacter aerogenes, with phenelzine demonstrating complete ineffectiveness in bacterial growth suppression. In conclusion, the current study elucidates the efficacy of fluoxetine in clinical isolates, thereby positioning it as a promising contender for the advancement of novel antimicrobial agents. Additionally, our data raises questions regarding the proposed mechanisms of antibacterial action for selective serotonin reuptake inhibitors (SSRIs) and challenges the notion of dysbiosis as a potential mode of action for antidepressants.

Serotonin is a common thread linking different classes of antidepressants

Depression pathology remains elusive. The monoamine hypothesis has placed much focus on serotonin, but due to the variable clinical efficacy of monoamine reuptake inhibitors, the community is looking for alternative therapies such as ketamine (neurogenesis theory of antidepressant action). There is evidence that different classes of antidepressants may affect serotonin levels; a notion we test here. We measure hippocampal serotonin in mice with voltammetry and study the effects of acute challenges of escitalopram, fluoxetine, reboxetine, and ketamine. We find that pseudo-equivalent doses of these drugs similarly raise ambient serotonin levels, despite their differing pharmacodynamics because of differences in Uptake 1 and 2, rapid SERT trafficking, and modulation of serotonin by histamine. These antidepressants have different pharmacodynamics but have strikingly similar effects on extracellular serotonin. Our findings suggest that serotonin is a common thread that links clinically effective antidepressants, synergizing different theories of depression (synaptic plasticity, neurogenesis, and the monoamine hypothesis).

Prospective Association Between the Dispensing of Antidepressants and of Medications to Treat Osteoporosis in Older Age

Osteoporosis is a common condition associated with fragility fractures, especially in older individuals and women. Antidepressants have emerged as a potential risk factor, but their association with bone fragility remains uncertain because the results of past studies are difficult to generalize. We aimed to investigate the association between antidepressant exposure and subsequent treatment for osteoporosis in a nationally representative sample of Australians. Cohort study using a 10% random sample of the Pharmaceutical Benefits Scheme (PBS) data for 2012, that included 566,707 individuals aged older than or equal to 50 years not dispensed osteoporosis medications. The effect of exposure to antidepressants during 2012 (prevalent or incident) or later (up to 2022) was examined using Cox regression models adjusted for age, sex, comorbidities and other psychotropic medications. Over 10 years, 73,360 (12.94%) received osteoporosis medications; 16,216 (22.10%) had been dispensed antidepressants in 2012. The hazard of osteoporosis medication dispensing was higher among those exposed to antidepressants (HR = 1.16, 99% CI = 1.14-1.18; average duration of follow up: 8.0 ± 3.1 years, range: 1-10 years). The hazard of osteoporosis medication diminished with increasing age, and the effect of antidepressants was 37%-76% more pronounced among men in the 50s and 60s. Different classes of antidepressants had a similar risk profile. The dispensing of antidepressants in older age is associated with higher hazard of subsequent dispensing of medications for osteoporosis, and this association is more marked for young older adults, particularly men. Clinicians should monitor the bone health of older individuals treated with antidepressants in order to decrease the morbidity associated with fragility fractures.

Efficacy and tolerability of desvenlafaxine in the real-world treatment of patients with major depression: a narrative review and an expert opinion paper

