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Nathan Rothenberg married his first cousin, Rieke Kleinstrass she is listed below, under the children of Helena Rosenstern.

Rieke married her first cousin, Nathan, see above. They have a separate line for each spouse. Later the family moved to Höxter and to Paderborn.

Thanks to Janet Rosenstern and to Michael Plaut for their work in assembling much of this data. He spent his time there collecting information on the Jewish families of the region, from town and synagogue records, by visiting cemeteries, and by talking with people.

His data, now in the collection of the Leo Baeck Institute in New York, is one of the best sources of information on the Jews of Höxter, Brakel, Steinheim, and nearby towns in that part of Westphalia.

Thanks to Fritz Ostkämper in Höxter for pointing me in their direction. Click here for HOME page. Whether these potential neural phenotypes are meaningfully linked to newly identified genetic contributors to this trait remains untested.

Additionally, participants were genotyped and, using data derived from a meta-analysis of GWAS studies examining neuroticism in , individuals Nagel et al, , a series of neuroticism polygenic association scores were derived using a range of p-value thresholds, and the first principal component of these scores PAS was carried forward for voxel-wise analyses within the striatum.

There were no striatal findings with [11C]NNC Conclusions: Individuals with greater polygenic risk for neuroticism may have lower presynaptic dopamine synthesis and dopamine receptor availability in regions important for mood, anxiety, and reinforcement learning, consistent with the literature on neuroticism itself, but also increased presynaptic dopamine synthesis in limbic temporal lobes.

These results lend support for associations between putative molecular foundations of neuroticism and dopamine systems in the healthy human brain and merit further study in patient populations.

While treatments like cognitive-behavioral therapy are effective at reducing overall anxiety, they are largely ineffective in reducing worry severity in older adults.

In this study we investigate the neural basis of both induction and reappraisal of worry using an in-scanner personalized worry task.

We identified several regions that were associated with worry severity and conducted an open-label treatment using intermittent theta-burst stimulation iTBS [a form of transcranial magnetic stimulation TMS ] of an identified target in 5 participants.

Based on the clinical interview with each participant, we built a participant-specific list of worry induction and worry reappraisal sentences.

These sentences one per block were presented to participants during functional magnetic resonance imaging fMRI with fixation in between blocks.

Worry induction blocks were followed either by neutral blocks control condition, included random factual sentences — e. Following each block, participants rated their worry severity After motion correction, spatial normalization to a standard anatomical space, and smoothing we conducted mass-univariate general linear modeling to model worry induction, reappraisal, and neutral blocks.

Using statistical non-parametric mapping SnPM12 , we performed a paired t-test to identify regions that were significantly more parametrically modulated during worry induction compared to worry reappraisal.

We also conducted paired t-tests to identify regions that were activated more during worry induction and reappraisal compared to neutral.

We identified several regions that had activation that increased parametrically with in-scanner worry severity.

We targeted the right supramarginal gyrus see results. Neuronavigation software was used to target the right supramarginal gyrus identified in our study.

The same regions had greater activation associated with lower in-scanner worry severity rating following worry reappraisal.

Conclusions: The dACC and the temporoparietal junction showed greater activation during worry induction when participants reported higher levels of worry at the end of worry-induction blocks.

This result may indicate an increased level of affective mentalizing SMG coupled with a more sustained effort toward implicit-controlled regulation dACC in participants who exhibit higher level of worry following induction.

In contrast, the activation in these regions was greater during reappraisal if the participants reported lower levels of worry at the end of worry-reappraisal blocks.

This result may be interpreted as a marker of successful reappraisal and points toward to role of both dACC and SMG in cognitively regulating worry severity.

These results indicate potential targets for future interventions designed to alleviate severe worry in older adults e.

TMS of the TPJ seems to show potential for reducing worry-modulated activation and while not significant due to small sample sizes , there is potential for its development as a treatment for severe worry.

