Time period of side effects To further understand side effects and their impact on patients’ quality of life and compliance, it. is also important to be aware of the time

when certain side effects present. While there is common belief that side effects can be classified as acute or chronic, a review by Papakostas9 challenged this idea. In it, he cites Hu et al’s1 study that. shows that although certain side effects may present, early or later in the course of treatment, many of those that arc considered acute persist #this website keyword# to a point that they should be considered chronic. In this stud}1, SSRI-induced side effects such as insomnia, sexual dysfunction, and drowsiness that are often considered acute persisted at 3 months. On the other hand, some side effects such as nausea do start early in the course of treatment, and then usually improve, while others such as weight, gain are not. present initially but emerge over time.

Inhibitors,research,lifescience,medical Another naturalistic study by Demyttenaere et al3 of 272 outpatients Inhibitors,research,lifescience,medical on an SSRI, trazodone, venlafaxine, or moclobemide looked at the time period that patients discontinue treatment secondary to side effects, and found that patients who cited side effects as their reason for discontinuation dropped out. of treatment at a mean period of 6.5 weeks. This study showed that side effects and lack of efficacy led to the earliest, discontinuation of antidepressants (at 6.5 weeks and 7 weeks respectively), followed by other reasons such as “fear of drug dependence” and “feeling better” that Inhibitors,research,lifescience,medical occurred at 8 weeks and later. Reinforcing the conclusion that side effects often account for early discontinuation, Bull et al10 found that significantly more patients discontinued or switched their SSRI because of an adverse effect, within the first. 3 months of treatment compared with the second 3 months. Side effects as predictors of response Although there are no systematic studies to our knowledge that address specific treatment-emergent adverse effects as predictors of response, we are aware that optimistic colleagues

Inhibitors,research,lifescience,medical sometimes look for certain early side effects, such as activation or insomnia, as favorable prognosticators. the Emerging biomarkers, such as quantitative electroencephalography11 or neuroimaging,12 alone or in conjunction with clinical features at. baseline and during treatment, represent, an important area of current research. Nevertheless, while the presence of particular side effects has no known prognostic significance, when patients have no side effects and minimal response despite full doses of an antidepressant, it is reasonable to rc-cvaluate medication adherence as well as to consider the possibility of drug-drug interactions (particularly metabolic induction) and genetic polymorphism that might call for higher doses to achieve an optimal outcome.

Selected abbreviations and acronyms α2-AR α2-adrenoceptor β-AR β-adrenoceptor DAT dopamine transporter GPCR G protein-coupled receptor 5-HT 5-hydroxytryptamine (serotonin) LC locus ceruleus Notes The contributions of former and current members of the Clinical Neurobiology Laboratory at the German Primate Center are gratefully acknowledged. The work summarized here was in part supported by the German Science Foundation, the DAAD, and the EC.
Depression is a common, chronic, and often disabling psychiatric illness, which is estimated to affect 5% to 10% of the population. It frequently appears Inhibitors,research,lifescience,medical in early life, has a

chronic course, and is considered a risk factor for other medical illnesses, such as coronary vascular disease, diabetes, and osteoporosis. This is not altogether

surprising given the extensive bidirectional “mind-body” interactions mediated Inhibitors,research,lifescience,medical via the autonomic nervous system, immune system, and a host of neuroendocrine factors. According to the World Health Organization (WHO), depression is the leading global cause of years of life lived with disability and the fourth leading cause of disability-adjusted Inhibitors,research,lifescience,medical life-years. Disability-adjusted life-years is defined as the reduction in an individual’s productive life, and takes into account premature mortality.1,2 Considering the high morbidity and mortality associated with depression, it is unfortunate that the psychological and neurobiological underpinnings of depression have not been specifically defined. Although major depression is currently diagnosed by means of a diagnostic system (Diagnostic and Statistical Manual of Mental Health Disorders, Fourth Edition [DSM-IV]) based upon phenomenology, Inhibitors,research,lifescience,medical this selleck chemicals llc disorder most likely embodies a heterogeneous set of disorders with multiple causes. Therefore, one of the major goals of current, and future research on depression is the development of a diagnostic system Inhibitors,research,lifescience,medical based on etiology.3 This goal

is becoming increasingly closer to reality due to recent progress in the identification of neural circuits, neurochemicals, and signal transduction mechanisms underlying the pathophysiology and treatment of depressive illness.4,5 Advances toward specifying the contribution of genetic factors,6 psychosocial stressors,7,8 and gene-environment interactions Calpain to susceptibility to depression are also taking place.9,10 It is anticipated that, in the next few years, combined use of genomic and proteomic strategies to refine complex psychiatric diseases into mechanism-based subcategories may ultimately facilitate the matching of specific target-based therapies to particular markers in certain patient subgroups.11 Of all brain systems, the monoaminergic neurotransmitter systems have received the greatest attention in neurobiological studies of depressive disorders.