ABSTRACT Introduction Major depressive disorder (MDD) is a common severe mental disorder, requiring a tailored and integrated treatment. Several approaches are available including different classes of antidepressants various psychotherapeutic approaches, and psychosocial interventions. The treatment plan for each patient with MDD should be differentiated on the basis of several clinical, personal, and contextual factors. Areas covered Desvenlafaxine – a serotonine-noradrenergic reuptake inhibitor (SNRI) antidepressant – has been approved in the United States in 2008 for the treatment of MDD in adults, and has been recently rediscovered by clinicians due to its good side-effect profile and its clinical effectiveness. A narrative review on efficacy, tolerability and use of desvenlafaxine in clinical practice was carried out. The keywords: ‘major depression’, ‘depression,’ ‘desvenlafaxine,’ ‘efficacy,’ ‘clinical efficacy,’ ‘side effects’, ‘tolerability,’ ‘elderly patients’, ‘consultation-liaison’, ‘menopausal’, ‘young people’, ‘adolescent’ were entered in PubMed, ISI Web of Knowledge, Scopus and Medline. No time limit was fixed, the search strategy was implemented on May 10, 2023. Expert opinion Desvenlafaxine should be listed among the optimal treatment strategies for managing people with MDD, whose main strengths are: 1) ease of dosing; 2) favorable safety and tolerability profile, 3) absence of sexual dysfunctions, weight gain and low rate of discontinuation symptoms; 4) low risk of drug–drug interactions.

Understanding target-specific effects of antidepressant drug pollution on molluscs: A systematic review protocol.

The environmental prevalence of widely prescribed human pharmaceuticals that target key evolutionary conserved biomolecules present across phyla is concerning. Antidepressants, one of the most widely consumed pharmaceuticals globally, have been developed to target biomolecules modulating monoaminergic neurotransmission, thus interfering with the endogenous regulation of multiple key neurophysiological processes. Furthermore, rising prescription and consumption rates of antidepressants caused by the burgeoning incidence of depression is consistent with increasing reports of antidepressant detection in aquatic environments worldwide. Consequently, there are growing concerns that long-term exposure to environmental levels of antidepressants may cause adverse drug target-specific effects on non-target aquatic organisms. While these concerns have resulted in a considerable body of research addressing a range of toxicological endpoints, drug target-specific effects of environmental levels of different classes of antidepressants in non-target aquatic organisms remain to be understood. Interestingly, evidence suggests that molluscs may be more vulnerable to the effects of antidepressants than any other animal phylum, making them invaluable in understanding the effects of antidepressants on wildlife. Here, a protocol for the systematic review of literature to understand drug target-specific effects of environmental levels of different classes of antidepressants on aquatic molluscs is described. The study will provide critical insight needed to understand and characterize effects of antidepressants relevant to regulatory risk assessment decision-making, and/or direct future research efforts. The systematic review will be conducted in line with the guidelines by the Collaboration for Environmental Evidence (CEE). A literature search on Scopus, Web of Science, PubMed, as well as grey literature databases, will be carried out. Using predefined criteria, study selection, critical appraisal and data extraction will be done by multiple reviewers with a web-based evidence synthesis platform. A narrative synthesis of outcomes of selected studies will be presented. The protocol has been registered in the Open Science Framework (OSF) registry with the registration DOI: 10.17605/OSF.IO/P4H8W.

TRKB interaction with PSD95 is associated with latency of fluoxetine and 2R,6R-hydroxynorketamine.

Brain derived neurotrophic factor (BDNF) and its receptor tropomyosin kinase receptor B (TRKB) are key regulators of activity-dependent plasticity in the brain. TRKB is the target for both slow- and rapid-acting antidepressants and BDNF-TRKB system mediates the plasticity-inducing effects of antidepressants through their downstream targets. Particularly, the protein complexes that regulate the trafficking and synapse recruitment of TRKB receptors might be crucial in this process. In the present study, we investigated the interaction of TRKB with the postsynaptic density protein 95 (PSD95). We found that antidepressants increase the TRKB:PSD95 interaction in adult mouse hippocampus. Fluoxetine, a slow-acting antidepressant, increases this interaction only after a long-term (7days) treatment, while (2R,6R)-hydroxynorketamine (RHNK), an active metabolite of rapid-acting antidepressant ketamine, achieves this within a short treatment regimen (3days). Moreover, the drug-induced changes of TRKB:PSD95 interaction correlate with drug latency in behaviour, observed in mice subjected to an object location memory test (OLM). While silencing of PSD95 by viral delivery of shRNA in hippocampus abolished the RHNK-induced plasticity in mice in OLM, overexpression of PSD95 shortened the fluoxetine latency. In summary, changes in the TRKB:PSD95 interaction contribute to differences observed in drug latency. This study sheds a light on a novel mechanism of action of different classes of antidepressants.

