Escitalopram Treatment Research Articles

Effects of escitalopram with a Chinese traditional compound Jiuweizhenxin-keli on mismatch negativity and P50 in patients with major depressive disorders

ObjectiveThe objective of this study was to investigate the therapeutic effects of escitalopram in conjunction with Jiuweizhenxin-keli on neuroelectrophysiology in patients with major depressive disorders (MDD).Patients and methodsPatients with depressive episode of MDD according to the criteria of Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, were randomly assigned to Esc group (30 patients) receiving escitalopram treatment and JK group (30 patients) treated with a combination of escitalopram and Jiuweizhenxin-keli. The healthy control (HC) group (30 persons with normal health condition) served as control. All groups were subject to examination of 24-item Hamilton Depression Rating Scale and Hamilton Anxiety Scale, mismatch negativity (MMN), and sensory gating potential P50 (SG-P50) of event-related potentials. Data were collected at three different time points: baseline (before treatment) and week 2 and week 6 post treatment.ResultsAt baseline, all electrophysiological parameters of patients with MDD were significantly higher than those of HCs. After treatment, in the Esc group, MMN latency, S2-P50 amplitude, and S2-P50/S1-P50 amplitude ratio decreased; however, the decrements were not statistically significant compared to either baseline or the HC group. Also, no significant changes were observed in the percentage of individuals whose S2-P50/S1-P50 ≥0.5 in the Esc group. On the other hand, in the JK group after a 6-week treatment, MMN latency (206.35±32.14 ms) was significantly shorter than that of the Esc group (219.57±36.51 ms), S2-P50 amplitude (7.27±4.85 μV) reduced significantly compared with the baseline level (10.21±4.10 μV), the percentage of individuals whose S2-P50/S1-P50 ≥0.5 in the JK group greatly decreased and this was not significantly different compared to that of the HC group (P≥0.05).ConclusionNeuroplasticity of patients with MDD is apparently disturbed, characterized by aberrant MMN latency and SG-P50-related event-related potential parameters. A combination of escitalopram and Jiuweizhenxin-keli treatment can markedly restore these neuroelectrophysiological features, and thus, could be a novel therapeutic solution for improving the impaired neuroplasticity of MDD patients.

Whole-genome expression analysis reveals genes associated with treatment response to escitalopram in major depression

The reasons for variability in treatment response in major depressive disorder (MDD) are not fully understood, but there is accumulating evidence suggesting that therapeutic outcomes of antidepressants can be influenced by genetic factors. In the present study we applied the microarray Illumina platform for whole genome expression profiling in depressive patients treated with escitalopram medication in order to identify genes underlying response to antidepressant treatment. The initial study sample consisted of 135 outpatients with major depressive disorder (mean age 31.1±11.6 years, 68% females) treated with escitalopram 10–20mg/day for 12 weeks, from which 87 patients (55 females) were included in gene expression analyzing. The gene expression profiles were measured on peripheral blood cells at baseline, at week 4 and at the end of treatment (week 12) using BeadChips Illumina. The fold change was used to demonstrate rate of changes in average gene expressions between studied groups. Statistical analyses were performed using the false discovery rate (FDR). The most interesting gene, which showed the predictive effect on treatment outcome by delineating low dose responders and treatment-resistant patients at the beginning of medication, was NLGN2, belonging to a family of neuronal cell surface proteins and involving in synapse formation. In addition, the several gene clusters, related to immune response, signal transduction and neurotrophin pathway, have distinguished responders from non-responders at the week 4 of treatment. After 4 weeks of escitalopram treatment (10mg/day), the YWHAZ gene has showed the highest transcriptional change in responders as compared with non-responders. Finally, at the end of the treatment we noticed that at least three genes (NR2C2, ZNF641, FKBP1A) have been strongly associated with resistance to escitalopram. Thus the results of this study support that exploration of peripheral gene expression is a useful tool in the further identification of novel genetic biomarkers for antidepressant treatment response.