On the first day postpartum, 5 mL of urine was taken from the mothers.

Urine samples were frozen at a temperature of −80°C and stored until urinary cotinine measurement was performed. Urinary cotinine concentration was see more measured by high-performance liquid chromatography with spectrophotometric detection and norephedrine was used as an internal marker, following earlier liquid–liquid extraction. The concentration Inhibitors,research,lifescience,medical of urinary cotinine was measured in ng/mL and then expressed as mg of creatinine (ng/mg of creatinine), in order to avoid errors associated with excessive dilution or concentration of the urine. Creatinine concentration was measured by spectrophotometry. The fetal age of the neonates in the study ranged from 26 to 42 weeks of gestation and the average birth age of neonates was 38 weeks of gestation. The majority (114) were term births (77.55%). There were 33 (22.45%) preterm births. There was Inhibitors,research,lifescience,medical no statistically significant difference

between the groups of subjects in terms of sex, method of delivery, or numbers of preterm births (Table 1). Measurement of the head circumference was made immediately after birth with the aid of a tape measure with an accuracy of up to 0.5 cm. The head circumference was measured by passing the tape measure over the opisthocranion and metopion. The cerebral mass was calculated according to the following equation: cerebral Inhibitors,research,lifescience,medical mass (g) = 0.037 × head Inhibitors,research,lifescience,medical circumference (cm)2.57 (Lindley et al. 2000). Table 1 Characteristics of the neonates. In order to determine the proportion of cerebral mass to body mass, the brain body ratio (BBR) was calculated according to the following equation: BBR = 100 × [0.037 × head circumference (cm)2.57]/body mass (g) (Lindley et al. 2000). The following tools were used for the statistical analysis: Descriptive statistics—average values, standard

deviations, medians, and ranges for quantitative variables. The Shapiro–Wilk test for testing the null hypothesis of no difference between the distribution of the subjects and the normal distribution. The Kruskal–Wallis one-way analysis of variance Inhibitors,research,lifescience,medical for the comparison of groups for quantitative variables with a non-Gaussian distribution. Wilcoxon’s test for analysis of found the differences between two groups for quantitative variables with a non-Gaussian distribution. Fisher’s exact test for analysis of the relationship between quantitative variables. The multi-dimensional logistic regression model (GLIMMIX) was used to calculate the odds ratio for the different patient groups as well as the multi equivalent risk ratio in the groups under comparison. The relationship between maternal urinary cotinine concentration and the cerebral mass of the neonates was confirmed by estimating Spearman’s rank correlation coefficient. A P-value of <0.05 was taken as statistically significant. Calculations were made using the SAS system.

2008). However, fDTI is a highly novel technique that has not been adequately validated and these studies were also excluded. This review thus focuses on fMRI and [15O] PET studies. Searches yielded 107 articles, of which only 40 used functional neuroimaging. Another 27 potentially relevant articles were found

through cross-referencing. Of these 67 articles, 37 were excluded because they included only polydrug users (n = 3), did not have a matched control group (n = 16), re-used an external (nonmatched) control group from a previous study (n = 2), did Inhibitors,research,lifescience,medical not match for alcohol and/or cannabis use (n = 7), or included other imaging techniques (n = 9). This review thus includes 26 studies using fMRI and four studies using [15O] PET. The most frequently

studied substance was cocaine (n = 17), Inhibitors,research,lifescience,medical followed by nicotine (n = 5), (meth-)amphetamine (n = 4), and ecstasy (n = 4). No studies were found in subjects with excessive use of caffeine compared with low or no caffeine consumers. For several details concerning the reviewed studies (e.g., neuroimaging technique, task, abused drug, time since last use, Inhibitors,research,lifescience,medical sample size, and summary of findings), four tables (Tables 1–4) are presented in the subsequent sections. Table 1 Overview of the selected reviewed studies on reward and punishment processing in stimulant abusers versus healthy controls Table 4 Overview of the selected reviewed articles on decision making and executive control Results and Discussion Section 1: Reward and punishment processing in stimulant dependence Task paradigms and behavioral findings during