Antidepressants for the treatment of depression in people with cancer.

Antidepressants for the treatment of depression in people with cancer.

Pharmacokinetic interactions between esketamine and different classes of antidepressants in patients with treatment-resistant depression

Pharmacokinetic interactions between esketamine and different classes of antidepressants in patients with treatment-resistant depression

Impact of different classes of antidepressants on sleep and wakefulness regulation in depression

Sleep disturbances are common in patients with mental disorders. Sleep disturbances, in particular insomnia, are widespread in depression. Depressed patients have a lot of sleep complaints that are often confirmed by polysomnography. Most antidepressants impair sleep, so drugs that help to restore sleep are of particular value in clinical practice. Agomelatine (valdoxan) rapidly improves sleep in depressed patients by making it easier to fall asleep, increasing total sleep time, duration of rapid eye movement (REM), and slow-wave sleep (SWS), and improving functioning during the day.

Antidepressants Usage and Risk of Pneumonia Among Elderly Patients With the Parkinson's Disease: A Population-Based Case-Control Study.

The patients with Parkinson's disease (PD) are associated with a higher risk of pneumonia. Antidepressants exert an anticholinergic effect in varying degrees and various classes of antidepressants also can produce a different effect on immune function. The relationship between the risk of pneumonia and the use of antidepressants among elderly patients with PD is unknown. The study investigated the risk of pneumonia associated with the use of antidepressants in elderly patients with PD. This case-control study was based on data from the longitudinal health insurance database in Taiwan. We analyzed the data of 551,975 elderly patients with PD between 2002 and 2018. To reduce the potential confounding caused by unbalanced covariates in non-experimental settings, we used propensity score matching to include older patients without pneumonia to serve as the comparison. The antidepressants in the study included tricyclic antidepressants (TCAs), monoamine oxidase inhibitors (MAOIs), selective serotonin reuptake inhibitors (SSRIs), serotonin, and norepinephrine reuptake inhibitors (SNRIs). The conditional logistic regression was used to investigate the association between antidepressants and pneumonia. Control variables in the study included sex, age, income level, urbanization, Charlson comorbidity index score, and comorbidities related to pneumonia. In terms of TCAs users, compared with patients not receiving TCAs, current users had a lower risk of incident pneumonia (adjusted odds ratio [aOR] = 0.86, 95% CI = 0.82–0.90) and recent users (aOR = 0.83, 95% CI = 0.80–0.87). In terms of MAOIs users, current users had a lower risk of incident pneumonia (aOR = 0.88, 95% CI = 0.83–0.93), recent users (aOR = 0.89, 95% CI = 0.85–0.93). In terms of SSRIs users, current users had a higher risk of incident pneumonia (a OR = 1.13, 95% CI = 1.01–1.17), recent users (aOR = 1.01, 95% CI = 1.06–1.13), and past users (aOR = 1.19, 95% CI = 1.17–1.21). In terms of SNRIs users, past users had a higher risk of incident pneumonia (aOR = 1.07, 95% CI = 1.03–1.10). The incident pneumonia is associated with the use of individuals of different classes of antidepressants. The use of TCAs (such as, amitriptyline and imipramine) had a lower odds of incident pneumonia. The use of MAOIs (such as, selegiline and rasagiline) had a lower odds of pneumonia during recent use. The use of SSRIs (such as, fluoxetine, sertraline, escitalopram, paroxetine, and citalopram) and SNRIs (such as, milnacipran, and venlafaxine) had a higher odds of incident pneumonia.

Modulation of microglial activation by antidepressants.

