Journal articles: 'Neural controls'

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Palmieri, Arianna, Federica Meconi, Antonino Vallesi, Mariagrazia Capizzi, Emanuele Pick, Sonia Marcato, Johann R. Kleinbub, Gianni Sorarù, and Paola Sessa. "Enhanced Neural Empathic Responses in Patients with Spino-Bulbar Muscular Atrophy: An Electrophysiological Study." Brain Sciences 11, no. 1 (December 24, 2020): 16. http://dx.doi.org/10.3390/brainsci11010016.

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Background: Spino-bulbar muscular atrophy is a rare genetic X-linked disease caused by testosterone insensitivity. An inverse correlation has been described between testosterone levels and empathic responses. The present study explored the profile of neural empathic responding in spino-bulbar muscular atrophy patients. Methods: Eighteen patients with spino-bulbar muscular atrophy and eighteen healthy male controls were enrolled in the study. Their event-related potentials were recorded during an “Empathy Task” designed to distinguish neural responses linked with experience-sharing (early response) and mentalizing (late response) components of empathy. The task involved the presentation of contextual information (painful vs. neutral sentences) and facial expressions (painful vs. neutral). An explicit dispositional empathy-related questionnaire was also administered to all participants, who were screened via neuropsychological battery tests that did not reveal potential cognitive deficits. Due to electrophysiological artefacts, data from 12 patients and 17 controls were finally included in the analyses. Results: Although patients and controls did not differ in terms of dispositional, explicit empathic self-ratings, notably conservative event-related potentials analyses (i.e., spatio-temporal permutation cluster analyses) showed a significantly greater experience-sharing neural response in patients compared to healthy controls in the Empathy-task when both contextual information and facial expressions were painful. Conclusion: The present study contributes to the characterization of the psychological profile of patients with spino-bulbar muscular atrophy, highlighting the peculiarities in enhanced neural responses underlying empathic reactions.

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PHILLIPS, M. L., I. M. MARKS, C. SENIOR, D. LYTHGOE, A. M. O'DWYER, O. MEEHAN, S. C. R. WILLIAMS, M. J. BRAMMER, E. T. BULLMORE, and P. K. McGUIRE. "A differential neural response in obsessive–compulsive disorder patients with washing compared with checking symptoms to disgust." Psychological Medicine 30, no. 5 (September 2000): 1037–50. http://dx.doi.org/10.1017/s0033291799002652.

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Background. Patients with obsessive–compulsive disorder (OCD) have symptoms that pre-dominantly concern washing (washers) or checking (checkers), or both. Functional neuroimaging has been used to identify the neural correlates of the urge to ritualize but has not distinguished between washing and checking symptoms in OCD. We used functional magnetic resonance imaging to compare the neural response to emotive pictures in washers and checkers.Methods. In one of two 5-minute experiments, washers (N = 7), checkers (N = 7) and age-matched normal controls (N = 14) were scanned while viewing alternating blocks of normally disgusting (rated as disgusting by all subjects) and neutral pictures. In the other experiment, all patients and a normal subgroup (N = 8) viewed alternating blocks of washer-relevant (rated as more disgusting by washers than normal controls or checkers) and neutral pictures.Results. In all subjects, normally disgusting pictures activated visual regions implicated in perception of aversive stimuli and the insula, important in disgust perception. Only in washers were similar regions activated by washer-relevant pictures. In checkers, these pictures activated fronto-striatal regions associated with the urge to ritualize in OCD. Normal controls were more similar in neural response to checkers than washers to these pictures. Both normal controls and checkers had frontal regions activated significantly more by washer-relevant than normally disgusting pictures, and had these regions activated significantly more than washers by washer-relevant pictures.Conclusions. We demonstrate a differential neural response to washer-relevant disgust in washers and checkers: only washers demonstrate a neural response to washer-relevant disgust associated with emotion perception rather than attention to non-emotive visual detail.

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Moran, Timothy H., and Ellen E. Ladenheim. "Physiologic and Neural Controls of Eating." Gastroenterology Clinics of North America 45, no. 4 (December 2016): 581–99. http://dx.doi.org/10.1016/j.gtc.2016.07.009.

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Thomas, E. J., R. Elliott, S. McKie, D. Arnone, D. Downey, G. Juhasz, J. F. W. Deakin, and I. M. Anderson. "Interaction between a history of depression and rumination on neural response to emotional faces." Psychological Medicine 41, no. 9 (February 9, 2011): 1845–55. http://dx.doi.org/10.1017/s0033291711000043.

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BackgroundBoth past depressive episodes and the personality trait of depressive rumination are strong risk factors for future depression. Depression is associated with abnormal emotional processing, which may be a neurobiological marker for vulnerability to depression. A consistent picture has yet to emerge as to how a history of depression and the tendency to ruminate influence emotional processing. The aim of this study was to investigate the relationship between rumination, past depression and neural responses when processing face emotions.MethodThe Ruminative Responses Scale (RRS) was completed by 30 remitted depressives and 37 controls who underwent functional magnetic resonance imaging (fMRI) scanning while viewing happy, sad, fearful and neutral faces.ResultsThe remitted depressives showed overall reductions in neural responses to negative emotions relative to the controls. However, in the remitted depressives, but not the controls, RRS scores were correlated with increased neural responses to negative emotions and decreased responses to happiness in limbic regions.ConclusionsAutomatic emotion processing biases and rumination seem to be correlated to aspects of vulnerability to depression. However, remission from depression may be maintained by a general suppression of limbic responsiveness to negative emotion.

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Schiefer, C., F. X. Rubenzucker, H. P. Jorgl, and H. R. Aberl. "A neural network controls the galvannealing process." IEEE Transactions on Industry Applications 35, no. 1 (1999): 114–18. http://dx.doi.org/10.1109/28.740854.

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Horan, W. P., G. Hajcak, J. K. Wynn, and M. F. Green. "Impaired emotion regulation in schizophrenia: evidence from event-related potentials." Psychological Medicine 43, no. 11 (January 28, 2013): 2377–91. http://dx.doi.org/10.1017/s0033291713000019.

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BackgroundAlthough several aspects of emotion seem to be intact in schizophrenia, there is emerging evidence that patients show an impaired ability to adaptively regulate their emotions. This event-related potential (ERP) study examined whether schizophrenia is associated with impaired neural responses to appraisal frames, that is when negative stimuli are presented in a less negative context.MethodThirty-one schizophrenia out-patients and 27 healthy controls completed a validated picture-viewing task with three conditions: (1) neutral pictures preceded by neutral descriptions (‘Neutral’), (2) unpleasant pictures preceded by negative descriptions (‘Preappraised negative’), and (3) unpleasant pictures preceded by more neutral descriptions (‘Preappraised neutral’). Analyses focused on the late positive potential (LPP), an index of facilitated attention to emotional stimuli that is reduced following cognitive emotion regulation strategies, during four time windows from 300 to 2000 ms post-picture onset.ResultsReplicating prior studies, controls showed smaller LPP in Preappraised neutral and Neutral versus Preappraised negative conditions throughout the 300–2000-ms time period. By contrast, patients showed (a) larger LPP in Preappraised neutral and Preappraised negative versus Neutral conditions in the initial period (300–600 ms) and (b) an atypical pattern of larger LPP to Preappraised neutral versus Preappraised negative and Neutral conditions in the 600–1500-ms epochs.ConclusionsModulation of neural responses by a cognitive emotion regulation strategy seems to be impaired in schizophrenia during the first 2 s after exposure to unpleasant stimuli.

