It is well-known that approximately 20% of patients who underwent Roux-en-Y gastric bypass (RYGB) and 11% of patients who undertook laparoscopic adjustable gastric banding acquired AUD within five years of surgery. Notably, decreases in BMI following RYGB have decreased food addiction symptoms (as measured by the Yale Food Addiction Scale) and increased alcohol intake 24 months post-operation. After many years of successful bariatric (weight-loss) surgeries targeted at the obesity epidemic, clinicians report that some patients replace compulsive overeating with newly acquired compulsive disorders such as alcoholism, gambling, drugs, and other addictions like compulsive shopping and exercise. Our laboratory previously coined the term Reward Deficiency Syndrome (RDS) for common genetic determinants in predicting addictive disorders and reported that the Bayesian predictive value for future RDS behaviors in subjects carrying the DRD2 Taq A1 allele was 74% [1]. Transfer potential, data from our laboratory has shown that in an obese cohort undergoing bariatric surgery based on genetic addiction risk testing showed that these individuals carried a high risk for illicit drug abuse as well as Alcohol Use Disorder (AUD) suggestive of addiction transfer potential. Arterburn, et al. summarized the literature on bariatric surgery benefits and risks. Obesity and associated health largest public health causing preventable et examined the current epidemiology of obesity and surgical and the beneficial effects on numerous obesity-related comorbidities type
Pioneering work reported by Anton, et al. [1] in this journal may be an important step in the treatment algorithm of patients with alcohol use disorder (AUD). Identifying patients who need and would benefit from treatment with naltrexone [2] might help to change clinicians’ hesitancy to utilize these medications in AUD where twelve step treatment programs have renewed interest and support [3]. Modern therapeutics and personalized medication are predicated on the basis of tests or measures that can provide potential matching of safe and effective medications with the population of patients who are most likely to benefit from these therapeutic interventions. Anton’s work might help to improve the utilization of medications in not only in classical AUD but also in a wider spectrum of alcohol misusing patients. The importance of genetic testing to predict Medical Assistance Treatment (MAT) response came to prominence by the initial discovery of the DRD2 Taq A1 allele and its relationship to alcoholism [4]. In addition, it also seems essential to analyze genetic polymorphisms related to opioid and dopaminergic genes as antecedent polymorphic predictors of clinical responses to naltrexone [5]. We also applaud the efforts of Anton’s team in evaluating whether response to naltrexone depends on or is predicted by potential interactions of the OPRM1 SNP rs1799971 with the dopamine transporter gene DAT1/SLC6A3
This study aimed to identify strengths and weaknesses in a cognitive profile of children with Autism Spectrum Disorders (ASD) and to study relationship between the triad of impairments in ASD, delayed achievement of speech milestones and cognitive abilities.Our sample consisted of 30 children, male-to-female ratio 5:1, diagnosed with ASD using the Autism Diagnostic Interview -Revised and the Autism Diagnostic Observation Schedule.Results showed significant variations in their cognitive abilities as measured the Woodcock-Johnson International Editions.Cognitive efficiency, consisting of Processing speed and working memory, has been significantly reduced, yet individuals with ASD performed well on fluid intelligence, suggesting possible underestimation of their performance assessed with tests standardized for neurotypical population.We also identified three negative predictors of their overall IQ: inflexible adherence to specific non-functional routines or rituals, persistent preoccupation with parts of objects or non-functional elements of play materials and a delayed use of sentences.
The Center for Devices and Radiological Health (CDRH) of the Food and Drug Administration (FDA) has completed its review of your de novo request for classification of the Neuropsychiatric EEG-Based Assessment Aid for Attention Deficit Hyperactivity Disorder (ADHD), referred to as the NEBA System, a prescription device under 21 CFR Part 801.109 that is indicated as follows:The Neuropsychiatric EEG-Based ADHD Assessment Aid (NEBA) uses the theta/beta ratio of the EEG measured at electrode CZ on a patient 6-17 years of age combined with a clinician's evaluation to aid in the diagnosis of ADHD.NEBA should only be used by a clinician as confirmatory support for a completed clinical evaluation or as support for the clinician's decision to pursue further testing following a clinical evaluation.The device is NOT to be used as a stand-alone in the evaluation or diagnosis of ADHD.FDA concludes that this device, and substantially equivalent devices of this generic type, should be classified into class II.This order, therefore, classifies the Neuropsychiatric EEG-Based Assessment Aid for ADHD (NEBA) System, and substantially equivalent devices of this generic type, into class II under the generic name, Neuropsychiatric Interpretive Electroencephalograph Assessment Aid.FDA identifies this generic type of device as:Neuropsychiatric Interpretive Electroencephalograph Assessment Aid.The Neuropsychiatric Interpretive Electroencephalograph Assessment Aid is a prescription device that uses a patient's electroencephalograph (EEG) to provide an interpretation of the patient's neuropsychiatric condition.The Neuropsychiatric Interpretive EEG
The unpredictable chronic mild stress (UCMS) mouse model of depression causes a variety of neuronal structural alterations ranging from dendritic spines loss and dendrite arbor retraction to spine proliferation in brain regions involved in the control of mood.Based on data showing that the plant stress hormone methyl jasmonate (MJ: methyl acetate-2,2-d2) mimics the effect of imipramine in rescuing the UCMS-induced depressive behavioral phenotype, here we examine whether the UCMS protocol used to demonstrate the antidepressant action of the compound triggers structural alterations in basolateral amygdala, hippocampus and prefrontal cortex which can be rescued by MJ treatment.Male C57BL/6 mice were injected with MJ (50 mg/kg) or saline (SAL) before each of the two daily exposures to UCMS administered over a 10-day period.Home cage, daily manipulated, SAL-injected mice served as controls (CTRL).On day 11, mice were sacrificed for Golgi-staining.Results show that in comparison with CTRL mice, SAL+UCMS mice exhibit a massive reduction in spine density and dendritic arbor extension/complexity in the three regions examined.Remarkably, MJ+UCMS mice show an alleviation of neuronal structural alterations in the three regions, with a more complete recovery observed in the prefrontal cortex.Our data provide further validation of the antidepressant action of the compound by revealing its efficacy in globally preventing the collapse in synaptic density and neuronal connectivity identified as key nodes of the mood circuitry.