Prenatal stress-induced increases in hippocampal von Willebrand factor expression are prevented by concurrent prenatal escitalopram

Prenatal stress has been linked to deficits in neurological function including deficient social behavior, alterations in learning and memory, impaired stress regulation, and susceptibility to adult disease. In addition, prenatal environment is known to alter cardiovascular health; however, limited information is available regarding the cerebrovascular consequences of prenatal stress exposure. Vascular disturbances late in life may lead to cerebral hypoperfusion which is linked to a variety of neurodegenerative and psychiatric diseases. The known impact of cerebrovascular compromise on neuronal function and behavior highlights the importance of characterizing the impact of stress on not just neurons and glia, but also cerebrovasculature. Von Willebrand factor has previously been shown to be impacted by prenatal stress and is predictive of cerebrovascular health. Here we assess the impact of prenatal stress on von Willebrand factor and related angiogenic factors. Furthermore, we assess the potential protective effects of concurrent anti-depressant treatment during in utero stress exposure on the assessed cerebrovascular endpoints. Prenatal stress augmented expression of von Willebrand factor which was prevented by concurrent in utero escitalopram treatment. The functional implications of this increase in von Willebrand factor remain elusive, but the presented data demonstrate that although prenatal stress did not independently impact total vascularization, exposure to chronic stress in adulthood decreased blood vessel length. In addition, the current study demonstrates that production of reactive oxygen species in the hippocampus is decreased by prenatal exposure to escitalopram. Collectively, these findings demonstrate that the prenatal experience can cause complex changes in adult cerebral vascular structure and function.

Excessive nest building is a unique behavioural phenotype in the deer mouse model of obsessive-compulsive disorder.

Obsessive-compulsive disorder (OCD) is a phenotypically heterogeneous condition characterised by time-consuming intrusive thoughts and/or compulsions. Irrespective of the symptom type diagnosed, the severity of OCD is characterised by heterogeneity in symptom presentation that complicates diagnosis and treatment. Heterogeneity of symptoms would be invaluable in an animal model. Nest building behaviour forms part of the normal behavioural repertoire of rodents and demonstrates profound between-species differences. However, it has been proposed that within-species differences in nest building behaviour (i.e. aberrant vs. normal nest building) may resemble obsessive-compulsive-like symptoms. In an attempt to investigate whether other obsessive-compulsive-like behaviours are present in an animal model of OCD, or if aberrant nest building behaviour may represent a unique obsessive-compulsive phenotype in such a model, the current study assessed nest building behaviour in high (H, viz obsessive-compulsive) and non (N, viz normal) stereotypical deer mice. Subsequently, 12 N and H animals, respectively, were provided with an excess of cotton wool daily for one week prior to and following four weeks of high-dose oral escitalopram treatment (50 mg/kg/day). Data from the current investigation demonstrate daily nesting activity to be highly variable in deer mice, with stereotypy and nest building being independent behaviours. However, we identified unique aberrant large nest building behaviour in 30% of animals from both cohorts that was attenuated by escitalopram to pre-treatment nesting scores of the larger group. In summary, behavioural and drug-treatment evidence confirms that deer mouse behaviour does indeed resemble symptom heterogeneity related to OCD, and as such expands its face and predictive validity for the disorder.

Plasminogen Activator Inhibitor-1 in depression: Results from Animal and Clinical Studies.

Evidence suggests that plasminogen activator inhibitor-1 (PAI-1) is a stress-related factor, and serum PAI-1 levels are increased in patients with major depressive disorders (MDD). Herein, we analysed PAI-1 protein levels in the brain, cerebrospinal fluid (CSF) and serum of rodents exposed to chronic unpredictable mild stress or treated with escitalopram. In addition, we examined PAI-1 concentrations in serum obtained from 17 drug-free depressed patients before and after escitalopram treatment. We found that PAI-1 expression was increased in area 1 of the cingulate cortex and prelimbic cortex of the medial prefrontal cortex as well as in the hippocampal cornu ammonis 3 and dentate gyrus in stressed rats. A downregulation of PAI-1 following chronic escitalopram treatment was also found. PAI-1 levels were higher in the CSF and serum in stressed rats than in controls, although the difference did not reach statistical significance in the serum. Escitalopram treatment significantly decreased PAI-1 levels in the serum, but not in the CSF. MDD patients had significantly greater serum PAI-1 concentrations than controls. Our results suggest that PAI-1 is implicated in the pathophysiology of depression.