Background: The ability to flexibly respond to changes in the environment is critical for adaptive behavior.

Reversal learning is a form of associative learning that tests the ability of an organism to change responses when contingencies are altered.

For example, conditions that were once rewarding may become threatening and vice versa. Successful reversal learning is thought to be mediated by cortico-striatal and medial temporal lobe MTL systems.

Interestingly, a previous study in patients with confirmed MTL atrophy reported specific deficits in reversal of contextual associations, but intact reversal of cue associations, independent of the outcome valence.

Reversal learning of contextual versus cue associations may rely on different components on this system; however, this has not been investigated.

Methods: 34 adults mean age Pairs of cues objects and contexts background color were presented with one of two outcomes money or bomb , and then the outcome association of either the cue or context was reversed, requiring participants to form new associations between the context or cue and outcome.

Neural activation during contextual versus cue reversal learning was compared in MTL subregions e. Conclusions: These findings support previous evidence that the MTL is critical for the reversal of associations that involve contextual but not cue information.

Furthermore, our results implicate cortico-striatal regions in the reversal of cue-based associations.

Background: Mitochondria are responsive to both acute and chronic exposure to psychosocial stress. A few recent studies suggest that circulating cell-free mitochondrial DNA ccf-mtDNA may rise with psychopathology and acute psychosocial stress.

No prior work has examined ccf-mtDNA in relation to adversity or trauma exposure. This study assessed ccf-mtDNA at baseline and in the context of an acute stressor in a sample of healthy young adults, with or without a history of parental loss and maltreatment.

Conclusions: These preliminary findings add to the evidence that cell-free DNA may be involved in the response to acute psychosocial stressors.

Because elevations in ccf-mtDNA are known to be elevated in physiologic stress, such as exercise or illness, elevations in response to a psychosocial stressor may indicate the role of mitochondrial signaling in broader systemic responses to psychosocial stress.

Higher ratio of ccf-mtDNA to ccf-nDNA was also linked to current trauma and stressor-related disorders, suggesting the possibility of mitochondrial changes may be associated with underlying psychological functioning.

Human studies using actigraphy-based tracking in real time have revealed the central role of disturbances in motor activity in mood disorders, particularly Bipolar Disorder BD that is characterized by dysregulation of patterns of motor activity.

Likewise, the atypical subtype of depression, characterized by overeating and oversleeping is associated with disrupted patterns of both activity and sleep based on objectively tracked assessments.

At present, there are well-established methods for measuring motor activity in different species, such as non-human primates and rodents.

However, the widespread variability of tools limits comparisons across these studies as well as applying the findings to human research.

This presentation will examine the use of actigraphy in humans and monkeys as a first step in developing cross species approaches to examine patterns of motor activity.

Second, we present data on the definitions, measures and correlates of motor activity in rodents based on infrared motion detectors.

The monkey data are derived from a sample of adult female rhesus monkeys from a study of predictors of degeneration of nigrostriatal dopaminergic neurons.

Results: First, we asked how similar were daily activity patterns in monkeys and humans? Moreover, the 4 highest loading components of monkeys explained Conversely, the 4 highest loading components from human explain Second, we asked if there were detectable differences in activity patterns in humans with Bipolar disorder?

In addition, the general activity of single-housed adult male mice was monitored using both infrared motion detectors mounted to the top of the cages and wheels.

Patterns of motor activity in response to light were examined to identify whether there were particular light conditions that led to depression like behaviors.

Conclusions: These findings demonstrate the value of studying a core component of behavior across humans and animals.

The use of motor activity as a core behavioral measure of depression can in part minimize the limitation of current behavioral models of depression in basic science.

Harmonization of measures that distinguish motor activity from exercise in humans, and motor activity from motivation in animals will be critical to provide valid comparisons both within basic science and between basic and human studies.

Background: The human prefrontal cortex PFC is a region of the cerebral cortex expanded in primates and associated with higher-order cognitive function including abstract thinking, moral reasoning, and language.