Background:Recent studies have suggested that microglial activation plays a key role in the pathogenesis of depression. In fact, neuroinflammation is associated with a phenotypic change of microglia, consisting of morphological differences, increased release of cytokines and oxidative stress products, which may contribute to the development and maintenance of depression. Antidepressants, including selective serotonin re-uptake inhibitors and serotonin–norepinephrine reuptake inhibitors, have been shown to act on the immune and oxidative stress mechanisms commonly found to be disrupted in depression. Thus, the inhibition of microglial activation may be one of the mechanisms through which they exert an antidepressant action.Aim:This is the first review summarising in vitro and ex vivo studies investigating the effects of different classes of antidepressants on microglia activation, by examining cellular changes and/or via measuring the production of immune and/or oxidative stress signalling molecules, in microglia models of neuroinflammation with either lipopolysaccharide (LPS) or cytokines. A total of 23 studies were identified, 18 using LPS stimulation and 5 using cytokines stimulation.Results:Overall, the studies show that antidepressants, such as selective serotonin re-uptake inhibitors, serotonin–norepinephrine reuptake inhibitors, monoamine oxidase inhibitors and tricyclic antidepressants prevented microglial activation, including reduced microglial reactivity and decreased immune and oxidative stress products, in both models. However, specific antidepressants, such as bupropion and agomelatine did not prevent interferon-gamma (IFN-γ)-induced microglial activation; and for other antidepressants, including phenelzine, venlafaxine and sertraline, the results of different studies were inconsistent.Conclusions:Overall, results summarised in this review support the hypothesis that the action of at least certain classes of antidepressants may involve regulation of microglial activation, especially when in presence of increased levels of inflammation.

Atypical antipsychotics in major depressive disorder

The antipsychotics are used among pharmacological treatment of depression. Atypical antipsychotics have been used as monotherapy or adjunctively with antidepressants to treat depressive disorders with or without psychotic symptoms. The antidepressant effect of atypical antipsychotics involves regulation of monoamine, glutamate, gamma-aminobutyric acid, cortisol, and neurotrophic factors. To date, the United States Food and Drug Administration has approved aripiprazole and quetiapine slow-release tablets as adjunctive treatment for depressive disorders, and the combination of olanzapine and fluoxetine for the treatment of treatment-resistant depression. When using atypical antipsychotics in the treatment of depressed patients, clinicians need to monitor patients for the emergence of adverse effects, including hyperglycemia, weight gain, cholesterol levels, and extrapyramidal symptoms. These agents are effective for depression only at subantipsychotic doses. Receptor profiles predict that all second‐generation antipsychotics will have anxiolytic effects as subantipsychotic doses but that all will be dysphorogenic at full antipsychotic doses (i.e. produce a depression-like clinical picture). The antidepressant effect appears to be unique to some agents. Also, despite the availability of a large number of antidepressants of different classes, a significant portion of patients do not achieve remission, and treatment resistance is common. This paper reviews the antipsychotics that are effective for the treatment of depressive disorders, and the pharmacological mechanisms of antipsychotics in the treatment of depressive disorders.

Global geriatric depression situation: A critical evaluation

Introduction: Ageing is a natural process. The world is rapidly aging, the number of people aged 60 and over as a proportion of the global population will double from 11% in 2006 to 22% by 2050 and the absolute population increase is expected to be from 605 million to 2000 million. Of this, 80% people will be living in low- and middle-income countries. Late-life depression is a major mental health problem that challenges clinicians and will remain so as the population grows older than 65. Late-life depression contributes to adverse functional, social, and medical outcomes, and can interfere with treatment for medical problems such as stroke. Methodology: Survey of secondary literature is the prime methodology for preparing this research article.Research Findings: Mental and behavioural disorders are estimated to account for 12% of the global burden of disease which affects approximately 450 million people. However, most countries allocate less than 1% of their total health expenditures to mental health budgets. It is estimated that depression affects approximately 350 million people worldwide. Conclusion: An effective approach to this treatable disorder includes recognition of risk factors, detection, and assessment. The Geriatric Depression Scale and the Cornell Scale for Depression in Dementia can assist in diagnosis, while both psychotherapy and pharmacotherapy are options for management. When psychotherapies are compared, the strongest evidence for effectiveness has been found for cognitive behavioural therapy, problem-solving therapy, and interpersonal therapy. When pharmacotherapies are compared, efficacy is similar for different classes of antidepressants and adjuvant medications, but side effect profiles differ and must be considered to avoid adverse events. Patients with severe clinical features of late-life depression, including suicidal ideation and psychosis, should be referred to mental health services.