Long-term administration of escitalopram in patients with social anxiety disorder in Japan.

PurposeTo investigate the safety, tolerability, and effectiveness of escitalopram in patients with social anxiety disorder in Japan.MethodsA 52-week, open-label study was conducted in Japanese patients with social anxiety disorder with a total score ≥60 on the Liebowitz Social Anxiety Scale – Japanese Version (LSAS-J) and ≥4 on the Clinical Global Impression – Severity Scale. Escitalopram 10 mg/day was administered for the first week and could be increased to 20 mg/day.ResultsThe study included 158 patients: 81.0% (128/158) completed 52 weeks of escitalopram treatment, 68.4% (108/158) increased their dose to 20 mg/day, and 56.3% (89/158) remained on 20 mg/day. Adverse drug reactions were reported by 57.6% (91/158) of patients. The most common (incidence ≥10%) were somnolence and nausea. The incidence of adverse drug reactions was similar in extensive and poor metabolizers of cytochrome P450 2C19. No adverse drug reactions increased in incidence by >5% after week 12. The incidence of serious adverse events was 1.3% (2/158). No deaths occurred. The LSAS-J total scores improved until week 52. The LSAS-J response rate (≥30% improvement in LSAS-J) was 69.0%, the Clinical Global Impression – Improvement Scale response rate (≤2) was 73.0%, and the LSAS-J remission rate (≤30) was 27.0%.ConclusionIn this first 52-week clinical study of social anxiety disorder, escitalopram 10–20 mg/day was safe, well tolerated, and effective in Japanese patients.

A Chronic Psychogenic Vomiting Case of Dramatic Response to Escitalopram

This case report describes the treatment of an interesting patient with vomiting for years. The patient admitted to the family health center with chronic vomiting and weight loss. Her physical examination was unremarkable. The complaint of patient in who organic pathogen were excluded by biochemical and radiological examinations was evaluated psychologically; her complaints were ended following the initiation of escitalopram therapy unlike previous treatment. In this report, we represent a specific patient for the escitalopram treatment and thanks to this, it contributes a unique sample to the literature about escitalopram usage in the treatment of chronic vomiting.

Determinants and escitalopram treatment effects on suicidal ideation in patients with acute coronary syndrome: Findings from the K-DEPACS and EsDEPACS studies

BackgroundThis study is aimed to investigate the determinants of suicidal ideation as well as to assess escitalopram treatment effects on suicidal ideation in patients with acute coronary syndrome (ACS). MethodsA total of 1152 patients were consecutively recruited at baseline, 2 to 14weeks after a confirmed ACS episode. Of 446 baseline participants with comorbid depressive disorders, 300 were randomized to a 24-week double-blind trial of escitalopram or placebo treatment. Suicidal ideation was determined using the “suicidal thoughts” item of the Montgomery and Asberg Depression Rating Scale. Socio-demographic and clinical characteristics, including depressive and anxiety symptoms, cardiovascular risk factors, and current cardiac status, were assessed. ResultsSuicidal ideation was independently associated with past history of depression, depressive and anxiety disorders, and higher troponin I levels. Escitalopram treatment was significantly more efficacious in reducing and treating suicidal ideation than placebo treatment over a 24-week period. These effects were largely explained by remission status of depressive and anxiety disorders. ConclusionsSuicidal ideation is associated with unfavorable psychiatric and ACS status during the acute phase of ACS. Successful treatment of depression and anxiety with escitalopram had significant beneficial effects on suicidal ideation in these patients.