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Prajapati, Ravindra S., Mark Hintze, and Andrea Streit. "PRDM1 controls the sequential activation of neural, neural crest and sensory progenitor determinants." Development 146, no. 24 (December 5, 2019): dev181107. http://dx.doi.org/10.1242/dev.181107.

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Tada, S., T. Yasui, T. Okuno, Y. Nakatsuji, H. Mochizuki, S. Sakoda, and H. Kikutani. "BAFF controls neural cell survival through BAFF receptor." Journal of the Neurological Sciences 333 (October 2013): e689. http://dx.doi.org/10.1016/j.jns.2013.07.2380.

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Krauss, Patrick, Marc Schuster, Verena Dietrich, Achim Schilling, Holger Schulze, and Claus Metzner. "Weight statistics controls dynamics in recurrent neural networks." PLOS ONE 14, no. 4 (April 9, 2019): e0214541. http://dx.doi.org/10.1371/journal.pone.0214541.

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Fortin, D. L. "Neural Activity Controls the Synaptic Accumulation of -Synuclein." Journal of Neuroscience 25, no. 47 (November 23, 2005): 10913–21. http://dx.doi.org/10.1523/jneurosci.2922-05.2005.

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Kuriyama, Shigeru, Yoshimi Kurihara, Yusuke Irino, and Toyohisa Kaneko. "Physiological gait controls with a neural pattern generator." Journal of Visualization and Computer Animation 13, no. 2 (2002): 107–19. http://dx.doi.org/10.1002/vis.284.

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Tada, Satoru, Teruhito Yasui, Yuji Nakatsuji, Tatsusada Okuno, Toru Koda, Hideki Mochizuki, Saburo Sakoda, and Hitoshi Kikutani. "BAFF Controls Neural Cell Survival through BAFF Receptor." PLoS ONE 8, no. 7 (July 29, 2013): e70924. http://dx.doi.org/10.1371/journal.pone.0070924.

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Peever, John, and Patrick M. Fuller. "Neuroscience: A Distributed Neural Network Controls REM Sleep." Current Biology 26, no. 1 (January 2016): R34—R35. http://dx.doi.org/10.1016/j.cub.2015.11.011.

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Cuervo-Lombard, Christine, Cédric Lemogne, Fabien Gierski, Céline Béra-Potelle, Eric Tran, Christophe Portefaix, Arthur Kaladjian, Laurent Pierot, and Frédéric Limosin. "Neural basis of autobiographical memory retrieval in schizophrenia." British Journal of Psychiatry 201, no. 6 (December 2012): 473–80. http://dx.doi.org/10.1192/bjp.bp.111.099820.

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BackgroundAutobiographical memory retrieval is impaired in schizophrenia.AimsTo determine the neural basis of this impairment.MethodThirteen patients with schizophrenia and 14 healthy controls performed an autobiographical memory retrieval task based on cue words during functional magnetic resonance imaging. Patients were selected on the basis of their ability to perform the task and all participants received training.ResultsAlthough patients and controls activated a similar brain network during autobiographical memory retrieval, patients displayed decreased activation in several of these regions, including the anterior cingulate cortex, left lateral prefrontal cortex, right cerebellum and ventral tegmental area (k ≥ 10, P < 0.001, uncorrected). In addition, activation of the caudate nuclei was negatively correlated with retrieval performance in controls but positively correlated with performance in patients.ConclusionsThe autobiographical memory retrieval brain network is impaired in schizophrenia. Patients with schizophrenia display decreased activation of the cognitive control network during retrieval, possibly due to aberrant functioning of the dorsal striatum.

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Wang, Lihong, Ying-Hui Chou, Guy G. Potter, and David C. Steffens. "Altered Synchronizations among Neural Networks in Geriatric Depression." BioMed Research International 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/343720.

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Although major depression has been considered as a manifestation of discoordinated activity between affective and cognitive neural networks, only a few studies have examined the relationships among neural networks directly. Because of the known disconnection theory, geriatric depression could be a useful model in studying the interactions among different networks. In the present study, using independent component analysis to identify intrinsically connected neural networks, we investigated the alterations in synchronizations among neural networks in geriatric depression to better understand the underlying neural mechanisms. Resting-state fMRI data was collected from thirty-two patients with geriatric depression and thirty-two age-matched never-depressed controls. We compared the resting-state activities between the two groups in the default-mode, central executive, attention, salience, and affective networks as well as correlations among these networks. The depression group showed stronger activity than the controls in an affective network, specifically within the orbitofrontal region. However, unlike the never-depressed controls, geriatric depression group lacked synchronized/antisynchronized activity between the affective network and the other networks. Those depressed patients with lower executive function has greater synchronization between the salience network with the executive and affective networks. Our results demonstrate the effectiveness of the between-network analyses in examining neural models for geriatric depression.

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Hilbert, Kevin, Ricarda Evens, Nina Isabel Maslowski, Hans-Ulrich Wittchen, and Ulrike Lueken. "Fear Processing in Dental Phobia during Crossmodal Symptom Provocation: An fMRI Study." BioMed Research International 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/196353.

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While previous studies successfully identified the core neural substrates of the animal subtype of specific phobia, only few and inconsistent research is available for dental phobia. These findings might partly relate to the fact that, typically, visual stimuli were employed. The current study aimed to investigate the influence of stimulus modality on neural fear processing in dental phobia. Thirteen dental phobics (DP) and thirteen healthy controls (HC) attended a block-design functional magnetic resonance imaging (fMRI) symptom provocation paradigm encompassing both visual and auditory stimuli. Drill sounds and matched neutral sinus tones served as auditory stimuli and dentist scenes and matched neutral videos as visual stimuli. Group comparisons showed increased activation in the insula, anterior cingulate cortex, orbitofrontal cortex, and thalamus in DP compared to HC during auditory but not visual stimulation. On the contrary, no differential autonomic reactions were observed in DP. Present results are largely comparable to brain areas identified in animal phobia, but also point towards a potential downregulation of autonomic outflow by neural fear circuits in this disorder. Findings enlarge our knowledge about neural correlates of dental phobia and may help to understand the neural underpinnings of the clinical and physiological characteristics of the disorder.

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Lakis, Nadia, and Adrianna Mendrek. "Individuals Diagnosed with Schizophrenia Assign Emotional Importance to Neutral Stimuli: An fMRI Study." ISRN Psychiatry 2013 (December 5, 2013): 1–7. http://dx.doi.org/10.1155/2013/965428.

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The majority of functional neuroimaging studies investigating neural correlates of emotion processing in schizophrenia report a significant deficit in limbic structures activation in patients relative to control participants. Recently it has been suggested that this apparent “deficit” could be due to an enhanced sensitivity of the neutral material in individuals diagnosed with schizophrenia, rather than due to their inefficiency in emotion processing. The purpose of the present study was to test this supposition and verify if the potential effect is present in both men and women diagnosed with schizophrenia. In order to do that we examined the pattern of cerebral activation associated with processing of neutral stimuli in schizophrenia. Thirty-seven schizophrenia patients and 37 healthy controls viewed neutral and emotional images while in a functional magnetic resonance imaging scanner. Schizophrenia patients rated the neutral images as more emotionally salient than controls. Additionally, patients showed significant activation during processing of neutral images in limbic and prefrontal regions; similar areas were underactivated in patients relative to controls during processing of emotional information. Investigation of sex differences revealed that the enhanced responsiveness to the emotionally neutral material was attributed primarily to men with schizophrenia.