Comparative analyses of the PFC have identified human-specific changes in cell number, morphology, and types as well as microcircuitry and long-range connections, which are thought to underlie human advanced cognitive capabilities and possibly, susceptibility to disease.

These changes in circuitry are likely mediated by divergent changes in spatiotemporal patterns of gene expression and cis-regulatory element activity, most evident during early fetal and mid-fetal stages.

Linking these genomic changes with human-specific changes in cortical anatomy will be integral to modeling and understanding development of human and primate-specific cortical circuitry, as well as how dysfunction in this circuitry lead to neuropsychiatric disease.

However, this process has been arduous due to difficulty accessing high-quality human and primate expression data. To remedy this problem, our laboratory along with multiple other laboratories have created a spatiotemporal atlas of gene expression in humans and macaques spanning from embryonic ages to adulthood, as part of the PsychEncode initiative, called BrainSpan.

Using this database, we are able to identify candidate genes differentially expressed in the human and primate PFC during important periods of development, which can be then be studied in animal models to identify their role in development and dysfunction of the cerebral cortex.

Methods: We used the BrainSpan database to identify genes and signaling pathways enriched in the frontal lobe during mid-fetal development, a crucial developmental period for the formation of neuronal circuits with an enrichment of expression of genes implicated in schizophrenia and ASD.

Expression of select candidate genes was further profiled in various species including mouse, macaque, and human using In Situ Hybridization and RNA-sequencing.

In addition, we utilized comparative genetics combined with both in vitro and in vivo assays to identify non-coding elements that underlie these species-specific shifts in expression.

Finally, we studied the function of select candidate genes and regulatory elements in mouse using CRISPR-Cas9 technology and in utero electroporation combined with a diverse set of assays including diffusion tensor imaging DTI and RNA-sequencing to study the functional significance of this network.

Results: We identified an enrichment of genes involved in synaptogenesis and axon development in the frontal lobe during human mid-fetal development PCW Pathway analysis identified that many of these enriched genes are regulated by the same upstream signaling pathway, whose function in later cortical development has not been explored.

Reduction in activity of this signaling pathway in the early postnatal mouse medial frontal cortex leads to selective loss of reciprocal thalamocortical connectivity both through DTI Furthermore, expansion of this signaling pathway in mouse frontal cortex, to replicate the lateral expansion of activity of this signaling pathway seen in humans, leads to an increase in the thickness of layer IV in motor regions.

In addition, we identified an enhancer regulated by this pathway with a hominini-specific human, great apes deletion.

Targeted replacement with the human enhancer in mouse leads to increased excitatory synapses of both upper Conclusions: Using the BrainSpan database, we were able to identify genes enriched in the human PFC which are co-regulated by a signaling pathway previously linked to schizophrenia.

Using mouse models, we identified that this signaling pathway is required for mediodorsal thalamus innervation and density of excitatory synapses in the PFC.

Connections between the mediodorsal thalamus and PFC are implicated in working memory, behavioral flexibility and goal-directed behaviors and are disrupted in schizophrenia.

Together, we have identified a possible mechanistic link between a previously described dysregulation in a specific signaling pathway, cognitive dysfunction, and schizophrenia.

Background: Behavioral activation system BAS and behavioral inhibition system BIS traits play a central role in determining individual variations in behavioral disposition and vulnerability.

With voxel-based morphometry VBM Li et al. In addition to whole-brain analyses, we also conducted ROI analyses to replicate the findings of Li et al.

We only considered subjects for which raw images were available. Structural magnetic resonance imaging MRI was acquired using optimized protocol for 3T machines including Siemens Prisma, GE and Philips with voxel size 1 mm isotropic.

This modified version shortens the Reward Responsiveness subscale but includes the BAS Fun known to be a reliable predictor of substance involvement in older samples.