reward and punishment processing Reduced sensitivity for reward or punishment, Inhibitors,research,lifescience,medical or negative affect, is hypothesized to cause persistent drug-taking behavior by reducing aversive states (Baker et al. 2004) or by inducing lowered self-control (Segarra et al. 2000). With regard to addictive disorders, we like to notice that altered sensitivity to both natural reinforcers (this section) and drug (related) cues (next section) was found. Sensitivity for reward and punishment of natural reinforcers can be measured using neurocognitive Inhibitors,research,lifescience,medical TCL tasks with positive (monetary) feedback (reward) after a correct HDAC assay response or negative (monetary) feedback (punishment) following an incorrect response. Tasks that measure reward and punishment sensitivity include the stimulus-response learning task, and the probabilistic reversal learning task (PRLT), and a variety of gambling tasks which focus on processes like risk taking strategies regarding wins and losses, or on learning reward and punishment contingencies. The PRLT is a task in which the individual is required to adapt his or her response to changing contingencies (shifts) to win the largest amount of money. Tasks may feature several reward contingencies, representing high and low reward options or measure response differences during reward and punishment processing.

However, these levels had returned to normal after 10 days of withdrawal.45 As found

in our previous studies, adaptation or tolerance to the cocaine effects on the HPA axis activation also was observed during chronic binge cocaine.45 However there were still modestly elevated levels of ACTH during acute withdrawal. As expected, naloxone produced modest elevations in ACTH levels in cocaïne-naïve rats; naloxone did not have such an effect in the acute or subacute cocaine-withdrawn animals. There were no changes in arginine vasopressin, or POMC, or mu-opioid receptor Inhibitors,research,lifescience,medical mRNA levels in the hypothalamus following chronic cocaine administration, and acute withdrawal from cocaine.45 These findings suggested that opioid receptors may mediate the increase in arginine vasopressin Inhibitors,research,lifescience,medical in the amygdala during acute cocaine withdrawal, and suggest a potential role for arginine vasopressin in the amygdala in some of the adversive effects of withdrawal from cocaine as well as in withdrawal from opiates.45 A recent set of laboratory-based studies in rats affirm, and further suggest a mechanism, for observations

which we have made in two separate clinical studies, around 7 years apart, and in two parts of the world.46-48 We have determined that steady-state methadone may attenuate or eliminate the liking Inhibitors,research,lifescience,medical of cocaine, and may do so by a mu-opioid receptor-mediated mechanism49,50 In several earlier studies, as

discussed above, we have shown that chronic binge-pattern cocaine administration results in an increase in mu-opioid receptor Inhibitors,research,lifescience,medical density in multiple, but not all, brain regions, and specifically in regions where there are abundant dopaminergic terminals from dopamine neurons Inhibitors,research,lifescience,medical in the ventral tegmental area and substantia nigra compecta.31-33 Further, we have shown that acute and subacute, but not chronic, cocaine administration results in an increase in mu-opioid receptor mRNA levels.30 in these recent studies, different paradigms were used.41 In one set of studies, rats were implanted with STAT inhibitor either salineor Edoxaban methadone-filled osmotic minipumps and then conditioned with 1, 5, or 20 mg/kg cocaine intraperltoneally. Animals with the 20 mg/kg/day or 55 mg/kg/day methadone-filled osmotic pumps did not express cocaine-induced place preference.46 However, methadone pumps at two doses (30 and 55 mg/kg/day) did not alter intravenous self-administration of cocaine using a continuous schedule of reinforcement with different doses of cocaine (0.1, 0.5, and 2.0 mg/kg/infusion) studied. Mu-opioid receptor mRNA levels were measured in animals treated with cocaine as part of conditioning for place preference. As in earlier studies, it was shown that this subacute cocaine administration resulted in increased mu-opioid receptor mRNA levels in the nucleus accumbens core and in the frontal cortex 10 days after cocaine conditioning.