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McCarthy, Hazel, Jessica Stanley, Richard Piech, Norbert Skokauskas, Aisling Mulligan, Gary Donohoe, Diane Mullins, et al. "Childhood-Diagnosed ADHD, Symptom Progression, and Reversal Learning in Adulthood." Journal of Attention Disorders 22, no. 6 (August 9, 2016): 561–70. http://dx.doi.org/10.1177/1087054716661233.

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Objective: ADHD persists in up to 60% into adulthood, and the reasons for persistence are not fully understood. The objective of this study was to characterize the neurofunctional basis of decision making in those with a childhood diagnosis of ADHD with either persistent or remitted symptoms in adulthood versus healthy control participants. Method: Thirty-two adults diagnosed with ADHD as children were split into persistent ( n = 18) or remitted ( n = 14) ADHD groups. Their neural activity and neurofunctional connectivity during a probabilistic reversal learning task were compared with 32 healthy controls. Results: Remitters showed significantly higher neural connectivity in final reversal error and probabilistic error conditions, and persisters depict higher neural connectivity in reversal errors than controls at a family-wise error (FWE) corrected whole-brain corrected threshold. Conclusion: Remitters may have utilized higher neural connectivity than controls to make successful decisions. Also, remitters may have utilized compensatory strategies to override any potential underlying ADHD deficits.

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Mitterschiffthaler, M. T., S. C. R. Williams, N. D. Walsh, A. J. Cleare, C. Donaldson, J. Scott, and C. H. Y. Fu. "Neural basis of the emotional Stroop interference effect in major depression." Psychological Medicine 38, no. 2 (September 10, 2007): 247–56. http://dx.doi.org/10.1017/s0033291707001523.

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BackgroundA mood-congruent sensitivity towards negative stimuli has been associated with development and maintenance of major depressive disorder (MDD). The emotional Stroop task assesses interference effects arising from the conflict of emotional expressions consistent with disorder-specific self-schemata and cognitive colour-naming instructions. Functional neuroimaging studies of the emotional Stroop effect advocate a critical involvement of the anterior cingulate cortex (ACC) during these processes.MethodSubjects were 17 medication-free individuals with unipolar MDD in an acute depressive episode (mean age 39 years), and 17 age-, gender- and IQ-matched healthy volunteers. In an emotional Stroop task, sad and neutral words were presented in various colours, and subjects were required to name the colour of words whilst undergoing functional magnetic resonance imaging (fMRI). Overt verbal responses were acquired with a clustered fMRI acquisition sequence.ResultsIndividuals with depression showed greater increases in response time from neutral to sad words relative to controls. fMRI data showed a significant engagement of left rostral ACC (BA 32) and right precuneus during sad words in patients relative to controls. Additionally, rostral ACC activation was positively correlated with latencies of negative words in MDD patients. Healthy controls did not have any regions of increased activation compared to MDD patients.ConclusionsThese findings provide evidence for a behavioural and neural emotional Stroop effect in MDD and highlight the importance of the ACC during monitoring of conflicting cognitive processes and mood-congruent processing in depression.

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Shahzad, Nadeem, Afshan Riaz, Uzma Ameer, and Daniyal Nadeem. "NEURAL TUBE DEFECTS (NTDS);." Professional Medical Journal 24, no. 12 (November 29, 2017): 1878–83. http://dx.doi.org/10.29309/tpmj/2017.24.12.573.

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Background: The most common congenital malformations are Neural tubedefects (NTDs) occurring in 0.6 per 1,000 live births in the United States, and almost 4000pregnancies are recorded of babies with neural tube defects, among them anencephalyand Spina bifida are the most common and their annual incidence is 2,500 to 3,000 births inthe United States. The etiology of NTDs is still an enigma, however, in the past few decadesvaluable advances has been made in understanding the causation and measures to preventNTDs and many risk factors are indentified which are associated with it. Objectives: This studywas designed to determine the risk factors and their association with neural tube defects. StudyDesign: Case control study. Place and Duration of Study: This study was conducted at unit111 Lady Willingdon Hospital Lahore and duration was one year from 1.1.2016 to 31.12.2016.Methodology: A total of 120 mothers were included in the study, of which 30 were having ofbabies delivered with NTDs, matched with 90 mothers delivered babies without NTDs (Threecontrols for each NTD case). Informations were collected on special Performa, data was analyzedon SPSS version 20. Results: Majority of the patients in both groups were found between 31-40 years of age, 43.33 %( n13) in patients with NTD group and 56.67 %( n51) in controls whileonly 16.67% (n5) in NTD and 17.78 % (n16) were found between 21-30 years. The mean agewas recorded as 33.06+1.21 and 32.12+ 0.89 respectively. Regarding parity, 23.33% (n7) werefound between P1-2, 26.67% (n11) were P2-3 while 40% (n12) with Parity >4 in the NTD group,while 21.11% (n19) were p1-2, 37.77% (n 34) with P 3-4 and 41.12% (n37) were P >4 in controlgroup. 86.67% (n 26) were found with poor economic status and 13.33% (n4) were found withrich status in NTDs, while 18.89% (n17) were found with poor and 81.11% (n73) with rich statusin control group. Distribution of fetuses according to their gender revealed that 20% (n6) weremales, and 80% (n24) were females in NTDs while 47.77 %( n43) were found males and 52.23%(n47) were females in controls. Regarding family history 80% (n24) with positive history of NTDsin patients of NTD group and 20% (n6) with no history while 4.44% (n4) had positive history and95.56% (n86) had no familial history of NTD in control cases. About previous history of NTDs,93.33% (n28) were found with positive previous history of NTDs and only 6.67% (n2)with noprevious history of NTDs in NTD group, while only 5.56% (n5) were found with positive previoushistory of NTDs and 94.44%(n85) with no previous history in controls. Conclusions: Poor socioeconomic status, family history and previous history of a baby with Neural tube defects are themajor risk factors.

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Banack, Sandra Anne, Rachael Anne Dunlop, and Paul Alan Cox. "An miRNA fingerprint using neural-enriched extracellular vesicles from blood plasma: towards a biomarker for amyotrophic lateral sclerosis/motor neuron disease." Open Biology 10, no. 6 (June 2020): 200116. http://dx.doi.org/10.1098/rsob.200116.

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Biomarkers for amyotrophic lateral sclerosis/motor neuron disease (ALS/MND) are currently not clinically available for disease diagnosis or analysis of disease progression. If identified, biomarkers could improve patient outcomes by enabling early intervention and assist in the determination of treatment efficacy. We hypothesized that neural-enriched extracellular vesicles could provide microRNA (miRNA) fingerprints with unequivocal signatures of neurodegeneration. Using blood plasma from ALS/MND patients and controls, we extracted neural-enriched extracellular vesicle fractions and conducted next-generation sequencing and qPCR of miRNA components of the transcriptome. We here report eight miRNA sequences which significantly distinguish ALS/MND patients from controls in a replicated experiment using a second cohort of patients and controls. miRNA sequences from patient blood samples using neural-enriched extracellular vesicles may yield unique insights into mechanisms of neurodegeneration and assist in early diagnosis of ALS/MND.

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Zhao, Zheng-Dong, Wen Z. Yang, Cuicui Gao, Xin Fu, Wen Zhang, Qian Zhou, Wanpeng Chen, et al. "A hypothalamic circuit that controls body temperature." Proceedings of the National Academy of Sciences 114, no. 8 (January 4, 2017): 2042–47. http://dx.doi.org/10.1073/pnas.1616255114.