Blood oxygen level-dependent signals via fMRI in the mood-regulating circuit using two animal models of depression are reversed by chronic escitalopram treatment

BackgroundPeople exposed to stressful experience are at increased risk of the development of depression. A number of functional imaging studies have found disturbances in the mood-regulating circuit of the stress-exposed depressed patients, although few animal imaging studies have been undertaken addressing the brain functional changes of depression. MethodsTwo rat models of depression: maternal separation (MS) and chronic unpredictable mild stress (CUMS), imitating early life stress and adult stress respectively, were administered with escitalopram. The differences in functional brain changes were determined by blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI). ResultsIncreased BOLD activation was observed in some brain regions of MS and CUMS animals, such as the bilateral hypothalamus, limbic system, hippocampus and frontal lobe, which were parts of mood-regulating circuit. Furthermore, the MS- and CUMS-induced increases in BOLD activation were partially attenuated by chronic escitalopram treatment. ConclusionsThese results suggested hyperactivation of mood-regulating circuit at baseline in the depressed animals exposed to stressful experience, and escitalopram can at least partially reverse these effects.

Characteristics of Escitalopram Discontinuation Syndrome

Antidepressant discontinuation syndrome (ADS) frequently occurs in patients who undergo an abrupt discontinuation of their antidepressant medication. We evaluated 25 consecutive outpatients with depression who discontinued their use of escitalopram. The presence of ADS was evaluated according to the Antidepressants Discontinuation Syndrome checklist. Antidepressant discontinuation syndrome was observed in 14 of 25 patients. Frequent symptoms were dizziness (44%), muscle tension (44%), chills (44%), confusion or trouble concentrating (40%), amnesia (28%), and crying (28%). The treatment doses and plasma concentrations of escitalopram were significantly higher in patients with ADS than in patients without ADS. No group differences were observed regarding age, sex, or duration of escitalopram treatment before the discontinuation. These findings suggest that a higher dose and lower clearance of escitalopram lead to a higher risk of ADS. Very slow tapering is recommended for all patients.

Transcriptome composition of the preoptic area in mid-age and escitalopram treatment in male mice

The decrease in serotonergic neurotransmission during aging can increase the risk of neuropsychiatric diseases such as depression in elderly population and decline the reproductive system. Therefore, it is important to understand the age-associated molecular mechanisms of brain aging. In this study, the effect of aging and chronic escitalopram (antidepressant) treatment to admit mice was investigated by comparing transcriptomes in the preoptic area (POA) which is a key nucleus for reproduction. In the mid-aged brain, the immune system-related genes were increased and hormone response-related genes were decreased. In the escitalopram treated brains, transcription-, granule cell proliferation- and vasoconstriction-related genes were increased and olfactory receptors were decreased. Since homeostasis and neuroprotection-related genes were altered in both of mid-age and escitalopram treatment, these genes could be important for serotonin related physiologies in the POA.

Escitalopram orally-disintegrating tablets (ODT) in major depression treatment

IntroductionThe growing rate of depressive disorders causes needs for more effective and more innovative solutions. The modern patients’ challenges make them fail mostly in the treatment compliance. Some reports have described that escitalopram orally disintegrating tablets (ODT) induce faster response and lower dropout rate than oral standard tablets (OST), although both forms have equal bioavailability.AimWe tried to clarify effectiveness rates between escitalopram ODT and OST treatments in depressive patients.MethodAn open-label, 6-month, randomized, flexible-dose study was conducted for direct comparison of the effects of escitalopram ODT (N16) and OST (N15) on dropout rate and clinical outcomes in patients with major depression.ResultsOutcome measures included Hamilton Depression Rating Scale (HDRS), Drug Attitude Inventory-10 (DAI), Clinical Global Improvement Scale (CGI), and Psychological General Well-Being Scale (PGWB). The tolerability was assessed by the UKU scale. No significant difference was found in HDRS, CGI, PGWB and GAF between the two forms of tablets. No significant difference was found in any tolerability rates. However, dropout rate favored escitalopram ODT group (N5, 31.3%) vs escitalopram OST (N7, 47.0%). DAI-10 outcomes, both in patients’ general attitude and subjective feelings, were significantly improved in ODT group (P = 0.000), comparing with OST.DiscussionEscitalopram in its classical form (OST) has become a leader in a group of antidepressants, thanks to safety of use, efficacy and tolerability. In the ODT form, escitalopram can meet additional needs, both clinical and lifestyle. ODT may reduce dropout rate and costs of long-term treatment improving the patients’ compliance.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Plasma micro-RNA profiles in patients with major depressive disorder (MDD)

