rudyvdbrink/CitationDatabase huggingface dataset:
What the left and right anterior fusiform gyri tell us about semantic memory.
Brain : a journal of neurology, 2010

The study of patients with semantic dementia, a variant of frontotemporal lobar degeneration, has emerged over the last two decades as an important lesion model for studying human semantic memory. Although it is well-known that semantic dementia is associated with temporal lobe degeneration, controversy remains over whether the semantic deficit is due to diffuse temporal lobe damage, damage to only a sub-region of the temporal lobe or even less severe damage elsewhere in the brain. The manner in which the right and left temporal lobes contribute to semantic knowledge is also not fully elucidated. In this study we used unbiased imaging analyses to correlate resting cerebral glucose metabolism and behavioural scores in tests of verbal and non-verbal semantic memory. In addition, a region of interest analysis was performed to evaluate the role of severely hypometabolic areas. The best, indeed the only, strong predictor of semantic scores across a set of 21 patients with frontotemporal lobar degeneration with semantic impairment was degree of hypometabolism in the anterior fusiform region subjacent to the head and body of the hippocampus. As hypometabolism in the patients' rostral fusiform was even more extreme than the abnormality in other regions with putative semantic relevance, such as the temporal poles, the significant fusiform correlations cannot be attributed to floor-level function in these other regions. More detailed analysis demonstrated more selective correlations: left anterior fusiform function predicted performance on two expressive verbal tasks, whereas right anterior fusiform metabolism predicted performance on a non-verbal test of associative semantic knowledge. This pattern was further supported by an additional behavioural study performed on a wider cohort of patients with semantic dementia, in which the patients with more extensive right-temporal atrophy (when matched on degree of naming deficit to a set of cases with more extensive left temporal atrophy) were significantly more impaired on the test of non-verbal semantics. Our preferred interpretation of this laterality effect involves differential strength of connectivity between different regions of a widespread semantic network in the human brain.
Love flows downstream: mothers' and children's neural representation similarity in perceiving distress of self and family.
Social cognitive and affective neuroscience, 2017

The current study aimed to capture empathy processing in an interpersonal context. Mother-adolescent dyads (N = 22) each completed an empathy task during fMRI, in which they imagined the target person in distressing scenes as either themselves or their family (i.e. child for the mother, mother for the child). Using multi-voxel pattern approach, we compared neural pattern similarity for the self and family conditions and found that mothers showed greater perceptual similarity between self and child in the fusiform face area (FFA), representing high self-child overlap, whereas adolescents showed significantly less self-mother overlap. Adolescents' pattern similarity was dependent upon family relationship quality, such that they showed greater self-mother overlap with higher relationship quality, whereas mothers' pattern similarity was independent of relationship quality. Furthermore, adolescents' perceptual similarity in the FFA was associated with increased social brain activation (e.g. temporal parietal junction). Mediation analyses indicated that high relationship quality was associated with greater social brain activation, which was mediated by greater self-mother overlap in the FFA. Our findings suggest that adolescents show more distinct neural patterns in perceiving their own vs their mother's distress, and such distinction is sensitive to mother-child relationship quality. In contrast, mothers' perception for their own and child's distress is highly similar and unconditional.
Autoimmune channelopathies in paraneoplastic neurological syndromes.
Biochimica et biophysica acta, 2015

Paraneoplastic neurological syndromes and autoimmune encephalitides are immune neurological disorders occurring or not in association with a cancer. They are thought to be due to an autoimmune reaction against neuronal antigens ectopically expressed by the underlying tumour or by cross-reaction with an unknown infectious agent. In some instances, paraneoplastic neurological syndromes and autoimmune encephalitides are related to an antibody-induced dysfunction of ion channels, a situation that can be labelled as autoimmune channelopathies. Such functional alterations of ion channels are caused by the specific fixation of an autoantibody upon its target, implying that autoimmune channelopathies are usually highly responsive to immuno-modulatory treatments. Over the recent years, numerous autoantibodies corresponding to various neurological syndromes have been discovered and their mechanisms of action partially deciphered. Autoantibodies in neurological autoimmune channelopathies may target either directly ion channels or proteins associated to ion channels and induce channel dysfunction by various mechanisms generally leading to the reduction of synaptic expression of the considered channel. The discovery of those mechanisms of action has provided insights on the regulation of the synaptic expression of the altered channels as well as the putative roles of some of their functional subdomains. Interestingly, patients' autoantibodies themselves can be used as specific tools in order to study the functions of ion channels. This article is part of a Special Issue entitled: Membrane channels and transporters in cancers.
Reduced Voluntary Activation During Brief and Sustained Contractions of a Hand Muscle in Secondary-Progressive Multiple Sclerosis Patients.
Neurorehabilitation and neural repair, 2016