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The homeostatic control of body temperature is essential for survival in mammals and is known to be regulated in part by temperature-sensitive neurons in the hypothalamus. However, the specific neural pathways and corresponding neural populations have not been fully elucidated. To identify these pathways, we used cFos staining to identify neurons that are activated by a thermal challenge and found induced expression in subsets of neurons within the ventral part of the lateral preoptic nucleus (vLPO) and the dorsal part of the dorsomedial hypothalamus (DMD). Activation of GABAergic neurons in the vLPO using optogenetics reduced body temperature, along with a decrease in physical activity. Optogenetic inhibition of these neurons resulted in fever-level hyperthermia. These GABAergic neurons project from the vLPO to the DMD and optogenetic stimulation of the nerve terminals in the DMD also reduced body temperature and activity. Electrophysiological recording revealed that the vLPO GABAergic neurons suppressed neural activity in DMD neurons, and fiber photometry of calcium transients revealed that DMD neurons were activated by cold. Accordingly, activation of DMD neurons using designer receptors exclusively activated by designer drugs (DREADDs) or optogenetics increased body temperature with a strong increase in energy expenditure and activity. Finally, optogenetic inhibition of DMD neurons triggered hypothermia, similar to stimulation of the GABAergic neurons in the vLPO. Thus, vLPO GABAergic neurons suppressed the thermogenic effect of DMD neurons. In aggregate, our data identify vLPO→DMD neural pathways that reduce core temperature in response to a thermal challenge, and we show that outputs from the DMD can induce activity-induced thermogenesis.

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Luria, Victor. "Genetic noise controls binary decisions in neural circuit assembly." Developmental Biology 331, no. 2 (July 2009): 473–74. http://dx.doi.org/10.1016/j.ydbio.2009.05.326.

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Li, Song, and Hongyan Wang. "An Intrinsic Mechanism Controls Reactivation of Neural Stem Cells." Mechanisms of Development 145 (July 2017): S22. http://dx.doi.org/10.1016/j.mod.2017.04.590.

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Chapnik, Elik, Vered Sasson, Robert Blelloch, and Eran Hornstein. "Dgcr8 controls neural crest cells survival in cardiovascular development." Developmental Biology 362, no. 1 (February 2012): 50–56. http://dx.doi.org/10.1016/j.ydbio.2011.11.008.

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Nishimura, I., J. Y. Sakoda, and K. Yoshikawa. "Drosophila MAGE controls neural precursor proliferation in postembryonic neurogenesis." Neuroscience 154, no. 2 (June 2008): 572–81. http://dx.doi.org/10.1016/j.neuroscience.2008.03.075.

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Li, Xin, Ted Erclik, Claire Bertet, Zhenqing Chen, Roumen Voutev, Srinidhi Venkatesh, Javier Morante, Arzu Celik, and Claude Desplan. "Temporal patterning of Drosophila medulla neuroblasts controls neural fates." Nature 498, no. 7455 (June 2013): 456–62. http://dx.doi.org/10.1038/nature12319.

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Shi, J., C. Severson, J. Yang, D. Wedlich, and M. W. Klymkowsky. "Snail2 controls mesodermal BMP/Wnt induction of neural crest." Development 138, no. 15 (June 29, 2011): 3135–45. http://dx.doi.org/10.1242/dev.064394.

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Zengqi, Sun, and Deng Zhidong. "A fuzzy neural network and its application to controls." Artificial Intelligence in Engineering 10, no. 4 (November 1996): 311–15. http://dx.doi.org/10.1016/0954-1810(96)00011-8.

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Shi, Lei, and Xing Cheng Wang. "The Application of Neural Network in Nonlinear System." Advanced Materials Research 179-180 (January 2011): 128–34. http://dx.doi.org/10.4028/www.scientific.net/amr.179-180.128.

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Neural network theory is widely applied to predictive control system because of its superiority in dealing with nonlinearities therein. Meanwhile, various algorithms for neural network predictive control have been put forward..The paper investigates the application of neural network-based control in nonlinear system. Especially, some current important nerual network-based controls are remarked and the developments are prospected.

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Azambuja, Ana Paula, and Marcos Simoes-Costa. "A regulatory sub-circuit downstream of Wnt signaling controls developmental transitions in neural crest formation." PLOS Genetics 17, no. 1 (January 19, 2021): e1009296. http://dx.doi.org/10.1371/journal.pgen.1009296.

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The process of cell fate commitment involves sequential changes in the gene expression profiles of embryonic progenitors. This is exemplified in the development of the neural crest, a migratory stem cell population derived from the ectoderm of vertebrate embryos. During neural crest formation, cells transition through distinct transcriptional states in a stepwise manner. The mechanisms underpinning these shifts in cell identity are still poorly understood. Here we employ enhancer analysis to identify a genetic sub-circuit that controls developmental transitions in the nascent neural crest. This sub-circuit links Wnt target genes in an incoherent feedforward loop that controls the sequential activation of genes in the neural crest lineage. By examining the cis-regulatory apparatus of Wnt effector gene AXUD1, we found that multipotency factor SP5 directly promotes neural plate border identity, while inhibiting premature expression of specification genes. Our results highlight the importance of repressive interactions in the neural crest gene regulatory network and illustrate how genes activated by the same upstream signal become temporally segregated during progressive fate restriction.

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Walther, S., A. Federspiel, T. Bracht, H. Horn, N. Razavi, W. Strik, and T. J. Müller. "Neural correlates of disturbed motor behavior in schizophrenia." European Psychiatry 26, S2 (March 2011): 1527. http://dx.doi.org/10.1016/s0924-9338(11)73231-x.

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IntroductionMotor behavior is altered in schizophrenia. Most patients have less physical activity than the general population. We have shown that actigraphic means of motor activity are influenced by negative syndrome scores, schizophrenia subtype and antipsychotic use.ObjectivesThe neural correlates of reduced motor activity in schizophrenia are widely unknown.AimsTo elucidate possible mechanisms, we correlated objective motor activity with measures of grey and white matter structure, as well as resting state perfusion.MethodsWe report the results of four studies from our lab. Schizophrenia patients and controls were scanned using a 3 T MRI scanner assessing resting perfusion (arterial spin labeling), structure and diffusion tensor imaging. In all participants, continuous actigraphy was performed for 24 hours in order to measure motor activity.ResultsResting perfusion in schizophrenia correlated with activity in bilateral prefrontal areas in patients, while in controls correlations were exclusively in the ventral anterior nucleus of the thalamus. In both groups, white matter integritiy in various frontal regions and the corticospinal tract correlated with motor activity. The group difference, however, was the inverse correlation of integrity and activity underneath the right supplemental motor area in patients. Grey matter volume did not correlate with activity in controls, but it did correlate in the posterior cingulate in patients.ConclusionsInterindividual differences in brain structure and perfusion are associated with varying motor activity. Multiple imaging approaches point to altered cortical motor control in schizophrenia.

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Wesley, Michael J., Terry Lohrenz, Mikhail N. Koffarnus, Samuel M. McClure, Richard De La Garza, Ramiro Salas, Daisy G. Y. Thompson-Lake, Thomas F. Newton, Warren K. Bickel, and P. Read Montague. "Choosing Money over Drugs: The Neural Underpinnings of Difficult Choice in Chronic Cocaine Users." Journal of Addiction 2014 (2014): 1–14. http://dx.doi.org/10.1155/2014/189853.