In addition, the complex receptor binding profile of clozapine has suggested to

some that attempts to simulate this effect should involve combining multiple drugs. There are several reports indicating a high prevalence of antipsychotic polypharmacy in recent clinical practice.55 #PRT062607 randurls[1|1|,|CHEM1|]# Despite widespread use, there is relatively little evidence that this strategy is helpful, particularly when clozapine is not involved. Correll et al56 reviewed 19 randomized trials including 1216 subjects. Although the overall results could be interpreted Inhibitors,research,lifescience,medical as suggesting an advantage for combination therapy in comparison with monotherapy, the factors which appeared to contribute to this effect limit the conclusions that can be drawn for the present context. Combination therapy was more likely to be efficacious when administered from the start of treatment rather than waiting to identify poor or partial responders and when clozapine was involved. Studies which took place in China and studies which lasted longer than 10 weeks were also more likely to be positive. This leaves the question unresolved Inhibitors,research,lifescience,medical as to whether or not adding a second antipsychotic is likely to be helpful when a patient fails Inhibitors,research,lifescience,medical to derive an adequate response from an initial trial of monotherapy with drugs other than clozapine. Adding a second antipsychotic to mitigate adverse effects from another medication is a different situation, and there is some suggestion

that, for Inhibitors,research,lifescience,medical example, adding aripiprazole to clozapine can lead to a reduction in weight and/or lipid abnormalities.57,58 Clozapine Since the Kane et al6 study, clozapine has been considered the best established treatment for refractory patients. In addition, clozapine has been shown to be superior to second-generation Inhibitors,research,lifescience,medical antipsychotics even among patients who were only moderately ill7 and would not necessarily have met criteria for true treatment resistance. The superiority of clozapine has been demonstrated in subsequent individual studies59,28,24 and metaanalysis.60,61,62 However, as mentioned previously, in a recent metaanalysis by Leucht et al14 of 28 randomized, head-to-head comparisons of clozapine with other second-generation

antipsychotic drugs, clozapine did not show consistent superiority. Nevertheless, many if not most of these studies used low or very low doses Cytidine deaminase of clozapine or patients were not truly poor responders. Other pharmacologic classes in augmentation strategies Numerous other classes of agents have been studied to determine their ability to augment the effects of antipsychotics in the treatment of patients with schizophrenia, either in general or in poor or partial responders. Cochrane reviews of benzodiazipines,63 lithium,64 and valproate65 could find no clear evidence of efficacy. A systematic review of carbamazepine66 was also negative. Lamotrigine has been examined in a Cochrane review including five studies involving 537 participants.

These new versions of the cholinergic and glutamatergic hypotheses make it necessary for us to reappraise our models. The goal of an acute pharmacological model is to transiently reproduce the hypoactive, symptomatic stage. According to the scheme proposed by Newcomer et al elsewhere in this issue, NMDA blockers induce transient hyperactivity of basal forebrain cholinergic, anterior thalamic glutamatergic, and cortical

NPY neurons. It is likely that the mechanism by which acute administration of NMDA blockers produces memory impairment Inhibitors,research,lifescience,medical is different and does not involve the two-stage sequence proposed as a chronic model. The finding that pretreatment with haloperidol reduces ketamineinduced impairment in executive cognitive functions91 nonetheless suggests that the cognitive effect of NMDA blockade is indirect and nonselective.

Higher selectivity, which would also avoid psychotomimetic symptomatology, might be achieved by acting downstream of the NMDA receptor. For the particular posterior cingulate and retrosplenial region, the best choice would be to give m3 and/or Inhibitors,research,lifescience,medical kainate receptor blockers. Another MLN8237 target of choice is the hippocampus, in which the most common muscarinic receptor is the mi subtype; the m2 subtype represents 15% and the m3 subtype globally less than 12%.120 Moreover, specific blockade of the m1 receptors would best reproduce their status in AD, where they are hypostimulatcd (because Inhibitors,research,lifescience,medical of presynaptic neuronal loss) and dysfunctional. The only molecule which is more or less selective for the mi receptor121 and available for human use is pirenzepine. Inhibitors,research,lifescience,medical It is said to cross the blood-brain barrier poorly,122 but very few studies have assessed its central effects in man123-125 and we think it deserves further study. Do neurotransmitter-based

