rudyvdbrink/CitationDatabase huggingface dataset:
Association between exposure to polycyclic aromatic hydrocarbons and brain cortical thinning: The Environmental Pollution-Induced Neurological EFfects (EPINEF) study.
The Science of the total environment, 2020

Although some studies have suggested that exposure to polycyclic aromatic hydrocarbons (PAHs) induces neurodevelopmental disturbances in children and neurodegeneration in animals, the neurotoxic effect of PAH exposure is unclear in adults. The aim was to examine the associations of PAH exposure with brain structure and neuropsychological function in adults without known neurological diseases.
Diabetic rats are more susceptible to cognitive decline in a model of microemboli-mediated vascular contributions to cognitive impairment and dementia.
Brain research, 2020

Vascular disease plays an important role in all kinds of cognitive impairment and dementia. Diabetes increases the risk of vascular disease and dementia. However, it is not clear how existing vascular disease in the brain accelerates the development of small vessel disease and promotes cognitive dysfunction in diabetes. We used microemboli (ME) injection model in the current study to test the hypothesis that cerebrovascular dysfunction in diabetes facilitates entrapment of ME leading to inflammation and cognitive decline. We investigated cognitive function, axonal/white matter (WM) changes, neurovascular coupling, and microglial activation in control and diabetic male and female Wistar rats subjected to sham or low/high dose ME injection. Diabetic male animals had cognitive deficits, WM demyelination and greater microglial activation than the control animals even at baseline. Functional hyperemia gradually declined in diabetic male animals after ME injection. Both low and high ME injection worsened WM damage and increased microglial activation in diabetic male and female animals. Low ME did not cause cognitive decline in controls, while promoting learning/memory deficits in diabetic female rats and no further decline in diabetic male animals. High ME led to cognitive decline in control male rats and exacerbated the deficits in diabetic cohort. These results suggest that the existing cerebrovascular dysfunction in diabetes may facilitate ME-mediated demyelination leading to cognitive decline. It is important to integrate comorbidities/sex as a biological variable into experimental models for the development of preventive or therapeutic targets.
[Cognitive impairment].
Revue neurologique, 2009

Cognitive impairment is common in multiple sclerosis (MS), occurring at all stages of the disease, even at the earliest, and can be a major source of disability, social impairment, and impoverished quality of life. Cognitive dysfunction is mainly focused on working memory, conceptual reasoning, verbal fluency, speed of information processing, attention and executive function. Measures of information-processing speed appear to be the most robust and sensitive markers of cognitive impairment in MS patients. Cognitive testing in MS patients is complex and cognitive screening tests are time- and cost-saving test instruments. A comprehensive and sensitive cognitive test procedure should be administered to detect cognitive dysfunction, and recent studies demonstrate that single, predominantly speed-related cognitive tests may be superior to extensive and time-consuming test batteries in screening cognitive decline. Additional clinical factors, including disease course, fatigue, and affective disturbance, can impact the degree of MS-related cognitive impairment. Despite weak correlation with disease duration and physical disability status, the degree of cognitive impairment in MS has been related to the extent of topographically specific neuronal tissue damage and loss. Numerous studies have applied conventional and quantitative magnetic resonance imaging (MRI) techniques to correlate the profile and degree of cognitive impairment with various MRI-detectable abnormalities. The burden of MRI-visible lesions does not fully account for the degree of MS-related cognitive impairment. Nonconventional MRI findings suggest the extent of subtle tissue damage in normal-appearing white and grey matter to correlate best with the severity of cognitive impairment in MS patients. Structural MRI approaches have recently been extended by functional MRI studies scrutinizing the brain's ability for adaptive functional reorganization in the presence of widespread tissue damage. Cognitive impairment in MS seems to be not simply the result of tissue destruction, but also a balance between tissue destruction, tissue repair, and adaptive functional reorganization. These findings highlight the need to screen for cognitive deficits in MS patients to conduct potential cognitive rehabilitation intervention.
Bilateral Hydronephrosis Secondary to Giant Cell Tumor of the Sacrum.
Cureus, 2020