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Addiction is considered a disorder that drives individuals to choose drugs at the expense of healthier alternatives. However, chronic cocaine users (CCUs) who meet addiction criteria retain the ability to choose money in the presence of the opportunity to choose cocaine. The neural mechanisms that differentiate CCUs from non-cocaine using controls (Controls) while executing these preferred choices remain unknown. Thus, therapeutic strategies aimed at shifting preferences towards healthier alternatives remain somewhat uninformed. This study used BOLD neuroimaging to examine brain activity as fifty CCUs and Controls performed single- and cross-commodity intertemporal choice tasks for money and/or cocaine. Behavioral analyses revealed preferences for each commodity type. Imaging analyses revealed the brain activity that differentiated CCUs from Controls while choosing money over cocaine. We observed that CCUs devalued future commodities more than Controls. Choices for money as opposed to cocaine correlated with greater activity in dorsal striatum of CCUs, compared to Controls. In addition, choices for future money as opposed to immediate cocaine engaged the left dorsolateral prefrontal cortex (DLPFC) of CCUs more than Controls. These data suggest that the ability of CCUs to execute choices away from cocaine relies on activity in the dorsal striatum and left DLPFC.

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Fett, Anne-Kathrin J., Elias Mouchlianitis, Paula M. Gromann, Lucy Vanes, Sukhi S. Shergill, and Lydia Krabbendam. "The neural mechanisms of social reward in early psychosis." Social Cognitive and Affective Neuroscience 14, no. 8 (August 2019): 861–70. http://dx.doi.org/10.1093/scan/nsz058.

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Abstract In chronic psychosis, reduced trust is associated with a neural insensitivity to social reward and reduced theory of mind (ToM). Here we investigate whether these mechanisms could underlie emerging social impairments in early psychosis. Twenty-two participants with early psychosis and 25 controls (male, 13–19 years) participated in two interactive trust games against a cooperative and unfair partner. Region of interest neuroimaging analyses included right caudate, medial prefrontal cortex (mPFC) and right temporoparietal junction (rTPJ), involved in reward and ToM processing. Both groups showed similar levels of trust (i.e. investments). However, individuals with psychosis failed to activate the caudate differentially in response to cooperation and unfairness while making decisions to trust. During cooperative returns, patients showed reduced and controls increased caudate activation. Patients demonstrated greater rTPJ activation than controls, possibly pointing towards compensatory mechanisms. Effects were associated with Wechsler Abbreviated Scale of Intelligence vocabulary scores. No group differences emerged in mPFC activation. Early psychosis is associated with an aberrant neural sensitivity to social reward. This could foster reduced social motivation and social isolation. Absent behavioural differences in early, relative to chronic psychosis could indicate that trust is achieved through increased compensatory demand on ToM.

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Piggins, Hugh D., and Clare Guilding. "The neural circadian system of mammals." Essays in Biochemistry 49 (June 30, 2011): 1–17. http://dx.doi.org/10.1042/bse0490001.

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Humans and other mammals exhibit a remarkable array of cyclical changes in physiology and behaviour. These are often synchronized to the changing environmental light–dark cycle and persist in constant conditions. Such circadian rhythms are controlled by an endogenous clock, located in the suprachiasmatic nuclei of the hypothalamus. This structure and its cells have unique properties, and some of these are reviewed to highlight how this central clock controls and sculpts our daily activities.

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Aotani, Daisuke, Ken Ebihara, Nobukatsu Sawamoto, Toru Kusakabe, Megumi Aizawa-Abe, Sachiko Kataoka, Takeru Sakai, et al. "Functional Magnetic Resonance Imaging Analysis of Food-Related Brain Activity in Patients with Lipodystrophy Undergoing Leptin Replacement Therapy." Journal of Clinical Endocrinology & Metabolism 97, no. 10 (October 1, 2012): 3663–71. http://dx.doi.org/10.1210/jc.2012-1872.

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Abstract Context: Lipodystrophy is a disease characterized by a paucity of adipose tissue and low circulating concentrations of adipocyte-derived leptin. Leptin-replacement therapy improves eating and metabolic disorders in patients with lipodystrophy. Objective: The aim of the study was to clarify the pathogenic mechanism of eating disorders in lipodystrophic patients and the action mechanism of leptin on appetite regulation. Subjects and Interventions: We investigated food-related neural activity using functional magnetic resonance imaging in lipodystrophic patients with or without leptin replacement therapy and in healthy controls. We also measured the subjective feelings of appetite. Results: Although there was little difference in the enhancement of neural activity by food stimuli between patients and controls under fasting, postprandial suppression of neural activity was insufficient in many regions of interest including amygdala, insula, nucleus accumbens, caudate, putamen, and globus pallidus in patients when compared with controls. Leptin treatment effectively suppressed postprandial neural activity in many of these regions of interest, whereas it showed little effect under fasting in patients. Consistent with these results, postprandial formation of satiety feeling was insufficient in patients when compared with controls, which was effectively reinforced by leptin treatment. Conclusions: This study demonstrated the insufficiency of postprandial suppression of food-related neural activity and formation of satiety feeling in lipodystrophic patients, which was effectively restored by leptin. The findings in this study emphasize the important pathological role of leptin in eating disorders in lipodystrophy and provide a clue to understanding the action mechanism of leptin in human, which may lead to development of novel strategies for prevention and treatment of obesity.

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Hortensius, Ruud, David Terburg, Barak Morgan, Dan J. Stein, Jack van Honk, and Beatrice de Gelder. "The role of the basolateral amygdala in the perception of faces in natural contexts." Philosophical Transactions of the Royal Society B: Biological Sciences 371, no. 1693 (May 5, 2016): 20150376. http://dx.doi.org/10.1098/rstb.2015.0376.

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The amygdala is a complex structure that plays its role in perception and threat-related behaviour by activity of its specific nuclei and their separate networks. In the present functional magnetic resonance imaging study, we investigated the role of the basolateral amygdala in face and context processing. Five individuals with focal basolateral amygdala damage and 12 matched controls viewed fearful or neutral faces in a threatening or neutral context. We tested the hypothesis that basolateral amygdala damage modifies the relation between face and threatening context, triggering threat-related activation in the dorsal stream. The findings supported this hypothesis. First, activation was increased in the right precentral gyrus for threatening versus neutral scenes in the basolateral amygdala damage group compared with the control group. Second, activity in the bilateral middle frontal gyrus, and left anterior inferior parietal lobule was enhanced for neutral faces presented in a threatening versus neutral scene in the group with basolateral amygdala damage compared with controls. These findings provide the first evidence for the neural consequences of basolateral amygdala damage during the processing of complex emotional situations.

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Buff, C., C. Schmidt, L. Brinkmann, B. Gathmann, S. Tupak, and T. Straube. "Directed threat imagery in generalized anxiety disorder." Psychological Medicine 48, no. 4 (July 24, 2017): 617–28. http://dx.doi.org/10.1017/s0033291717001957.

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BackgroundWorrying has been suggested to prevent emotional and elaborative processing of fears. In cognitive-behavioral therapy (CBT), generalized anxiety disorder (GAD) patients are exposed to their fears during the method of directed threat imagery by inducing emotional reactivity. However, studies investigating neural correlates of directed threat imagery and emotional reactivity in GAD patients are lacking. The present functional magnetic resonance imaging (fMRI) study aimed at delineating neural correlates of directed threat imagery in GAD patients.MethodNineteen GAD patients and 19 healthy controls (HC) were exposed to narrative scripts of either disorder-related or neutral content and were encouraged to imagine it as vividly as possible.ResultsRating results showed that GAD patients experienced disorder-related scripts as more anxiety inducing and arousing than HC. These results were also reflected in fMRI data: Disorder-related v. neutral scripts elicited elevated activity in the amygdala, dorsomedial prefrontal cortex, ventrolateral prefrontal cortex and the thalamus as well as reduced activity in the ventromedial prefrontal cortex/subgenual anterior cingulate cortex in GAD patients relative to HC.ConclusionThe present study presents the first behavioral and neural evidence for emotional reactivity during directed threat imagery in GAD. The brain activity pattern suggests an involvement of a fear processing network as a neural correlate of initial exposure during directed imagery in CBT in GAD.