Secondary-progressive multiple sclerosis (SPMS) patients have structural cortical damage resulting in increased compensatory cortical activity during (submaximal) performance. However, functional effects of changed cortical output are difficult to measure. The interpolated-twitch technique allows for measurement of voluntary activation (VA) necessary for force production. This study aimed to determine VA, force, and muscle fatigue during brief and sustained contractions in SPMS patients. Because fatigue effects are not confined to the motor system, we additionally examined fatiguing effects on cognitive performance.
Impact of fingolimod on CD4+ T cell subset and cytokine profile of relapsing remitting multiple sclerosis patients.
Journal of neuroimmunology, 2019

Fingolimod inhibits the egress of lymphocytes from lymphatic tissues and also directly affects their functions by modulation of the sphingosine-1-phosphate receptor 1 (S1P1). Our aim was to evaluate the impact of fingolimod on diverse CD4+ T cell subsets, and cytokines. Sixty-six relapsing remitting multiple sclerosis (RRMS) patients were treated with oral fingolimod (0.5 mg) for 6 months, and blood samples were collected at baseline, 3 months, and 6 months. Serum levels of seven cytokines and five chemokines were measured by multiplex immunoassay, and frequencies of peripheral blood mononuclear cell subsets were assessed by flow cytometry, and compared with those of 60 healthy controls. CCL2 (p = 0.039), and CCL5 (p = 0.001) levels were significantly higher in fingolimod-treated patients than healthy controls, whereas end-of-study serum levels of IL-6, IL-8, IL-17A, IL-22, IL-23, TNF-α, CXCL10, and CXCL13 were comparable to the baseline levels. Six months of fingolimod treatment reduced CD3+ T cell (mean ± standard deviation, 72.9% ± 5.5 vs. 60.1% ± 11.1, p < 0.001), CD4+ T cell (62.2% ± 8.5 vs. 24.6% ± 12.9, p < 0.001), CD4+CD25hi regulatory T cell (Treg) (3.4% ± 1.3 vs. 2.0% ± 1.4, p < 0.01), and CD19+ B cell (13.2% ± 5.8 vs. 5.3% ± 2.7, p < 0.001) frequencies, while CD8+ T cells (31.8% ± 7.8 vs. 57.8% ± 13.2, p < 0.001) were increased, and NK and NKT cells remained unchanged. The proportions of intracytoplasmic IL-4, IL-10, IFN-γ, and TNF-α-producing T cells were increased, whereas IL-17-producing cells remained relatively constant as measured by flow cytometry. Fingolimod appears to primarily diminish lymphocyte subsets involved in antigen presentation (CD19+ B and CD4+ T cells) rather than immune cells (CD8+ T, NK, and NKT cells) in charge of host defense against pathogens. In contrast, a relative increase is observed in pro- and anti-inflammatory cytokine-producing T helper subsets (IFN-γ, TNF-α, IL-4, and IL-10-producing CD4+ T cells), suggesting that effector T cells are suppressed to a lesser degree by S1P1 modulation.
Individuals with episodic amnesia are not stuck in time.
Neuropsychologia, 2014

The metaphor that individuals with episodic amnesia due to hippocampal damage are "stuck in time" persists in science, philosophy, and everyday life despite mounting evidence that episodic amnesia can spare many central aspects of temporal consciousness. Here we describe some of this evidence, focusing specifically on KC, one of the most thoroughly documented and severe cases of episodic amnesia on record. KC understands the concept of time, knows that it passes, and can orient himself with respect to his personal past and future. He expresses typical attitudes toward his past and future, and he is able to make future-regarding decisions. Theories claiming that the hippocampus plays an essential role in temporal consciousness need to be revised in light of these findings.
Reduced EGFR signaling in progenitor cells of the adult subventricular zone attenuates oligodendrogenesis after demyelination.
Neuron glia biology, 2007