Antidepressant use during pregnancy and development of preeclampsia: A focus on classes of action and specific transporters/receptors targeted by antidepressants

ObjectiveThe association between antidepressants and preeclampsia has been inconsistently reported. Given the compound-specific variable affinity for different transporters/receptors, their effect on preeclampsia risk could differ. Our study examined the risk of preeclampsia (and its subtypes) following exposure to different classes of antidepressants, also accounting for specific transporters/receptors targeted by antidepressants. MethodsWe conducted a cohort study, combining data from the Netherlands Perinatal Registry and the PHARMO Database Network. Exposure to antidepressants was examined from conception to week 20 of gestation; extended use thereafter was also studied. Antidepressants were categorized according to classes [selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs), serotonin-norepinephrine reuptake inhibitors (SNRIs), monoamine oxidase inhibitors (MAOIs) and other antidepressants] and according to target transporters/receptors. Women not using any antidepressants during 15 months before delivery were included as reference. ResultsWe included 2,103 exposed and 95,376 reference women. Preeclampsia occurred in 70 exposed women (15 early-onset, 55 late-onset) and in 2,582 reference women (387 early-onset, 2,195 late-onset). TCA monotherapy (214 women) was associated with an increased risk of preeclampsia (n = 15, RR 2.46, 95% CI 1.51–4.02) and late-onset preeclampsia (n = 12, RR 2.41, 95% CI 1.39–4.17, early-onset could not be evaluated). No association was detected with SSRIs, SNRIs and MAOIs. We did observe an increased risk of early-onset preeclampsia following exposure to 5-HT2A antagonizing antidepressants (6/405 women, excluding TCA users, RR 3.56, 95% CI 1.60–7.94). ConclusionsOur results support an increased risk of preeclampsia and the late-onset subtype among TCA users. The association between 5-HT2A antagonists and the early-onset subtype needs to be interpreted with caution based on the relatively small number of exposed cases.

Association of different antidepressant classes with clinical attachment level and alveolar bone loss in patients with periodontitis: A retrospective study.

Our study aimed to determine the relationship of antidepressant medicine use with periodontal diseases, exploring the association of different pharmacological classes of antidepressant with observations of clinical attachment loss (CAL) and alveolar bone level (BL) in patients with periodontitis. Existing evidence on the impact of antidepressant medication on periodontal tissues has focused on some classes only and is still unclear. Therefore, this retrospective study evaluated the association of different antidepressant classes with clinical attachment loss (CAL) and alveolar bone level (BL). This study was carried out in a population of patients aged≥30years old with periodontitis who sought treatment at the University of Florida from 2014 to 2018. The following variables were obtained from patients' records; usage of antidepressant medications and their pharmacological classes (selective serotonin reuptake inhibitors [SSRI], serotonin-norepinephrine reuptake inhibitors [SNRI], tricyclic, atypical, and monoamine oxidase inhibitors [MAO]), age, gender, smoking habit, mild systemic diseases, CAL, and cement-enamel junction (CEJ) and alveolar bone crest (BC) distance, defined as BL, in the Ramfjord index teeth. Five hundred and eighty-two periodontitis patients were evaluated, of which 113 (19.4%) were antidepressant users. Antidepressant users exhibited significantly lower BL and fewer sites with severe CAL (≥5mm), than non-users (p<.05). Among all single-class antidepressant users, the SSRI users showed significantly less CAL and lower BL than non-users (p<.05). Patients taking combinations of the different classes of antidepressants also showed better CAL and BL than non-users. Generalized linear models, including variables such as gender, age, systemic diseases, and smoking, demonstrated that antidepressant users were more likely to have lower mean BL and fewer sites with severe bone loss (i.e. BL>3 and >5mm) than non-users (p<.05). Antidepressant medications were associated with higher alveolar bone level and less clinical attachment loss in patients with periodontitis. When the different classes of antidepressants were analyzed individually, only the SSRI class users and the multiple-class users showed significantly less periodontal breakdown than non-users.