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Allin, M. P. G., N. Marshall, K. Schulze, M. Walshe, M. H. Hall, M. Picchioni, R. M. Murray, and C. McDonald. "A functional MRI study of verbal fluency in adults with bipolar disorder and their unaffected relatives." Psychological Medicine 40, no. 12 (February 11, 2010): 2025–35. http://dx.doi.org/10.1017/s0033291710000127.

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BackgroundIndividuals with a history of bipolar disorder demonstrate abnormalities of executive function, even during euthymia. The neural architecture underlying this and its relationship with genetic susceptibility for illness remain unclear.MethodWe assessed 18 remitted individuals with bipolar disorder, 19 of their unaffected first degree relatives and 19 healthy controls using functional magnetic resonance imaging (fMRI) and a paced verbal fluency task with two levels of difficulty.ResultsBipolar patients made significantly more errors in the easy level of the verbal fluency task than their relatives or controls. Analysis of variance of fMRI data demonstrated a significant main effect of group in a large cluster including retrosplenial cortex and adjacent precuneate cortex (x=7, y=−56, x=15). All three groups showed deactivation in these areas during task performance relative to a neutral or rest condition. Group differences comprised a lesser amount of deactivation in unaffected relatives compared with controls in the easy condition [F(2, 55)=3.42, p=0.04] and in unaffected relatives compared with bipolar patients in the hard condition [F(2, 55)=4.34, p=0.018]. Comparison with the control group indicated that both bipolar patients and their relatives showed similar deficits of deactivation in retrosplenial cortex and reduced activation of left prefrontal cortex.ConclusionsBipolar disorder may be associated with an inherited abnormality of a neural network incorporating left prefrontal cortex and bilateral retrosplenial cortex.

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Ortiz-Gil, Jordi, Edith Pomarol-Clotet, Raymond Salvador, Erick J. Canales-Rodríguez, Salvador Sarró, Jesús J. Gomar, Amalia Guerrero, et al. "Neural correlates of cognitive impairment in schizophrenia." British Journal of Psychiatry 199, no. 3 (September 2011): 202–10. http://dx.doi.org/10.1192/bjp.bp.110.083600.

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BackgroundCognitive impairment is an established feature of schizophrenia. However, little is known about its relationship to the structural and functional brain abnormalities that characterise the disorder.AimsTo identify structural and/or functional brain abnormalities associated with schizophrenic cognitive impairment.MethodWe carried out structural magnetic resonance imaging (MRI) and voxel-based morphometry in 26 participants who were cognitively impaired and 23 who were cognitively preserved, all with schizophrenia, plus 39 matched controls. Nineteen of those who were cognitively impaired and 18 of those who were cognitively preserved plus 34 controls also underwent functional MRI during performance of a working memory task.ResultsNo differences were found between the participants who were cognitively intact and those who were cognitively impaired in lateral ventricular volume or whole brain volume. Voxel-based morphometry also failed to reveal clusters of significant difference in grey and white matter volume between these two groups. However, during performance of the n-back task, the participants who were cognitively impaired showed hypoactivation compared with those who were cognitively intact in the dorsolateral prefrontal cortex among other brain regions.ConclusionsCognitive impairment in schizophrenia is not a function of the structural brain abnormality that accompanies the disorder but has correlates in altered brain function.

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Ethridge, Lauren, Andrew Thaliath, Jeremy Kraff, Karan Nijhawan, and Elizabeth Berry-Kravis. "Development of Neural Response to Novel Sounds in Fragile X Syndrome: Potential Biomarkers." American Journal on Intellectual and Developmental Disabilities 125, no. 6 (November 1, 2020): 449–64. http://dx.doi.org/10.1352/1944-7558-125.6.449.

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Abstract Auditory processing abnormalities in fragile X syndrome (FXS) may contribute to difficulties with language development, pattern identification, and contextual updating. Participants with FXS (N = 41) and controls (N = 27) underwent auditory event-related potentials during presentation of an oddball paradigm. Data was adequate for analysis for 33 participants with FXS and 27 controls (age 4–51 y, 13 females [FXS]; 4–54 y, 11 females [control]). Participants with FXS showed larger N1 and P2 amplitudes, abnormal lack of modulation of P1 and P2 amplitudes and P2 latency in response to oddball stimuli ) relative to controls: Females with FXS were more similar to controls. Participants with FXS showed a marginal speeding of the P2 latency, suggesting potentiation to oddball stimuli rather than habituation. Participants with FXS showed a heightened N1 habituation effect compared to controls. Gamma power was significantly higher for participants with FXS. Groups did not differ on mismatch negativity. Both controls and participants with FXS showed similar developmental trajectories in P1 and N1 amplitude, P2 latency, and gamma power, but not for P2 amplitude. One month retest analyses performed in 14 participants suggest strong test-retest reliability for most measures. Individuals with FXS show previously demonstrated increased response amplitude and high frequency neural activity. Despite an overall normal developmental trajectory for most measures, individuals with FXS show age-independent but gender-dependent decreases in complex processing of novel stimuli. Many markers show strong retest reliability even in children and thus are potential biomarkers for clinical trials in FXS.

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Barriga, Elias H., Patrick H. Maxwell, Ariel E. Reyes, and Roberto Mayor. "The hypoxia factor Hif-1α controls neural crest chemotaxis and epithelial to mesenchymal transition." Journal of Cell Biology 201, no. 5 (May 27, 2013): 759–76. http://dx.doi.org/10.1083/jcb.201212100.

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One of the most important mechanisms that promotes metastasis is the stabilization of Hif-1 (hypoxia-inducible transcription factor 1). We decided to test whether Hif-1α also was required for early embryonic development. We focused our attention on the development of the neural crest, a highly migratory embryonic cell population whose behavior has been likened to cancer metastasis. Inhibition of Hif-1α by antisense morpholinos in Xenopus laevis or zebrafish embryos led to complete inhibition of neural crest migration. We show that Hif-1α controls the expression of Twist, which in turn represses E-cadherin during epithelial to mesenchymal transition (EMT) of neural crest cells. Thus, Hif-1α allows cells to initiate migration by promoting the release of cell–cell adhesions. Additionally, Hif-1α controls chemotaxis toward the chemokine SDF-1 by regulating expression of its receptor Cxcr4. Our results point to Hif-1α as a novel and key regulator that integrates EMT and chemotaxis during migration of neural crest cells.

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Zhao, Y., D. Zhang, S. Tan, C. Song, J. Cui, F. Fan, X. Zhu, Y. Zou, and Y. Luo. "Neural correlates of the abolished self-referential memory effect in schizophrenia." Psychological Medicine 44, no. 3 (May 31, 2013): 477–87. http://dx.doi.org/10.1017/s0033291713001177.