Sacral giant cell tumors (GCTs) are rare entities that exhibit slow progressive growth and become clinically apparent when they reach a considerable size. The current case report discusses the presentation, investigation, and management of a young male patient diagnosed with a large sacral mass. A 17-year-old male patient presented with uremia, bilateral lumbar pain, and severe weakness of his lower extremities. Imaging revealed a midline sacral mass causing bilateral upper tract obstruction. The patient underwent bilateral nephrostomies followed by a partial en bloc sacrectomy and curettage of the tumor bulk. Histopathology revealed a giant cell tumor of the sacrum. Postoperatively, the patient received adjuvant radiotherapy and rehabilitation for his neurological symptoms. Sacral GCTs are essentially benign but behave like a malignant tumor in view of frequent recurrences and reports of malignant transformation. Surgery with wide local excision remains the ideal modality for complete clearance of sacral tumors. Nevertheless, limitations include their large size, difficult operative access, risk of fatal intraoperative bleeding, and inevitable high postoperative morbidity.
Weight Gain in a Sample of Patients Affected by Overweight/Obesity with and without a Psychiatric Diagnosis during the Covid-19 Lockdown.
Nutrients, 2020

The present study aimed at identifying psychological and psychosocial variables that might predict weight gain during the COVID-19 lockdown in patients affected by overweight/obesity with and without a psychiatric diagnosis. An online survey was administered between 25 April and 10 May 2020, to investigate participants' changes in dietary habits during the lockdown period. 110 participants were recruited and allocated to two groups, 63 patients had no psychiatric diagnosis; there were 47 patients with psychiatric diagnosis. ANOVA analyses compared the groups with respect to psychological distress levels, risk perception, social support, emotion regulation, and eating behaviors. For each group, a binary logistic regression analysis was conducted, including the factors that were found to significantly differ between groups. Weight gain during lockdown was reported by 31 of the participants affected by overweight/obesity without a psychiatric diagnosis and by 31 patients with a psychiatric diagnosis. Weight gain predictors were stress and low depression for patients without a psychiatric diagnosis and binge eating behaviors for patients with a psychiatric diagnosis. Of patients without a psychiatric diagnosis, 60% reported much more frequent night eating episodes. The risk of night eating syndrome in persons affected by overweight/obesity with no psychiatric diagnosis should be further investigated to inform the development of tailored medical, psychological, and psychosocial interventions.
Assessment of metal concentrations in the SOD1
Molecular and cellular neurosciences, 2018

Amyotrophic lateral sclerosis (ALS) is among the most common of the motor neuron diseases, and arguably the most devastating. During the course of this fatal neurodegenerative disorder, motor neurons undergo progressive degeneration. The currently best-understood animal models of ALS are based on the over-expression of mutant isoforms of Cu/Zn superoxide dismutase 1 (SOD1); these indicate that there is a perturbation in metal homeostasis with disease progression. Copper metabolism in particular is affected in the central nervous system (CNS) and muscle tissue.
Severe Impairment of TNF Post-transcriptional Regulation Leads to Embryonic Death.
iScience, 2020

Post-transcriptional regulation mechanisms control mRNA stability or translational efficiency via ribosomes, and recent evidence indicates that it is a major determinant of the accurate levels of cytokine mRNAs. Transcriptional regulation of
Akirin proteins in development and disease: critical roles and mechanisms of action.
Cellular and molecular life sciences : CMLS, 2020