Voxel-based morphometry or VBM is used to identify differences in the local composition of brain tissue and its association with behavioral and cognitive measures, while discounting large scale differences in gross anatomy and position.

CAT12 provides several components optimized for morphometry, including an internal interpolation, affine preprocessing affine registration of bias-corrected images , partial volume segmentation, denoising, DARTEL normalization, local adaptive segmentation, skull-stripping, an adaptive maximum a posteriori AMAP segmentation, and a final clean-up.

We used the ABCD raw images as opposed to the preprocessed data supposedly optimized to be used with Freesurfer in order to avoid any interference with the CAT12 preprocessing pipeline.

In regions of interest analyses, we focused on the left parahippocampal gyrus, ventromedial prefrontal cortex, and right parietal cortex, regions that were identified from Li et al.

Girls showed higher BIS score than boys 7. In contrast, girls demonstrated lower BAS score than boys Further, replicating Li et al.

Background: The striatum is associated with goal-directed behaviors and has been mapped extensively in primate models.

One complex limbic-cognitive task for both human and nonhuman primates is living in social groups. We assessed the literature to determine striatal sites implicated in these functions in humans, and used Macaques to place retrograde tracer injections in each region.

Our goal was to assess the range and combinatorial profile of cortical inputs across striatal zones associated with social activity. Methods: Regions of interest were chosen from a meta-analysis of fMRI studies that assessed a variety of social behavior in the human Baez-Mendoza and Schultz, Following a 2-week survival period, animals were sacrificed, and the brains were prepared for visualization of tracer using immunocytochemical and histologic techniques.

In the current study we mapped retrogradely labeled cells in the prefrontal cortex, insula, and amygdala. A subset of these injection sites additionally resulted in high concentrations of labeled cells in the agranular, dysgranular, and in some cases posterior granular insula.

The latter sites also had many retrogradely labeled cells in the amygdala. In addition to these inputs, striatal regions in the caudal ventral striatum receive strong inputs from the insula, area 32, and the amygdala, regions implicated in many affiliative behavioral paradigms.

Together, these data suggest networks to the caudal ventral striatum that code for behavioral responses involving social stimuli.

However, the molecular mechanism underlying this process and the pathophysiological consequences that occur when it is disrupted during prenatal development remain unclear.

In this study, we investigated a potential protein-protein interaction between D1R and SynGAP, and its role in GABAergic interneuron migration and physiological consequences in the behaviors of adulthood.

Immunofluorescent staining was used to analyze the distribution of GABAergic interneurons at various developmental stages. Locomotor, pre-pulse inhibition, visual discrimination and social behaviors were assessed to determine whether the prenatal impairment of GABAergic interneuron migration caused behavioral deficits in adulthood.

Interestingly, disrupting this complex during embryonic development resulted in pronounced GABAergic interneuron tangential migration deficits, possibly due to altered actin and microtubule dynamics.

More importantly, administration of TAT-D1Rpep to pregnant mice led to abnormalities in locomotor activity, pre-pulse inhibition, sociability and visual discrimination in the offspring.

Conclusions: Our study discovered a novel protein-protein interaction between D1R and SynGAP, and this interaction plays a critical role in the prenatal GABAergic interneuron migration and development of important behaviors in adulthood.

Background: Methylphenidate has been used to treat patients with attention-deficit hyperactivity disorder ADHD since the s with significant effects on clinical symptoms and functional improvement.

The data on the neural substrates for brain activity changes after treatment with methylphenidate is limited.

These brain regions might play a role as biological markers for the treatment effectiveness of methylphenidate. One challenge in FXS treatment development is a lack of rigorous, synchronized outcome readouts across animal and human study.

We have developed across the mouse fmr1 KO and human FXS lab EEG evaluations that 1 present stimuli in a similar manner; 2 have EEG data processed using the same analysis methods across mouse and human study; and 3 show baseline results indicating a similar aberrant patterns of brain activity across mouse and human study.