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BackgroundThe self-referential memory (SRM) effect refers to the phenomenon that stimuli processed with reference to the self are better remembered than those referenced to others. Studies have shown that schizophrenia patients do not have this memorial advantage for self-referenced information. The current study investigated the electrophysiological mechanism of the abolished SRM effect in schizophrenia.MethodTwenty schizophrenia patients and 22 controls were recruited to complete an SRM task. We used a high-time resolution event-related potential (ERP) technique to analyze the electrophysiological differences between patients and controls during self- and other-reflection processing.ResultsBehavior data indicated that healthy controls had a typical SRM bias that was absent in the schizophrenia patients. ERP comparison between groups showed that the schizophrenia patients presented smaller voltages in both self- and other-reflection conditions in the 160–260 ms (P2 component) and 800–1200 ms (positive slow wave) time windows over the pre/frontal cortex. Furthermore, the N2 amplitudes (270–380 ms) differed between self- and other-reflection conditions in patients but not in normal controls. More importantly, we found that the P3 amplitudes in the parietal cortex correlated significantly with the SRM bias score in the patients (r = –0.688).ConclusionsThese results provide comprehensive and direct electrophysiological evidence for self- and other-reflective dysfunction in schizophrenia patients and contribute to our understanding of the underlying neural substrates of the abolished SRM effect in schizophrenia.

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Meier, Jacqueline Katharina, Mathias Weymar, and Lars Schwabe. "Stress Alters the Neural Context for Building New Memories." Journal of Cognitive Neuroscience 32, no. 12 (December 2020): 2226–40. http://dx.doi.org/10.1162/jocn_a_01613.

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Stressful events affect mnemonic processing, in particular for emotionally arousing events. Previous research on the mechanisms underlying stress effects on human memory focused on stress-induced changes in the neural activity elicited by a stimulus. We tested an alternative mechanism and hypothesized that stress may already alter the neural context for successful memory formation, reflected in the neural activity preceding a stimulus. Therefore, 69 participants underwent a stress or control procedure before encoding neutral and negative pictures. During encoding, we recorded high-density EEG and analyzed—based on multivariate searchlight analyses—oscillatory activity and cross-frequency coupling patterns before stimulus onset that were predictive of memory tested 24 hr later. Prestimulus theta predicted subsequent memory in controls but not in stressed participants. Instead, prestimulus gamma predicted successful memory formation after stress, specifically for emotional material. Likewise, stress altered the patterns of prestimulus theta–beta and theta–gamma phase–amplitude coupling predictive of subsequent memory, again depending on the emotionality of the presented material. Our data suggest that stress changes the neural context for building new memories, tuning this neural context specifically to the encoding of emotionally salient events. These findings point to a yet unknown mechanism through which stressful events may change (emotional) memory formation.

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Anderson, David, Matthew Garlinghouse, Arica Hauger, Alison Moody, Ann M. Berger, and Jean L. Grem. "Neural mechanisms of impaired executive function in untreated colorectal cancer patients." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e24170-e24170. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e24170.

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e24170 Background: Cancer-related cognitive impairment (CRCI) affects 45% of colorectal cancer (CRC) patients prior to treatment. This study aimed to explore the neural mechanisms of CRCI in this severely understudied population by using a combination of neuropsychological and cognitive neurophysiology assessments. Methods: Newly diagnosed Stage I-IV CRC patients were recruited at a Midwestern tertiary medical center. Enrollment criteria included normal or corrected to normal vision and no prior cancer within 3 years. Healthy comparisons were recruited and demographically-matched to Stage III/IV patients scheduled to receive chemotherapy. Participants completed neuropsychological measures of processing speed, psychomotor speed, executive function, and verbal memory at study baseline. We recorded scalp electroencephalography while participants performed a computer-based cognitive task designed to measure control over spatial attention. Two event-related potentials were measured following presentation of a task-irrelevant spatial cue: (1) N2, a neural correlate of stimulus selection emerging approximately 160 milliseconds after stimulus presentation; and (2) N2pc, a neural correlate of spatial attention allocation emerging approximately 200 milliseconds after stimulus presentation. Results: CRC patients were enrolled within 4-8 weeks following surgery for Stage I (11%), II (31%), and III (35%) CRC; Stage IV patients (23%) started chemotherapy without surgery. Patients (n = 26) and controls (n = 14) were matched on age and gender; patients were trending toward lower education than controls (p = .06). Patients performed worse than controls on executive function assessments (Trials B: p = .049; Stroop: p = .025). N2 amplitudes were smaller in patients than controls (p = 0.032. N2pc amplitudes were larger in patients than controls (p = .092). N2 amplitudes were associated with Stroop interference scores (r = 0.50, p = .068). Conclusions: CRC patients demonstrated impaired executive function performance at baseline. Neurophysiological data suggest impairments may emerge from limited neural resources available for stimulus selection and poor control over spatial attention. Correlations between neurophysiological data and executive function performance suggest participants better able to overcome task-irrelevant interference had relatively more neural resources available for stimulus selection. Overall, these results suggest patients may be limited in their ability to focus their attention on caregiver and health care team instructions. Clinical trial information: NCT03683004 .

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Yasaka, Koichiro, Koji Kamagata, Takashi Ogawa, Taku Hatano, Haruka Takeshige-Amano, Kotaro Ogaki, Christina Andica, et al. "Parkinson’s disease: deep learning with a parameter-weighted structural connectome matrix for diagnosis and neural circuit disorder investigation." Neuroradiology 63, no. 9 (January 22, 2021): 1451–62. http://dx.doi.org/10.1007/s00234-021-02648-4.

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Abstract Purpose To investigate whether Parkinson’s disease (PD) can be differentiated from healthy controls and to identify neural circuit disorders in PD by applying a deep learning technique to parameter-weighted and number of streamlines (NOS)–based structural connectome matrices calculated from diffusion-weighted MRI. Methods In this prospective study, 115 PD patients and 115 healthy controls were enrolled. NOS-based and parameter-weighted connectome matrices were calculated from MRI images obtained with a 3-T MRI unit. With 5-fold cross-validation, diagnostic performance of convolutional neural network (CNN) models using those connectome matrices in differentiating patients with PD from healthy controls was evaluated. To identify the important brain connections for diagnosing PD, gradient-weighted class activation mapping (Grad-CAM) was applied to the trained CNN models. Results CNN models based on some parameter-weighted structural matrices (diffusion kurtosis imaging (DKI)–weighted, neurite orientation dispersion and density imaging (NODDI)–weighted, and g-ratio-weighted connectome matrices) showed moderate performance (areas under the receiver operating characteristic curve (AUCs) = 0.895, 0.801, and 0.836, respectively) in discriminating PD patients from healthy controls. The DKI-weighted connectome matrix performed significantly better than the conventional NOS-based matrix (AUC = 0.761) (DeLong’s test, p < 0.0001). Alterations of neural connections between the basal ganglia and cerebellum were indicated by applying Grad-CAM to the NODDI- and g-ratio-weighted matrices. Conclusion Patients with PD can be differentiated from healthy controls by applying the deep learning technique to the parameter-weighted connectome matrices, and neural circuit disorders including those between the basal ganglia on one side and the cerebellum on the contralateral side were visualized.

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Woodruff, Peter, Georgios Ponirakis, Reem Ghandi, Amani Hussein, Anjushri Bhagat, Ioannis Petropoulos, Adnan Khan, et al. "T13. CORNEAL CONFOCAL MICROSCOPY DETECTS NEURAL CHANGES IN SCHIZOPHRENIA." Schizophrenia Bulletin 46, Supplement_1 (April 2020): S235—S236. http://dx.doi.org/10.1093/schbul/sbaa029.573.