IntroductionMicro-RNAs (miRs) are involved in processes associated with MDD such as neural plasticity, neurogenesis, synaptogenesis and stress response. MiRs are detectable in biological fluids; however, no data is available regarding the use of plasma circulating miRs as markers of MDD, only whole blood or serum being reported so far.ObjectivesWe investigated plasma miR profiles as potential markers for MDD in patients treated with antidepressants.AimsTo detect and characterize differentially expressed miRs in the plasma of MDD patients, before and after treatment with escitalopram.MethodsBlood was collected from patients with MDD before and after 12 weeks of treatment. Plasma profiles of 1008 miRs were measured by real time PCR. The fold change of expression between time points was calculated and a paired t test was used for statistical significance. Gene targets and pathways were assessed in miRWalk2.0.ResultsFrom 222 plasma miRs expressed, 40 were significantly different after treatment. Upregulated miRs (23) belonged to 43 pathways, down-regulated miRs (17) belonged to 46 pathways; the top 5 significant pathways identified being pathways in cancer, Wnt signalling, endocytosis, axon guidance and MAPK signalling. Six of these miRs are common to all five pathways: miR-146a-5p, miR-146b-5p, miR-221-3p, miR-24-3p, miR-26a-5p.ConclusionsOur analysis of significant changes in plasma miRs after escitalopram treatment of MDD might open new avenues for the understanding of its mode of action and its side effects. To our knowledge, this is the first study to assess miRs affected by antidepressant treatment in plasma of MDD patients.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Of mice and marbles: Novel perspectives on burying behavior as a screening test for psychiatric illness.

Burying forms part of the normal behavioral routine of rodents, although its expression is species-specific. However, it has been suggested that aberrant burying behavior, of which marble-burying (MB) is an example, may represent neophobic and/or compulsive-like behavior. In the present investigation, we assessed MB in an established animal model of obsessive-compulsive disorder (OCD)-namely, spontaneous stereotypy in the deer mouse-to establish whether high (H) stereotypy is associated with neophobia and/or another compulsive endophenotype, i.e. MB, as compared to nonstereotypical (N) controls. A three-trial, one-zone MB test was performed over three consecutive evenings both before and after chronic treatment with high-dose (50mg/kg/day) oral escitalopram. Neophobia was measured via the number of marbles buried during the first pre- and posttreatment MB trials, and compulsive-like behavior via the number of marbles buried over all pre- and posttreatment MB trials. The data from the present study support earlier findings that burying is a normal behavioral routine (inherent burying behavior, IBB) that is expressed by all deer mice, irrespective of stereotypical cohort, and is not associated with either neophobia or compulsiveness. Indeed, chronic escitalopram treatment, which is similarly effective in treating clinical anxiety and OCD, as well as in attenuating H behavior, failed to influence IBB. Although 11% of the animals presented with a unique burying endophenotype (high burying behavior), escitalopram also failed to attenuate said behavior, necessitating further investigation as to its relevance. In conclusion, MB cannot be regarded as a measure of anxiety-like or compulsive behavior in the deer mouse model of OCD.

Social behavior in deer mice as a novel interactive paradigm of relevance for obsessive-compulsive disorder (OCD)

ABSTRACTGreater obsessive-compulsive (OC) symptom severity may be associated with poor social adjustment. Rather than possessing deficits in social skill per se, OCD patients may be more socially isolative in the presence of normal controls. We aimed to apply a novel social interaction challenge (SIC) to an established animal model of OCD, viz., the deer mouse, to assess complex social behavior in animals by investigating group sociability and its response to chronic escitalopram treatment (50 mg/kg/day × 28 days), both within and between non (N)- (viz., normal) and high (H)- (viz., OCD-like) stereotypical cohorts. Using automated screening, we scored approach behavior, episodes of proximity, duration of proximity, and relative net weighted movement. H animals socialized more with one another within cohort in all of the above parameters compared to the within-cohort behavior of N animals. Furthermore, the social behavior of H animals toward one another, both within and between cohort demonstrated significant improvements following chronic escitalopram treatment. However, the study also demonstrates that the social interaction between H and N animals remain poor even after chronic escitalopram treatment. To conclude, findings from the current investigation support clinical data demonstrating altered sociability in patients with OCD.