Inhibitors,research,lifescience,medical pharmacological models have a future? The way the cognitive symptoms are produced in AD is complex and many therapeutic strategies already in development address βA metabolism and toxicity,126-128 rather than cholinergic deficiency. However, D-cycloserine, which does not act on the cholinergic system but modulates the NMDA receptor, has been shown to attenuate the effect of scopolamine on memory.50 Moclobemide, a selective monoamine oxidase A (MAOA) inhibitor,42,43 already and thyrotropin-releasing hormonc (TRH)129 were also able to partly reverse the scopolamine-induced deficits. In the animal, the same has been observed with estrogens130 and GM1 gangliosides.131 Given these data and the current view that we have on the involvement of the cholinergic deficiency, it is very possible that new compounds, which do not act directly on the cholinergic system, could be effective on cholinergic models. Neurotransmitter-based models still have a place in our armamentarium, although efforts should be made to develop other approaches. Conclusion Whatever the model chosen, we must admit that it is e impossible to reproduce the full AD cognitive pattern.

3-9 CBT is defined as: An amalgam of behavioral and cognitive interventions guided by principles of applied science. The behavioral interventions aim to decrease maladaptive behaviors and increase adaptive ones by modifying their antecedents and consequences and by behavioral practices that result in new learning. The cognitive interventions aim to Tivantinib solubility dmso modify maladaptive cognitions, self-statements or beliefs. The Inhibitors,research,lifescience,medical hallmark features of CBT are problem-focused intervention strategies that are derived from learning theory

[as well as] cognitive theory principles.8 , 10 While it is beyond the scope of this article to review specific treatment components of CBT, they generally include various combinations of the following: psychoeducation about the nature of fear and anxiety, self-monitoring of symptoms, somatic

exercises, cognitive restructuring (eg, logical empiricism Inhibitors,research,lifescience,medical and disconfirmation), imaginal and in vivo exposure to feared stimuli while weaning from safety signals, and relapse prevention.8 Depending on the specific anxiety disorder, these CBT techniques are weighted differentially during therapy. A plethora of studies have examined the efficacy of CBT for adult anxiety disorders. Furthermore, several meta-analyses have been conducted to quantitatively review the evidence of CBT for anxiety disorders.4,6,9,11 In meta-analysis, Inhibitors,research,lifescience,medical treatment efficacy is quantified in terms of an effect size. An effect size indicates the magnitude of an observed effect in a standard unit of measurement. However, it is important to realize that different types of effect sizes can be used to appraise the available evidence. For instance, effect sizes are sometimes categorized Inhibitors,research,lifescience,medical as ”controlled“ versus ”uncontrolled.“4 A controlled effect size expresses the magnitude of a specific Inhibitors,research,lifescience,medical treatment effect as compared with alternative treatments or control conditions. Most often, it is calculated by subtracting the post-treatment mean of the control group from the post-treatment mean of the treatment group divided by the pooled standard deviation. This effect size is called Cohen’s d. 12 An uncontrolled effect size expresses

the magnitude of improvement within a group from Idoxuridine pretreatment to post-treatment. It is calculated by subtracting a group’s post-treatment mean from its pretreatment mean divided by the pooled standard deviation. Uncontrolled effect sizes are less preferable than controlled effect sizes, since they are susceptible to threats to internal validity.4 Meta-analytic reviews of CBT studies in anxiety disorders have generally found large effect sizes for the majority of treatment studies. Accordingly, recent reviews that summarized the results of these numerous meta-analyses of CBT treatment in anxiety disorders concluded that CBT is highly effective.3 – 4 – 13 However, these existing meta-analyses are not without limitations.

The same work group performed a second study (13) in a smaller group [37] of DMD patients undergoing cardiac evaluation before and after steroid treatment. Furthermore they expanded the number of echocardiographic measures, including left ventricular wall stress (WS), contractility and the corrected velocity of circumferential fiber shortening (VCFc). The mean period of FU was 4.5 years and regarded 23 untreated and 14 treated DMD cases (mean age 7.5 ± 0.8 years, at the initial cardiac evaluation). The baseline echocardiographic measures did not differ in the two groups; Inhibitors,research,lifescience,medical however, at the final echocardiographic measure, DMD untreated boys had significantly larger left

ventricular diastolic diameter (LVDD) and evidence of left ventricular dysfunction. The wall stress was higher and the contractility (VCFc) less yielding a negative Inhibitors,research,lifescience,medical stress velocity relationship (VCFdiff). The frequency of ventricular dysfunction increased significantly with age for untreated cases. On the other hand, steroids treated DMD patients did not have a significant change in functional indices compared to baseline. At the time of the final evaluation, only 2 treated cases vs. 16 Inhibitors,research,lifescience,medical untreated had evidence of ventricular dysfunction (p < 0.001). ACE-inhibitors treatment Angiotensin-converting enzyme inhibitors (ACEIs) are a group