Racemic baclofen has been extensively evaluated in the mouse model of FXS and racemic baclofen is readily available for immediate use in human FXS study.

Following surgical implantation at days and then two days to recover the mice underwent pre-dose 5 minutes of resting EEG followed by trains of the up chirp auditory entrainment paradigm.

For chronic daily dosing, the mice received the same baclofen dose daily for 2 weeks and then EEG paradigms were repeated after repeated dosing.

In humans, thirteen 15 to year olds years with full mutation received 30mg of oral racemic baclofen or matching placebo with a two week washout period between dosing days.

Prior to drug dosing the patients completed resting state and auditory chirp EEG paradigms consistent with the EEG work in the mice.

Four hours post-dose the humans repeated all EEG measures. In addition, the humans completed pre- and post-dose clinical measures including the Woodcock Johnson auditory attention subscale, the Repeatable Battery of Neuropsychiatric Status RBANS , the KiTap computer-based continuous performance testing, and eye tracking.

The reductions in gamma band power were consistent across left and right frontal, medial, and temporal brain regions. Following chronic daily baclofen dosing over 2 weeks, the changes in gamma band power remained consistent with the impact of single dosing.

Additionally, single and chronic baclofen treatment in the fmr1 KO mouse was associated with enhanced increased entrainment to a modulated up chirp auditory stimuli in the gamma region.

Single 30mg baclofen dosing was well tolerated in the human study without significant adverse effects noted. In 13 humans with FXS, single dose baclofen compared to placebo administration was associated with significant reduction in excessive gamma band brain activity in the resting condition.

Work continues to evaluate the impact of single dose baclofen in humans with FXS using the chirp auditory paradigm.

Additionally, work continues to evaluate potential correlations between gamma reduction and clinical change in the human subjects.

Chronic dosing studies are underway in the mouse as are lower dose baclofen studies. EEG may be useful in future baclofen study in FXS to profile which humans may best respond to this treatment while also working to show target engagement early during the treatment course.

Future work will evaluate potential clinical correlation between baclofen EEG impact and clinical measures.

Future work is additionally report on the impact of baclofen of other EEG measures including auditory evoked potentials and auditory entrainment paradigms.

Background: One in five teens suffer from major depression before they reach adulthood. Early identification of adolescents at risk for depression is critical to prevention efforts.

Adults with depression show smaller volumes of the amygdala, orbitofrontal cortex, anterior cingulate cortex, and hippocampus, yet larger volumes of the cerebellum and lateral ventricle.

Whether these neural features are present in adolescents with depression, or develop after its onset, is unclear.

The additive role of trauma and stress is also important to consider. We hypothesized that subsequently depressed compared to continuously healthy youth would exhibit smaller volumes of the orbitofrontal cortex, amygdala, anterior cingulate cortex, hippocampus, and basal ganglia, and that stress and trauma would exacerbate these effects.

Results: We identified 22 neuroimaging features and 1 metric reflecting childhood trauma that were most predictive of transitioning from a healthy to depressed state in adolescence, with a specificity of 0.

Thicknesses and volumes were found to be lesser in several of these brain regions in depressed subjects compared to non-depressed subjects after a transition from a non-depressed baseline, consistent with lesser brain maturation and supporting our hypothesis.

Conclusions: Generally smaller frontal and limbic structures, and greater childhood trauma predicted increased probability of transitioning into major depression in adolescence.

Results may point to neural systems that could be explored as targets of early prevention programs. Background: The role of the neuropeptide oxytocin in social cognition has attracted tremendous interest in social neuroscience.

Autism spectrum disorders ASD has been characterized by deficits in oxytocin function and the exogenous application of oxytocin has been shown to improve social symptoms in ASD.

However, little is known about the role of epigenetic variations of the oxytocin receptor gene OXTR in symptom severity and brain function in ASD.

The analysis was specifically conducted in the MT2 region of the OXTR gene given its direct relevance to transcription.