The Akirin genes, which encode small, nuclear proteins, were first characterized in 2008 in Drosophila and rodents. Early studies demonstrated important roles in immune responses and tumorigenesis, which subsequent work found to be highly conserved. More recently, a multiplicity of Akirin functions, and the associated molecular mechanisms involved, have been uncovered. Here, we comprehensively review what is known about invertebrate Akirin and its two vertebrate homologues Akirin1 and Akirin2, highlighting their role in regulating gene expression changes across a number of biological systems. We detail essential roles for Akirin family proteins in the development of the brain, limb, and muscle, in meiosis, and in tumorigenesis, emphasizing associated signaling pathways. We describe data supporting the hypothesis that Akirins act as a "bridge" between a variety of transcription factors and major chromatin remodeling complexes, and discuss several important questions remaining to be addressed. In little more than a decade, Akirin proteins have gone from being completely unknown to being increasingly recognized as evolutionarily conserved mediators of gene expression programs essential for the formation and function of animals.
Dual Function of Primary Somatosensory Cortex in Cognitive Control of Language: Evidence from Resting State fMRI.
Neuroscience, 2020

Resting state functional connectivity can be leveraged to investigate bilingual individual differences in cognitive control of language; however, thus far no report is provided on how the connectivity profiles of brain functional networks at rest point to different language control behavior in bilinguals. In order to address this gap in state-of-the-art research we did a functional connectivity analysis on the resting state data acquired via multiband EPI to investigate three resting state networks of interest namely, the frontoparietal network (FPN), the salience network (SN), and the default mode network (DMN), which are related to cognitive control, between two groups of Dutch-English bilinguals based on how they performed in a language switching task. Results demonstrated that there is the increased coupling of the left primary somatosensory cortex with the dorsolateral prefrontal cortex in the group with better performance in cognitive control of language and the increased coupling of the right primary somatosensory cortex with the inferior parietal cortex in the group with poorer performance in this executive function. As regards these results, we claim that the primary somatosensory cortex has a dual function in coupling with the dorsolateral prefrontal cortex and the inferior parietal cortex in the FPN, and in fact, in what characterizes bilingual individual differences in cognitive control of language in healthy participants. The results of this study provide a model for future research in cognitive control of language and may serve as a reference in clinical neuroscience when bilinguals are diagnosed with dysfunction in cognitive control.
Blindness, Psychosis, and the Visual Construction of the World.
Schizophrenia bulletin, 2020

The relationship between visual loss and psychosis is complex: congenital visual loss appears to be protective against the development of a psychotic disorder, particularly schizophrenia. In later life, however, visual deprivation or visual loss can give rise to hallucinosis, disorders of visual insight such as blindsight or Anton syndrome, or, in the context of neurodegenerative disorders, more complex psychotic presentations. We draw on a computational psychiatric approach to consider the foundational role of vision in the construction of representations of the world and the effects of visual loss at different developmental stages. Using a Bayesian prediction error minimization model, we describe how congenital visual loss may be protective against the development of the kind of computational deficits postulated to underlie schizophrenia, by increasing the precision (and consequent stability) of higher-level (including supramodal) priors, focusing on visual loss-induced changes in NMDA receptor structure and function as a possible mechanistic substrate. In simple terms, we argue that when people cannot see from birth, they rely more heavily on the context they extract from the other senses, and the resulting model of the world is more impervious to the false inferences, made in the face of inevitably noisy perceptual input, that characterize schizophrenia. We show how a Bayesian prediction error minimization framework can also explain the relationship between later visual loss and other psychotic symptoms, as well as the effects of visual deprivation and hallucinogenic drugs, and outline experimentally testable hypotheses generated by this approach.
Threat, hostility and violence in childhood and later psychotic disorder: population-based case-control study.
The British journal of psychiatry : the journal of mental science, 2020

A growing body of research suggests that childhood adversities are associated with later psychosis, broadly defined. However, there remain several gaps and unanswered questions. Most studies are of low-level psychotic experiences and findings cannot necessarily be extrapolated to psychotic disorders. Further, few studies have examined the effects of more fine-grained dimensions of adversity such as type, timing and severity.
Subsampled brain MRI reconstruction by generative adversarial neural networks.
Medical image analysis, 2020