Early life stress increases stress vulnerability through BDNF gene epigenetic changes in the rat hippocampus

Early life stress (ELS) exerts long-lasting epigenetic influences on the brain and makes an individual susceptible to later depression. It is poorly understood whether ELS and subsequent adult chronic stress modulate epigenetic mechanisms. We examined the epigenetic mechanisms of the BDNF gene in the hippocampus, which may underlie stress vulnerability to postnatal maternal separation (MS) and adult restraint stress (RS). Rat pups were separated from their dams (3 h/day from P1–P21). When the pups reached adulthood (8 weeks old), we introduced RS (2 h/day for 3 weeks) followed by escitalopram treatment. We showed that both the MS and RS groups expressed reduced levels of total and exon IV BDNF mRNA. Furthermore, RS potentiated MS-induced decreases in these expression levels. Similarly, both the MS and RS groups showed decreased levels of acetylated histone H3 and H4 at BDNF promoter IV, and RS exacerbated MS-induced decreases of H3 and H4 acetylation. Both the MS and RS groups had increased MeCP2 levels at BDNF promoter IV, as well as increased HDAC5 mRNA, and the combination of MS and RS exerted a greater effect on these parameters than did RS alone. In the forced swimming test, the immobility time of the MS + RS group was significantly higher than that of the RS group. Additionally, chronic escitalopram treatment recovered these alterations. Our results suggest that postnatal MS and subsequent adult RS modulate epigenetic changes in the BDNF gene, and that these changes may be related to behavioral phenotype. These epigenetic mechanisms are involved in escitalopram action.

Cross-trial prediction of treatment outcome in depression: a machine learning approach

Antidepressant treatment efficacy is low, but might be improved by matching patients to interventions. At present, clinicians have no empirically validated mechanisms to assess whether a patient with depression will respond to a specific antidepressant. We aimed to develop an algorithm to assess whether patients will achieve symptomatic remission from a 12-week course of citalopram. We used patient-reported data from patients with depression (n=4041, with 1949 completers) from level 1 of the Sequenced Treatment Alternatives to Relieve Depression (STAR*D; ClinicalTrials.gov, number NCT00021528) to identify variables that were most predictive of treatment outcome, and used these variables to train a machine-learning model to predict clinical remission. We externally validated the model in the escitalopram treatment group (n=151) of an independent clinical trial (Combining Medications to Enhance Depression Outcomes [COMED]; ClinicalTrials.gov, number NCT00590863). We identified 25 variables that were most predictive of treatment outcome from 164 patient-reportable variables, and used these to train the model. The model was internally cross-validated, and predicted outcomes in the STAR*D cohort with accuracy significantly above chance (64·6% [SD 3·2]; p<0·0001). The model was externally validated in the escitalopram treatment group (N=151) of COMED (accuracy 59·6%, p=0.043). The model also performed significantly above chance in a combined escitalopram-buproprion treatment group in COMED (n=134; accuracy 59·7%, p=0·023), but not in a combined venlafaxine-mirtazapine group (n=140; accuracy 51·4%, p=0·53), suggesting specificity of the model to underlying mechanisms. Building statistical models by mining existing clinical trial data can enable prospective identification of patients who are likely to respond to a specific antidepressant. Yale University.