We also examined the associations between OXTR methylation and social responsiveness and resting-state functional connectivity rsFC between networks involved in social cognition and reward processing in ASD.

The data used in this study in relation to rsFC was collected as part of a larger clinical trial that is registered on clinicaltrials.

The rsFC data used in this study is only related to placebo intake. Higher methylation levels are associated with more ASD symptom severity.

Conclusions: These findings provide first evidence for the implication of OXTR methylation in ASD symptom severity particularly regarding social motivation, restricted interests and reward processing.

Future longitudinal studies can reveal whether these epigenetic modifications are genetically inherited or acquired through environmental exposures.

Background: Major depressive disorder MDD is the most prevalent mental disorder worldwide. Several stress animal models have been used to study the neurobiology of this disorder, including learned helplessness LH , in which susceptible animals show a failure to escape a noxious stimulus along with a downregulation of ventral tegmental area VTA dopamine DA system activity.

In LH, the prelimbic portion of the prefrontal cortex plPFC is known to regulate stress and anxiety, and as such plays an important role in the modulation of helpless behavior, but so far there is no evidence indicating that its developmental disruption alters susceptibility to this behavior.

The aim of this study was to investigate the impact of plPFC lesion, performed at adolescence or adulthood, on the susceptibility to helpless behavior and its corresponding effects on VTA DA system activity in rats.

Two days after, the rats were submitted to the LH model to evaluate helpless behavior. Conclusions: These data suggest that the disruption of plPFC activity during adolescence increases susceptibility to helpless behavior in adult rats.

Therefore, a predisposition or early life adverse events that impair plPFC activity may enhance susceptibility to depression in adulthood.

Background: Early life is a critical period in the development and refinement of the central nervous system. Experience during this early life period plays an important role in shaping the maturation of the brain.

Exposure to early life adversity is implicated in increased susceptibility to many neuropsychiatric disorders such as depression, anxiety and addiction.

These processes are themselves linked to dysfunction of neuromodulatory systems. In particular, the serotonergic neurons of the dorsal raphe nucleus DRN exert widespread and complex neuromodulatory effects that are necessary for fine-tuning neural circuit formation.

While it is known that serotonin regulates a wide range of brain functions and behavior, it is not clear how their circuits regulating serotonergic function are modulated by development and early-life experience.

Methods: Here, we used slice electrophysiology to characterize the maturation of synaptic inputs received by serotonergic and GABAergic neurons in the DRN from juvenile to adult developmental stages in mice.

To examine the consequences of early life stress, we also subjected mice to a limited bedding and nesting protocol from PND Results: We found that the strength of excitatory transmission increased over the course of the juvenile and adolescent period and were maintained through early adulthood.

We then used slice electrophysiology to assess the maturation of DRN synaptic inputs. Our results indicate a decrease in excitatory neurotransmission mean spontaneous excitatory postsynaptic current frequency ELS 1.

Conclusions: Our results demonstrate that adverse experience during early life can cause persistent alterations in the synaptic architecture of the DRN.

We anticipate that our findings will be a starting point to understand the impact of adverse experiences on synaptic maturation of the DRN and to highlight targets for novel treatments for stress-related disorders.

Background: Neurodevelopmental disorders, especially autism spectrum disorders, are associated with multiple etiological mechanisms and symptom presentations.

However, a core symptom across autism-spectrum disorders are repetitive locomotor behaviors. Autism is a highly genetic disorder, and a frequently associated genetic variant with autism is 16p In a mouse model of 16p We therefore questioned whether molecular dysfunction in the striatum in these animals may be a common mechanism leading to both simple repetitive behaviors or stereotypies, as well as more complex compulsive behaviors in reward-guided decision making tasks.

Methods: In male and female mice modelling 16p In our first cohort, we measured delay discounting to assess compulsive choice in reward guided decision making.

In our second cohort, we measured amphetamine-induced locomotor sensitization to assess striatal dopaminergic function and resulting behavioral hyperactivity.