of pharmaceuticals primarily used in treatment of hypertension and congestive heart failure. ACE inhibitors block the conversion of angiotensin I to angiotensin II. They therefore lower arteriolar resistance and increase venous capacity, increase cardiac output and cardiac index, stroke work and volume, lower reno-vascular resistance and lead to increased natriuresis. ACE inhibitors can be divided into three groups based on their molecular structures: Sulphydril-containing Inhibitors,research,lifescience,medical agents; Dicarboxylate-containing agents; Phosphonate-containing Inhibitors,research,lifescience,medical agents. The first group BIO GSK-3 cell line includes Captopril – the first ACE inhibitor – and Zofenopril. The second group – the largest one – includes Enalapril, Ramipril, Quinapril, Perindopril, Lisinopril and Benazepril. Fosinopril is the only member of the third group. Treatment with

ACEIs has been shown to reduce mortality and hospitalization in patients with systolic heart failure or heart failure with reduced ejection fraction (14, 15). Furthermore a prophylactic effect of ACE-inhibitors has been reported in Syrian hamster cardiomyopathy, an experimental model of delta-sarcoglycanopathy, phenotypically similar to DMD (16, 17). Perindopril In 2005, Oxalosuccinic acid the group of Duboc in France (18) reported the results of a phase I three-year multicenter, randomised, double-blind trial of the ACEIs perindopril (2 to 4 mg/day) in a group of 57 DMD patients, aged 10.7 ± 1.2 years, with normal ejection fraction (group 1) vs. placebo (group 2). In phase II, all patients received open-label perindopril for 24 more months. Left ventricular ejection fraction (LVEF) was measured at 0, 36 and 60 months.

158 Summary The goal of this review is to highlight consistencies in the ASD fMRI literature. Given the array of imaging tasks reviewed, it is perhaps not surprising that findings are heterogenous. Despite variations in findings, there is a sufficient degree of consistency to #selleck compound randurls[1|1|,|CHEM1|]# draw a number of substantive conclusions. Studies of social processes have generally found evidence of hypoactivation in nodes of the “social Inhibitors,research,lifescience,medical brain,” including the medial prefrontal cortex, the inferior frontal gyrus and the anterior insula, the posterior superior temporal sulcus, the interparietal sulcus, the amygdala, and the fusiform gyrus. Studies addressing cognitive control,

designed to address neural mechanisms underlying restricted and repetitive behaviors and interests, have converged on aberrant frontostriatal functioning in ASDs, specifically Inhibitors,research,lifescience,medical in inferior and middle frontal gyri, anterior cingulate cortex, and the basal ganglia. Communication impairments in ASDs have been linked to differential patterns of language Inhibitors,research,lifescience,medical function lateralization, decreased synchrony- of brain regions processing language, and recruitment of brain regions that do not typically processing language. Reward processing studies have highlighted mesolimbic and mesocortical

impairments when processing both social and nonsocial incentives in ASDs. Finally, task-based functional connectivity Inhibitors,research,lifescience,medical studies in ASDs have reported local overconnectivity and long-distance (ie, between frontal and posterior regions) underconnectivity-, whereas resting state connectivity studies indicate decreased anterior-posterior connectivity and less coherent endogenous low-frequency oscillations across multiple regions. Future directions Most studies reviewed here focus on adulthood or adolescence, yet ASDs are present from very early childhood. It will be critical to address developmental profiles in children with ASDs to disambiguate proximal effects of altered brain function from downstream effects on learning and motivation. There also may be critical

nearly periods during early development Inhibitors,research,lifescience,medical when brain dysfunction creates a predisposition to develop a number of disorders, and understanding factors that influence these processes will be essential for the prevention of symptom onset. Indeed, emerging techniques allow for functional brain imaging in children as young as 12 months old, and future studies that focus on young samples are needed. Additionally, most studies reviewed here contain small samples, and larger samples will be needed to identify meaningful subgroups and track developmental profiles. Given the high costs associated with brain imaging and challenges recruiting large pediatric patient samples, it will be critical to leverage available bioinformatics tools to facilitate data sharing across research groups.