Chronic antidepressant treatment rescues abnormally reduced REM sleep theta power in socially defeated rats

The effects of chronic antidepressant (AD) treatment on sleep disturbances in rodent chronic stress models have not been thoroughly investigated. Here, we show that chronic social defeat stress (SDS) in rats induces prolonged social avoidance, alterations in sleep architecture (increased total rapid eye movement [REM] sleep duration, bout, and shortened REM latency), and contextual but not cued fear memory deficits, even 1 month after the last SDS. These abnormalities were associated with changes in electroencephalography (EEG) spectral powers, including reduced REM sleep theta power during the light phase. Chronic treatment with two different classes of antidepressants (ADs), imipramine and fluoxetine, significantly ameliorated these behavioral, sleep, and EEG abnormalities. Interestingly, REM theta power was normalized by chronic (1 month) but not 1 week AD administration and solely correlated with the ratio (an objective indicator) of social interaction 1 month after the last SDS. These data suggest that reductions in REM sleep theta power, an EEG parameter that has never been directly investigated in humans, is a core sleep symptom in socially defeated rats, and, potentially, also in patients with stress-related psychiatric disorders, including major depressive and posttraumatic stress disorders.

Associations Between Antidepressant Use and Advanced Diabetes Outcomes in Patients with Depression and Diabetes Mellitus.

Comorbid depression in patients with diabetes deteriorates the prognosis. Antidepressants might attenuate the adverse effects of depression; however, they are associated with cardiometabolic adverse effects. This study aimed to explore the association between antidepressant treatment and advanced diabetic complications and mortality among patients with depression and diabetes mellitus. We conducted a nationwide retrospective cohort study of 36 276 patients with depression and newly treated diabetes mellitus using Taiwan's universal health insurance database. Antidepressant treatment patterns within a 6-month window were classified into none, poor, partial, and regular use, and we accounted for time-dependent variables in the Cox proportional hazards regression analysis with adjustment for time-dependent comorbidity and concomitant use of medications. Different classes of antidepressants were compared. Macro- and microvascular complications, as well as all-cause mortality, were the main outcomes. Benzodiazepines were chosen as negative control exposure. Compared with poor use of antidepressants, regular use was associated with a 0.92-fold decreased risk of macrovascular complications and a 0.86-fold decreased risk of all-cause mortality but not associated with microvascular complications. Regular use of selective serotonin reuptake inhibitors was associated with a 0.83- and 0.75-fold decreased risk of macrovascular complications and all-cause mortality, respectively. Regular use of tricyclic or tetracyclic antidepressants was associated with a 0.78-fold decreased risk of all-cause mortality. Regular use of benzodiazepine showed no association with diabetic outcomes. Regular antidepressant use was associated with lower risk of advanced diabetic complications compared with poor adherence. Clinicians should emphasize antidepressant treatment adherence among patients with depression and diabetes mellitus.

Different Classes of Antidepressants Inhibit the Rat α7 Nicotinic Acetylcholine Receptor by Interacting within the Ion Channel: A Functional and Structural Study.