Results: In delay discounting, 16p In contrast, wildtype males and females of both genotypes show strong discounting as delay lengths for a large reward increase.

This is despite similar levels of trials completed and overall motivation, suggesting that the flexible expression of changes in preference is impaired in 16p11 hemideletion males.

In amphetamine locomotor sensitization, wildtype mice increased their distance traveled, reflective of psychostimulant-induced hyperactivity, but this was suppressed in 16p Instead, 16p Conclusions: In a mouse model of an autism-associated genotype, repetitive and inflexible behavior patterns were elicited in response to behavioral challenges reward delay and pharmacological challenges amphetamine that were not seen in these mice at baseline.

Further, these two behaviors may result from a common molecular and circuit neurodevelopmental adaptations, possibly centered around dopamine release in the striatum.

Background: Adolescence is a critical period of development when symptoms of many psychiatric illnesses, including depression, anxiety, and behavioral disorders, first emerge Belfer ML, These nascent clinical symptoms frequently entail dysregulation of the reward system, manifestations of which include anhedonia i.

A growing body of literature indicates that the habenula Hb , a small nucleus bordering the dorsomedial thalamus, plays a critical regulatory role by inhibiting dopaminergic reward signaling Boulos LJ et al, In animal models, Hb stimulation induces depressive phenotypes, whereas Hb inhibition and lesions result in impulsive behaviors Proulx CD et al, Despite these promising preclinical findings, the human Hb remains poorly understood due to its small size, which makes it difficult to study with traditional fMRI approaches.

Nevertheless, high-resolution fMRI work by our group and others has reported altered Hb responses to aversive task outcomes Lawson RP et al, and resting-state functional connectivity patterns Ely BA et al, in people with depressive symptoms.

Building on our recent study mapping whole-brain Hb connectivity in healthy young adults using optimized Hb seeds and neuroanatomically accurate cortical surface-based analysis Ely BA et al, , we examined Hb connectivity and its association with psychiatric symptomatology in adolescents.

Correlations with symptom scales were controlled for the other two scales. However, the full adolescent cohort and each major clinical subset i.

The unthresholded contrast of clinical over healthy control adolescents further underscored this pattern, revealing elevated Hb connectivity throughout the entire cortical default mode network as well as associated subcortical areas.

Moreover, Hb connectivity with these default mode areas showed a highly specific positive correlation with anxiety scores in the full adolescent cohort, whereas stronger Hb connectivity with the salience network and early sensory cortex was associated with higher anhedonia severity; Hb connectivity was minimally correlated with overall depression severity.

These findings also strongly support the feasibility of our approach for studying the human Hb in clinical populations, reproducing all of the major Hb connectivity features we reported using high-quality fMRI data from the HCP Ely BA et al, in an independent sample of mixed clinical and healthy subjects scanned under typical laboratory conditions.

Background: Sensorimotor disturbances are common features of autism spectrum disorder ASD and they are present in some unaffected first-degree relatives.

Family studies assessing the extent to which different clinical issues are present in unaffected biological parents hold promise for clarifying trait dimensions that track with distinct pathophysiological processes.

Two sensorimotor behaviors implicated in ASD were examined: ballistic eye movements reflective of feedforward motor processes and visually guided precision gripping behavior dependent upon sensory feedback processes.

Methods: Forty family trios were studied. Participants completed visually guided saccade and precision gripping tasks.

During the precision gripping test, participants pressed with their thumb and index finger on separate load cells while viewing a white FORCE bar on a screen that moved upwards with increased force toward a fixed green TARGET bar.

For both tests, the accuracy and variability of motor output were examined. No differences in trial-to-trial variability of saccade accuracy were found between ASD parents and parent controls.

Conclusions: Sensorimotor alterations were seen in ASD probands and their parents relative to healthy controls. Flüge Ferienwohnungen Restaurants Aktivitäten.

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