Neural progenitor cells that express the NG2 proteoglycan are present in different regions of the adult mammalian brain where they display distinct morphologies and proliferative rates. In the developing postnatal and adult mouse, NG2(+) cells represent a major cell population of the subventricular zone (SVZ). NG2(+) cells divide in the anterior and lateral region of the SVZ, and are stimulated to proliferate and migrate out of the SVZ by focal demyelination of the corpus callosum (CC). Many NG2(+) cells are labeled by GFP-retrovirus injection into the adult SVZ, demonstrating that NG2(+) cells actively proliferate under physiological conditions and after demyelination. Under normal physiological conditions and after focal demyelination, proliferation of NG2(+) cells is significantly attenuated in wa2 mice, which are characterized by reduced signaling of the epidermal growth factor receptor (EGFR). This results in reduced SVZ-to-lesion migration of NG2(+) cells and oligodendrogenesis in the lesion. Expression of vascular endothelial growth factor (VEGF) and EGFR ligands, such as heparin binding-EGF and transforming growth factor alpha, is upregulated in the SVZ after focal demyelination of the CC. EGF-induced oligodendrogenesis and myelin protein expression in wild-type SVZ cells in culture are significantly attenuated in wa2 SVZ cells. Our results demonstrate that the response of NG2(+) cells in the SVZ and their subsequent differentiation in CC after focal demyelination depend on EGFR signaling.
Novel loci affecting iron homeostasis and their effects in individuals at risk for hemochromatosis.
Nature communications, 2014

Variation in body iron is associated with or causes diseases, including anaemia and iron overload. Here, we analyse genetic association data on biochemical markers of iron status from 11 European-population studies, with replication in eight additional cohorts (total up to 48,972 subjects). We find 11 genome-wide-significant (P<5 × 10(-8)) loci, some including known iron-related genes (HFE, SLC40A1, TF, TFR2, TFRC, TMPRSS6) and others novel (ABO, ARNTL, FADS2, NAT2, TEX14). SNPs at ARNTL, TF, and TFR2 affect iron markers in HFE C282Y homozygotes at risk for hemochromatosis. There is substantial overlap between our iron loci and loci affecting erythrocyte and lipid phenotypes. These results will facilitate investigation of the roles of iron in disease.
Detecting Functional Connectivity During Audiovisual Integration with MEG: A Comparison of Connectivity Metrics.
Brain connectivity, 2015

In typical magnetoencephalography and/or electroencephalography functional connectivity analysis, researchers select one of several methods that measure a relationship between regions to determine connectivity, such as coherence, power correlations, and others. However, it is largely unknown if some are more suited than others for various types of investigations. In this study, the authors investigate seven connectivity metrics to evaluate which, if any, are sensitive to audiovisual integration by contrasting connectivity when tracking an audiovisual object versus connectivity when tracking a visual object uncorrelated with the auditory stimulus. The authors are able to assess the metrics' performances at detecting audiovisual integration by investigating connectivity between auditory and visual areas. Critically, the authors perform their investigation on a whole-cortex all-to-all mapping, avoiding confounds introduced in seed selection. The authors find that amplitude-based connectivity measures in the beta band detect strong connections between visual and auditory areas during audiovisual integration, specifically between V4/V5 and auditory cortices in the right hemisphere. Conversely, phase-based connectivity measures in the beta band as well as phase and power measures in alpha, gamma, and theta do not show connectivity between audiovisual areas. The authors postulate that while beta power correlations detect audiovisual integration in the current experimental context, it may not always be the best measure to detect connectivity. Instead, it is likely that the brain utilizes a variety of mechanisms in neuronal communication that may produce differential types of temporal relationships.
Natural polymeric 3-alkylpyridinium salt affects vertebrate skeletal muscle contractility by preferentially blocking neuromuscular transmission.
Toxicology letters, 2017