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Abstract Background A combination of neurodevelopmental and degenerative neural changes are likely to underpin positive and negative symptoms in schizophrenia. However, there are currently no validated biomarkers to accurately quantify the extent of neural changes in schizophrenia. Corneal confocal microscopy (CCM) is a non-invasive ophthalmic imaging technique that has been used to demonstrate in vivo corneal nerve fiber abnormalities in a range of peripheral neuropathies and central neurodegenerative disorders including Parkinson’s disease, multiple sclerosis and dementia. We wished to test the hypothesis that corneal nerve abnormalities occur in patients with schizophrenia, particularly those with negative symptoms and cognitive impairment. Methods Patients with DSM-V schizophrenia without other causes of peripheral neuropathy other than metabolic syndrome underwent assessment of clinical ratings (Positive and Negative Symptoms Scale (PANSS), cognitive function (Montreal Cognitive Assessment (MOCA) and Corneal confocal microscopy (CCM), vibration perception threshold (VPT) and sudomotor function testing. Healthy controls underwent the same assessments apart from PANSS. Results 55 subjects without (n=38) and with schizophrenia (n=17) with comparable mean age (35.7±8.5 vs 35.6±12.2, P=0.96) were studied. Patients with schizophrenia had significantly higher body weight (93.9±25.5 vs 77.1±10.1, P=0.02) and lower Low Density Lipoproteins (2.6±1.0 vs 3.4±0.7, P=0.02) compared with healthy controls. The proportion of gender, systolic and diastolic blood pressure, HbA1c, cholesterol, triglyceride and High Density Lipoproteins were comparable between the two groups. Patients with schizophrenia had significantly lower corneal nerve fibre density (CNFD, fibers/mm2) (35.6±6.5 vs 23.5±7.8, p<0.0001), branch density (CNBD, branches/mm2) (98.1±30.6 vs 34.4±26.9, p<0.0001), and fibre length (CNFL, mm/mm2) (24.2±3.9 vs 14.3±4.7, p<0.0001) compared with healthy controls but no difference in peripheral neuropathy assessed by VPT and sudomotor function testing. The area under the Receiver Operating Characteristic Curve (95% CI) of CNFD, CNBD, CNFL to distinguish patients with schizophrenia from healthy controls were 87.0% (76.8–98.2%), 93.2% (84.2–102.3%), 93.2% (84.4–102.1%), respectively. Discussion These preliminary results:

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Johansen, Kirsten L., Julie Doyle, Giorgos K. Sakkas, and Jane A. Kent-Braun. "Neural and metabolic mechanisms of excessive muscle fatigue in maintenance hemodialysis patients." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, no. 3 (September 2005): R805—R813. http://dx.doi.org/10.1152/ajpregu.00187.2005.

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Dialysis patients have severe exercise limitations related to metabolic disturbances, but muscle fatigue has not been well studied in this population. We investigated the magnitude and mechanisms of fatigue of the ankle dorsiflexor muscles in patients on maintenance hemodialysis. Thirty-three dialysis patients and twelve healthy control subjects performed incremental isometric dorsiflexion exercise, beginning at 10% of their maximal voluntary contraction (MVC) and increasing by 10% every 2 min. Muscle fatigue (fall of MVC), completeness of voluntary activation, and metabolic responses to exercise were measured. Before exercise, dialysis subjects exhibited reduced strength and impaired peripheral activation (lower compound muscle activation potential amplitude) but no metabolic perturbation. During exercise, dialysis subjects demonstrated threefold greater fatigue than controls with evidence of central activation failure but no change in peripheral activation. All metabolic parameters were significantly more perturbed at end exercise in dialysis subjects than in controls, including lower phosphocreatine (PCr) and pH, and higher Pi, Pi/PCr, and H2PO4−. Oxidative potential was markedly lower in patients than in controls [62.5 (SD 27.2) vs. 134.6 (SD 31.7), P < 0.0001]. Muscle fatigue was negatively correlated with oxidative potential among dialysis subjects ( r = −0.52, P = 0.04) but not controls. Changes in central activation ratio were also correlated with muscle fatigue in the dialysis subjects ( r = 0.59, P = 0.001) but not the controls. This study provides new information regarding the excessive muscular fatigue of dialysis patients and demonstrates that the mechanisms of this fatigue include both intramuscular energy metabolism and central activation failure.

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Badenhorst, Paul. "Tramtrack controls glial number and identity in the Drosophila embryonic CNS." Development 128, no. 20 (October 15, 2001): 4093–101. http://dx.doi.org/10.1242/dev.128.20.4093.

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Neurons and glia are often derived from common multipotent stem cells. In Drosophila, neural identity appears to be the default fate of these precursors. Stem cells that generate either neurons or glia transiently express neural stem cell-specific markers. Further development as glia requires the activation of glial-specific regulators. However, this must be accompanied by simultaneous repression of the alternate neural fate. I show that the Drosophila transcriptional repressor Tramtrack is a key repressor of neuronal fates. It is expressed at high levels in all mature glia of the embryonic central nervous system. Analysis of the temporal profile of Tramtrack expression in glia shows that it follows that of existing glial markers. When expressed ectopically before neural stem cell formation, Tramtrack represses the neural stem cell-specific genes asense and deadpan. Surprisingly, Tramtrack protein levels oscillate in a cell cycle-dependent manner in proliferating glia, with expression dropping before replication, but re-initiating after S phase. Overexpression of Tramtrack blocks glial development by inhibiting S-phase and repressing expression of the S-phase cyclin, cyclin E. Conversely, in tramtrack mutant embryos, glia are disrupted and undergo additional rounds of replication. I propose that Tramtrack ensures stable mature glial identity by both repressing neuroblast-specific genes and controlling glial cell proliferation.

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Gazes, Yunglin, Minghao Liu, Melissa Sum, Elaine Cong, Jennifer Kuo, James A. Lee, Shonni Silverberg, Yaakov Stern, and Marcella Walker. "Functional magnetic resonance imaging in primary hyperparathyroidism." European Journal of Endocrinology 183, no. 1 (July 2020): 21–30. http://dx.doi.org/10.1530/eje-20-0123.

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Objective The neurophysiological mechanisms underlying cognitive dysfunction in primary hyperparathyroidism (PHPT) and the brain regions affected are not clear. We assessed neural activation during cognitive testing (matrix reasoning, paired associates, and logical memory) using functional MRI (fMRI) in 23 patients with PHPT and 23 healthy controls. A subset with PHPT was re-assessed 6 months post-parathyroidectomy (PTX). Design This is an observational study comparing neural activation by fMRI in patients with PHPT to normative controls. Postmenopausal women were studied at a tertiary referral center. Results There were no between-group differences in cognitive task performance. Patients with PHPT had lower neural activation vs controls (max Z = 4.02, all P < 0.01) during matrix reasoning in brain regions involved in executive function (left frontal lobe (k = 57) and right medial frontal gyrus (k = 72)) and motor function (right precentral gyrus (k = 51)). During paired associates (verbal memory), those with PHPT had greater activation in the right inferior parietal lobule (language/mathematical operations; k = 65, P < 0.01). Greater activation in this region bilaterally correlated with higher PTH (k = 96, P < 0.01). Post-PTX, activation decreased during matrix reasoning, but in different regions than those affected pre-PTX. Conclusions PHPT is associated with differences in task-related neural activation patterns, but no difference in cognitive performance. While this may indicate compensation to maintain the same cognitive function, there was no clear improvement in neural activation after PTX. Larger, longitudinal studies that include PHPT patients followed without surgery are needed to determine if PTX could prevent worsening of altered neural activation patterns in PHPT.

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Journal articles on the topic 'Neural controls'

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