A main challenge in magnetic resonance imaging (MRI) is speeding up scan time. Beyond improving patient experience and reducing operational costs, faster scans are essential for time-sensitive imaging, such as fetal, cardiac, or functional MRI, where temporal resolution is important and target movement is unavoidable, yet must be reduced. Current MRI acquisition methods speed up scan time at the expense of lower spatial resolution and costlier hardware. We introduce a practical, software-only framework, based on deep learning, for accelerating MRI acquisition, while maintaining anatomically meaningful imaging. This is accomplished by MRI subsampling followed by estimating the missing k-space samples via generative adversarial neural networks. A generator-discriminator interplay enables the introduction of an adversarial cost in addition to fidelity and image-quality losses used for optimizing the reconstruction. Promising reconstruction results are obtained from feasible sampling patterns of up to a fivefold acceleration of diverse brain MRIs, from a large publicly available dataset of healthy adult scans as well as multimodal acquisitions of multiple sclerosis patients and dynamic contrast-enhanced MRI (DCE-MRI) sequences of stroke and tumor patients. Clinical usability of the reconstructed MRI scans is assessed by performing either lesion or healthy tissue segmentation and comparing the results to those obtained by using the original, fully sampled images. Reconstruction quality and usability of the DCE-MRI sequences is demonstrated by calculating the pharmacokinetic (PK) parameters. The proposed MRI reconstruction approach is shown to outperform state-of-the-art methods for all datasets tested in terms of the peak signal-to-noise ratio (PSNR), the structural similarity index (SSIM), as well as either the mean squared error (MSE) with respect to the PK parameters, calculated for the fully sampled DCE-MRI sequences, or the segmentation compatibility, measured in terms of Dice scores and Hausdorff distance. The code is available on GitHub.
Gulliver's virtual travels: active embodiment in extreme body sizes for modulating our body representations.
Cognitive processing, 2020

It is noted that the perceptual experience of body and space can be modulated by changing the action capabilities or by manipulating the perceived body dimensions through a multisensory stimulation. This study adds to pre-existing literature by investigating the alterations in bodily experience following embodiment to both enlarged and shrunked bodies, while participants actively navigated in a virtual environment. A normal-sized body served as a reference condition. After each embodied navigation, participants estimated the height and width of three different body parts. Results revealed that the embodiment over shrunked body induced a significant reduction in participants' body image, while no changes were reported after the embodiment over the enlarged body. Findings were discussed in terms of previous literature exploring the constraints implicated in the ownership over different bodies.
Assessment of the electrophysiological properties of the muscle fibers of a transplanted hand.
Transplantation, 2011

The muscle fibers in a transplanted hand remain denervated for a long period of time after the transplant. This prolonged inactivity may change the electrophysiological membrane properties of muscle fibers, as observed in long-term denervation. We investigated whether electrophysiological properties of the muscle fibers are preserved in a transplanted hand even after several months of denervation. Specifically, we assessed the dependence of muscle fiber conduction velocity (CV) on discharge rate in motor units of the abductor digiti minimi muscle.
Identifying neuroanatomical signatures in insomnia and migraine comorbidity.
Sleep, 2021

While insomnia and migraine are often comorbid, the shared and distinct neuroanatomical substrates underlying these disorders and the brain structures associated with the comorbidity are unknown. We aimed to identify patterns of neuroanatomical substrate alterations associated with migraine and insomnia comorbidity.
Welcome to Neurology: Genetics.
Neurology. Genetics, 2015

The powers of human genetics and genetic technologies have transformed the complexities of neurology and neuroscience at the basic, translational, and now also the clinical level. We have left an era of black and white views of causative genetic variation and are entering a period of more than 50 shades of grey, fascinated with DNA variants that increase or decrease risk, epigenetic modification, and an unexpectedly large number of variants of unknown or potentially pathogenic significance. Loss-of-function alleles and even complete human gene knockouts for certain genes appear to be compatible with a normal phenotype.
Influences on help-seeking decisions for behavioral child sleep problems: Why parents do and do not seek help.
Clinical child psychology and psychiatry, 2021