The effects of natural polymeric alkylpyridinium salt (nPoly-3-APS), a potent acetylcholinesterase inhibitor isolated from the marine sponge Reniera sarai, were studied on isolated mouse phrenic nerve-hemidiaphragm muscle preparations using electrophysiological approaches. nPoly-3-APS inhibited nerve-evoked isometric muscle twitch and tetanic contraction in a concentration-dependent manner (IC
Prenatal alcohol exposure alters synaptic activity of adult hippocampal dentate granule cells under conditions of enriched environment.
Hippocampus, 2016

Prenatal alcohol exposure (PAE) results in fetal alcohol spectrum disorder (FASD), which is characterized by a wide range of cognitive and behavioral deficits that may be linked to impaired hippocampal function and adult neurogenesis. Preclinical studies in mouse models of FASD indicate that PAE markedly attenuates enrichment-mediated increases in the number of adult-generated hippocampal dentate granule cells (aDGCs), but whether synaptic activity is also affected has not been studied. Here, we utilized retroviral birth-dating coupled with whole cell patch electrophysiological recordings to assess the effects of PAE on enrichment-mediated changes in excitatory and inhibitory synaptic activity as a function of DGC age. We found that exposure to an enriched environment (EE) had no effect on baseline synaptic activity of 4- or 8-week-old aDGCs from control mice, but significantly enhanced the excitatory/inhibitory ratio of synaptic activity in 8-week-old aDGCs from PAE mice. In contrast, exposure to EE significantly enhanced the excitatory/inhibitory ratio of synaptic activity in older pre-existing DGCs situated in the outer dentate granule cell layer (i.e., those generated during embryonic development; dDGCs) in control mice, an effect that was blunted in PAE mice. These findings indicate distinct electrophysiological responses of hippocampal DGCs to behavioral challenge based on cellular ontogenetic age, and suggest that PAE disrupts EE-mediated changes in overall hippocampal network activity. These findings may have implications for future therapeutic targeting of hippocampal dentate circuitry in clinical FASD. © 2016 Wiley Periodicals, Inc.
Ursodeoxycholic Acid Improves Mitochondrial Function and Redistributes Drp1 in Fibroblasts from Patients with Either Sporadic or Familial Alzheimer's Disease.
Journal of molecular biology, 2018

Alzheimer's disease (AD) is the leading cause of dementia worldwide. Mitochondrial abnormalities have been identified in many cell types in AD, with deficits preceding the development of the classical pathological aggregations. Ursodeoxycholic acid (UDCA), a treatment for primary biliary cirrhosis, improves mitochondrial function in fibroblasts derived from Parkinson's disease patients as well as several animal models of AD and Parkinson's disease. In this paper, we investigated both mitochondrial function and morphology in fibroblasts from patients with both sporadic and familial AD. We show that both sporadic AD (sAD) and PSEN1 fibroblasts share the same impairment of mitochondrial membrane potential and alterations in mitochondrial morphology. Mitochondrial respiration, however, was decreased in sAD fibroblasts and increased in PSEN1 fibroblasts. Morphological changes seen in AD fibroblasts include reduced mitochondrial number and increased mitochondrial clustering around the cell nucleus as well as an increased number of long mitochondria. We show here for the first time in AD patient tissue that treatment with UDCA increases mitochondrial membrane potential and respiration as well as reducing the amount of long mitochondria in AD fibroblasts. In addition, we show reductions in dynamin-related protein 1 (Drp1) level, particularly the amount localized to mitochondria in both sAD and familial patient fibroblasts. Drp1 protein amount and localization were increased after UDCA treatment. The restorative effects of UDCA are abolished when Drp1 is knocked down. This paper highlights the potential use of UDCA as a treatment for neurodegenerative disease.
Certain, but incorrect: on the relation between subjective certainty and accuracy in sound localisation.
Experimental brain research, 2020