Changes in the regional cerebral blood flow detected by arterial spin labeling after 6-week escitalopram treatment for major depressive disorder

BackgroundA few studies have used pseudo-continuous arterial spin labeling (pCASL) to assess the regional cerebral blood flow (rCBF) in patients with major depressive disorder (MDD). However, rCBF changes during treatment with escitalopram have not been studied in detail. We used pCASL to investigate the effect of 6-week escitalopram treatment on the rCBF in MDD patients. MethodsWe subjected 53 MDD patients and 36 controls to pCASL (T1, baseline). The patients then received treatment with escitalopram for 6 weeks and 27 were scanned again (T2). We used selected regions of interest that exhibited differences between the controls and patients at T1 and compared the T2 rCBF in the patients with the T1 rCBF of the controls. We also compared the T1 and T2 rCBF in the patients to assess their response to escitalopram. ResultsAfter 6-week treatment with escitalopram, the rCBF in the patients' left inferior temporal gyri, the middle- and inferior frontal gyri, and the subgenual anterior cingulate, which had been higher at T1 than in the controls, was decreased. Their rCBF in the right lingual gyrus remained significantly lower at T2. LimitationWe did not have a placebo-control group and the number of patients available at T2 was small. ConclusionIn MDD patients, 6-week escitalopram treatment elicited significant rCBF changes toward normalization in most of the areas that had shown significant differences between the patients and the controls at T1. The persistence of rCBF anomalies in the right lingual gyrus may be a trait marker of MDD.

Plasma Brain-Derived Neurotrophic Factor as a Biomarker for the Main Types of Mild Neurocognitive Disorders and Treatment Efficacy: A Preliminary Study.

Decreased levels of brain-derived neurotrophic factor (BDNF) are assumed to play a crucial role in the pathophysiology of mild neurocognitive disorders (MNCDs). In this study, we compared plasma BDNF levels (at baseline and after two months of treatment with escitalopram) in patients with the main types of MNCDs and normal controls. 21 patients met the DSM-5 diagnostic criteria for possible MNCD due to Alzheimer's disease (MNCD-AD); 22 patients fulfilled the diagnostic criteria for subcortical vascular MNCD (ScVMNCD) according to Frisoni et al. (2002) and neuroimaging-supported probable diagnosis of vascular MNCD according to DSM-5; 16 subjects entered control group. At baseline, we detected lower BDNF levels in both MNCD groups, which was significant only in subjects with MNCD-AD. Moreover, plasma BDNF level of 21160 pg/mL showed high sensitivity (94%) to discriminate patients with MNCD-AD. Decreased plasma BDNF highly correlated with the severity of memory impairment and total MMSE score in MNCD-AD group. Escitalopram treatment in patients with MNCD-AD or ScVMNCD led to an increase of plasma BDNF concentrations and as a result to a decrease of cognitive, depressive, and anxiety symptom severity. In conclusion, plasma BDNF might be a reliable biomarker for the validation of MNCD-AD diagnosis and treatment efficacy.

Combined Treatment of Aripiprazole and Escitalopram Oxalate Therapy to Treat Major Depressive Disorders.

This review article presents the pharmacology of combined treatment of Aripiprazole and Escitalopram oxalate in treatment of Major Depressive Disorders. Aripiprazole is anti psychotic agent. Escitalopram Oxalate is also an antidepressant agent (Selective Serotonin Reuptake Inhibitor). Aripiprazole's antipsychotic activity is likely due to a combination of antagonism at D2 receptors in the mesolimbic pathway and 5HT2A receptors in the frontal cortex. Antagonism at D2 receptors relieves positive symptoms while antagonism at 5HT2A receptors relieves negative symptoms of schizophrenia. Escitalopram Oxalate is selective serotonin reuptake inhibitors (SSRIs) are a group of chemically diverse antidepressant drugs that specifically inhibit serotonin reuptake. The SSRIs block the reuptake of serotonin, leading to increased concentrations of the neurotransmitter in the synaptic cleft and, ultimately, to greater postsynaptic neuronal activity. The combination of both have decrease dose and improve Depression. Combination of both the drugs were approved by us government and has been used in Major Depressive Disorders. The main objective of this review article is to provide pharmacological information of combined therapy of of Aripiprazole and Escitalopram Oxalate to researcher in development of combined dosage form of this.