Several antidepressants inhibit nicotinic acetylcholine receptors (nAChRs) in a non-competitive and voltage-dependent fashion. Here, we asked whether antidepressants with a different structure and pharmacological profile modulate the rat α7 nAChR through a similar mechanism by interacting within the ion-channel. We applied electrophysiological (recording of the ion current elicited by choline, ICh, which activates α7 nAChRs from rat CA1 hippocampal interneurons) and in silico approaches (homology modeling of the rat α7 nAChR, molecular docking, molecular dynamics simulations, and binding free energy calculations). The antidepressants inhibited ICh with the order: norfluoxetine ~ mirtazapine ~ imipramine < bupropion ~ fluoxetine ~ venlafaxine ~ escitalopram. The constructed homology model of the rat α7 nAChR resulted in the extracellular vestibule and the channel pore is highly negatively charged, which facilitates the permeation of cations and the entrance of the protonated form of antidepressants. Molecular docking and molecular dynamics simulations were carried out within the ion−channel of the α7 nAChR, revealing that the antidepressants adopt poses along the receptor channel, with slightly different binding-free energy values. Furthermore, the inhibition of ICh and free energy values for each antidepressant-receptor complex were highly correlated. Thus, the α7 nAChR is negatively modulated by a variety of antidepressants interacting in the ion−channel.

P.734 Early effects of different classes of antidepressants on emotion recognition processing

Measuring the wax deposition inside pipelines is one of the critical parameters in the oil, gas and petrochemical industries to control the flow through the pipelines. This paper presents a novel method using artificial neural networks to measure the thickness of the wax. This method was based on counting the backscattered gamma-ray from different thicknesses of the wax inside the pipes with different diameters. For this purpose, the system was simulated by MCNPX code and the designed setup was optimized. The main analyses were based on the simulation results but the verification was performed using a real experimental setup. The results showed a good agreement between the simulation results and the experimental data with a root mean square error less than 1%. Response of the detector was simulated for a standard industrial nominal pipe ranged from 2 to 4.5 inches and for radiation sources 137Cs and 60Co. Using these data, a multilayer perceptron for different energy sources was trained. The best prediction of the wax thickness was obtained for the case of using two radiation sources, simultaneously. The output of the trained neural network showed that the proposed method is capable of measuring the wax thickness inside the pipe with a good accuracy.

Does Treatment for Depression With Collaborative Care Improve the Glycemic Levels in Diabetic Patients with Depression? A Systematic Review.

Diabetes is a chronic disease with a high prevalence in the United States. If not treated adequately, it can have serious complications. Furthermore, when depression affects concomitantly, adherence to treatment can be decreased. Therefore, a cascade of complications may develop, affecting the quality of life and increasing the risk of death.Depression is underdiagnosed in patients with diabetes, and even if diagnosed, the treatment for both diabetes and depression is not well established in primary care. This study aims to evaluate if treatment for depression with collaborative care can improve glycemic levels and depression treatment response in diabetic patients with depression. As well, we will investigate if treatment with antidepressants will aid in improving glycemic levels. For this systematic review, we followed Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines and used PubMed, PubMed Central, and MEDLINE as database. Keywords: “diabetes improvement with depression treatment’.For collaborative care intervention, we selected three systematic reviews and meta-analysis. These three studies gave us a total of 1637 patients evaluated for the glycemic outcome and 1793 patients for depression outcomes. For the intervention with antidepressants, we included two articles. One systematic review and meta-analysis that evaluated the effect of selective serotonin reuptake inhibitors (SSRIs) on glycemic levels and the second article involved was a systematic review that assessed the effect of antidepressants on glycemia. A total of 4119 diabetic patients taking antidepressants were evaluated for glucose levels of the outcome. For the collaborative care outcome: two of the three studies showed non-significant improvement of glycemic levels with intervention. However, one study that had a bigger sample size exhibited significant improvement of glycemia with collaborative care. It is necessary to elaborate on new studies to confirm this finding.For the glycemic outcome with antidepressants: SSRIs improve glycemic levels. This class of antidepressants is the most studied, and it would be interesting to perform trials comparing different classes of antidepressants with a bigger sample size and run for a more extended period. According to our review, collaborative care improves glycemia and depression treatment response. At the same time, it improves the adherence to treatment of both oral hypoglycemic drugs and antidepressants. SSRIs demonstrated to be more effective in glycemic control. The most studied and effective SSRIs are fluoxetine, escitalopram, and citalopram.