When asked to identify the position of a sound, listeners can report its perceived location as well as their subjective certainty about this spatial judgement. Yet, research to date focused primarily on measures of perceived location (e.g., accuracy and precision of pointing responses), neglecting instead the phenomenological experience of subjective spatial certainty. The present study aimed to investigate: (1) changes in subjective certainty about sound position induced by listening with one ear plugged (simulated monaural listening), compared to typical binaural listening and (2) the relation between subjective certainty about sound position and localisation accuracy. In two experiments (N = 20 each), participants localised single sounds delivered from one of 60 speakers hidden from view in front space. In each trial, they also provided a subjective rating of their spatial certainty about sound position. No feedback on response was provided. Overall, participants were mostly accurate and certain about sound position in binaural listening, whereas their accuracy and subjective certainty decreased in monaural listening. Interestingly, accuracy and certainty dissociated within single trials during monaural listening: in some trials participants were certain but incorrect, in others they were uncertain but correct. Furthermore, unlike accuracy, subjective certainty rapidly increased as a function of time during the monaural listening block. Finally, subjective certainty changed as a function of perceived location of the sound source. These novel findings reveal that listeners quickly update their subjective confidence on sound position, when they experience an altered listening condition, even in the absence of feedback. Furthermore, they document a dissociation between accuracy and subjective certainty when mapping auditory input to space.
Reduced default mode network connectivity following combat trauma.
Neuroscience letters, 2016

Recent studies show decreased functional connectivity in the default mode network (DMN) in PTSD; however, few have directly examined combat trauma specifically. There is limited understanding of how combat itself may affect the DMN. Some literature suggests that trauma exposure, rather than PTSD, can disrupt the DMN. To further elucidate the effect of trauma and PTSD on the DMN, we investigated DMN functional connectivity during the resting-state in veterans with PTSD, combat-exposed controls, and never-traumatized healthy controls. Results revealed that DMN connectivity was reduced in veterans exposed to combat trauma with and without PTSD compared to healthy civilian controls. Specifically, both groups of veterans demonstrated weaker connectivity within a network involving the precuneus, medial prefrontal cortex (mPFC) and right superior parietal lobule regardless of whether the mPFC or precuneus was chosen as a seed region. Findings suggest that the experience of trauma, rather than the pathology of PTSD, may be related to DMN changes.
Minimally Invasive Thoracolumbar Corpectomy and Stabilization for Unstable Burst Fractures Using Intraoperative Computed Tomography and Computer-Assisted Spinal Navigation.
World neurosurgery, 2019

Minimally invasive surgery using a mini-open lateral retropleural or retroperitoneal approach for corpectomy is a well-described procedure for treating unstable thoracolumbar burst fractures. Most surgeons have incorporated fluoroscopy for localization and determination of hardware placement accuracy; however, the utility of computer-assisted image-guided spinal navigation has not been well described. We report a series of mini-open lateral approach thoracolumbar corpectomy cases using either fluoroscopy or intraoperative computed tomography (iCT) with computer-assisted navigation and discuss the technical nuances and advantages of using iCT with navigation versus fluoroscopy.
Behavioural therapy based on distraction alleviates impaired fear extinction in male serotonin transporter knockout rats.
Journal of psychiatry & neuroscience : JPN, 2012

The "biological susceptibility" model posits that some individuals, by genetic predisposition, are highly sensitive to environmental stimuli. Exposure to adverse stimuli leads to negative outcomes, and better outcomes follow favourable stimuli. Recent studies indicate that individuals carrying the low-activity (short; s) variant of the serotonin transporter (5-HTT)-linked polymorphic region (5-HTTLPR) show an enhanced vulnerability to posttraumatic stress disorder (PTSD). Simultaneously, they respond poorly to exposure therapy, the first-line treatment to enhance fear extinction in individuals with PTSD. Given that s-allele carriers also show improved adaptive responding when exposed to positive stimuli, we hypothesized that this trait could be used to offset impaired fear extinction.
A neural model of schemas and memory encoding.
Biological cybernetics, 2020

The ability to rapidly assimilate new information is essential for survival in a dynamic environment. This requires experiences to be encoded alongside the contextual schemas in which they occur. Tse et al. (Science 316(5821):76-82, 2007) showed that new information matching a preexisting schema is learned rapidly. To better understand the neurobiological mechanisms for creating and maintaining schemas, we constructed a biologically plausible neural network to learn context in a spatial memory task. Our model suggests that this occurs through two processing streams of indexing and representation, in which the medial prefrontal cortex and hippocampus work together to index cortical activity. Additionally, our study shows how neuromodulation contributes to rapid encoding within consistent schemas. The level of abstraction of our model further provides a basis for creating context-dependent memories while preventing catastrophic forgetting in artificial neural networks.