Behavioral sleep problems affect 25% of children and impact functioning, but little is known about help-seeking for these problems. We identified (1) predictors for sleep problem perception and help-seeking, using nested-logit regression and (2) reasons why parents did not seek professional help for sleep problems, using chi-square.
Cross-Frequency Phase-Amplitude Coupling between Hippocampal Theta and Gamma Oscillations during Recall Destabilizes Memory and Renders It Susceptible to Reconsolidation Disruption.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2020

Avoidance memory reactivation at recall triggers theta-gamma hippocampal phase amplitude coupling (hPAC) only when it elicits hippocampus-dependent reconsolidation. However, it is not known whether there is a causal relationship between these phenomena. We found that in adult male Wistar rats, silencing the medial septum during recall did not affect avoidance memory expression or maintenance but abolished hPAC and the amnesia caused by the intrahippocampal administration of reconsolidation blockers, both of which were restored by concomitant theta burst stimulation of the fimbria-fornix pathway. Remarkably, artificial hPAC generated by fimbria-fornix stimulation during recall of a learned avoidance response naturally resistant to hippocampus-dependent reconsolidation made it susceptible to reactivation-dependent amnesia. Our results indicate that hPAC mediates the destabilization required for avoidance memory reconsolidation and suggest that the generation of artificial hPAC at recall overcomes the boundary conditions of this process.
Stage-specific links between plasma neurofilament light and imaging biomarkers of Alzheimer's disease.
Brain : a journal of neurology, 2020

Neurofilament light (NfL) is a marker of neuroaxonal injury, a prominent feature of Alzheimer's disease. It remains uncertain, however, how it relates to amyloid and tau pathology or neurodegeneration across the Alzheimer's disease continuum. The aim of this study was to investigate how plasma NfL relates to amyloid and tau PET and MRI measures of brain atrophy in participants with and without cognitive impairment. We retrospectively examined the association between plasma NfL and MRI measures of grey/white matter volumes in the Alzheimer's Disease Neuroimaging Initiative [ADNI: n = 1149; 382 cognitively unimpaired control subjects and 767 cognitively impaired participants (mild cognitive impairment n = 420, Alzheimer's disease dementia n = 347)]. Longitudinal plasma NfL was measured using single molecule array (Simoa) technology. Cross-sectional associations between plasma NfL and PET amyloid and tau measures were independently assessed in two cohorts: ADNI [n = 198; 110 cognitively unimpaired, 88 cognitively impaired (MCI n = 67, Alzheimer's disease dementia n = 21), data accessed October 2018]; and Translational Biomarkers in Aging and Dementia [TRIAD, n = 116; 74 cognitively unimpaired, 42 cognitively impaired (MCI n = 16, Alzheimer's disease dementia n = 26), data obtained November 2017 to January 2019]. Associations between plasma NfL and imaging-derived measures were examined voxel-wise using linear regression (cross-sectional) and linear mixed effect models (longitudinal). Cross-sectional analyses in both cohorts showed that plasma NfL was associated with PET findings in brain regions typically affected by Alzheimer's disease; associations were specific to amyloid PET in cognitively unimpaired and tau PET in cognitively impaired (P < 0.05). Longitudinal analyses showed that NfL levels were associated with grey/white matter volume loss; grey matter atrophy in cognitively unimpaired was specific to APOE ε4 carriers (P < 0.05). These findings suggest that plasma NfL increases in response to amyloid-related neuronal injury in preclinical stages of Alzheimer's disease, but is related to tau-mediated neurodegeneration in symptomatic patients. As such, plasma NfL may a useful measure to monitor effects in disease-modifying drug trials.