rudyvdbrink/CitationDatabase huggingface dataset:
Agent-based representations of objects and actions in the monkey pre-supplementary motor area.
Proceedings of the National Academy of Sciences of the United States of America, 2019

Information about objects around us is essential for planning actions and for predicting those of others. Here, we studied pre-supplementary motor area F6 neurons with a task in which monkeys viewed and grasped (or refrained from grasping) objects, and then observed a human doing the same task. We found "action-related neurons" encoding selectively monkey's own action [self-type (ST)], another agent's action [other-type (OT)], or both [self- and other-type (SOT)]. Interestingly, we found "object-related neurons" exhibiting the same type of selectivity before action onset: Indeed, distinct sets of neurons discharged when visually presented objects were targeted by the monkey's own action (ST), another agent's action (OT), or both (SOT). Notably, object-related neurons appear to signal self and other's intention to grasp and the most likely grip type that will be performed, whereas action-related neurons encode a general goal attainment signal devoid of any specificity for the observed grip type. Time-resolved cross-modal population decoding revealed that F6 neurons first integrate information about object and context to generate an agent-shared signal specifying whether and how the object will be grasped, which progressively turns into a broader agent-based goal attainment signal during action unfolding. Importantly, shared representation of objects critically depends upon their location in the observer's peripersonal space, suggesting an "object-mirroring" mechanism through which observers could accurately predict others' impending action by recruiting the same motor representation they would activate if they were to act upon the same object in the same context.
lnc'edin to Myelin.
Neuron, 2017

Long non-coding RNAs (lncRNAs) have been implicated in numerous developmental processes. In a technical and bioinformatics tour-de-force, He et al. (2017) provide critical insight into the dynamics of lncRNA expression, function, and mechanism during oligodendrocyte development and after injury.
HDAC6 inhibition restores TDP-43 pathology and axonal transport defects in human motor neurons with TARDBP mutations.
The EMBO journal, 2021

TDP-43 is the major component of pathological inclusions in most ALS patients and in up to 50% of patients with frontotemporal dementia (FTD). Heterozygous missense mutations in TARDBP, the gene encoding TDP-43, are one of the common causes of familial ALS. In this study, we investigate TDP-43 protein behavior in induced pluripotent stem cell (iPSC)-derived motor neurons from three ALS patients with different TARDBP mutations, three healthy controls and an isogenic control. TARDPB mutations induce several TDP-43 changes in spinal motor neurons, including cytoplasmic mislocalization and accumulation of insoluble TDP-43, C-terminal fragments, and phospho-TDP-43. By generating iPSC lines with allele-specific tagging of TDP-43, we find that mutant TDP-43 initiates the observed disease phenotypes and has an altered interactome as indicated by mass spectrometry. Our findings also indicate that TDP-43 proteinopathy results in a defect in mitochondrial transport. Lastly, we show that pharmacological inhibition of histone deacetylase 6 (HDAC6) restores the observed TDP-43 pathologies and the axonal mitochondrial motility, suggesting that HDAC6 inhibition may be an interesting therapeutic target for neurodegenerative disorders linked to TDP-43 pathology.
Age- and memory- related differences in hippocampal gray matter integrity are better captured by NODDI compared to single-tensor diffusion imaging.
Neurobiology of aging, 2020

Single-tensor diffusion imaging (DTI) has traditionally been used to assess integrity of white matter. For example, we previously showed that integrity of limbic white matter tracts declines in healthy aging and relates to episodic memory performance. However, multi-compartment diffusion models may be more informative about microstructural properties of gray matter. The current study examined hippocampal gray matter integrity using both single-tensor and multi-compartment (neurite orientation dispersion and density imaging, NODDI) diffusion imaging. Younger (20-38 years) and older (59-84 years) adults also completed the Mnemonic Similarity Task to measure mnemonic discrimination performance. Results revealed age-related declines in both single-tensor (lower fractional anisotropy, higher mean diffusivity) and multi-compartment (higher restricted, hindered and free diffusion) measures of hippocampal gray matter integrity. As expected, NODDI measures (hindered and free diffusion) captured more age-related variance than DTI measures. Moreover, mnemonic discrimination of highly similar lure items in memory was related to hippocampal gray matter integrity in younger but not older adults. These findings support the notion that age-related differences in gray matter integrity are better captured by multi-compartment versus single-tensor diffusion models and show that the relationship between mnemonic discrimination and hippocampal gray matter integrity is moderated by age.
PTSD is associated with increased DNA methylation across regions of HLA-DPB1 and SPATC1L.
Brain, behavior, and immunity, 2021

Posttraumatic stress disorder (PTSD) is characterized by intrusive thoughts, avoidance, negative alterations in cognitions and mood, and arousal symptoms that adversely affect mental and physical health. Recent evidence links changes in DNA methylation of CpG cites to PTSD. Since clusters of proximal CpGs share similar methylation signatures, identification of PTSD-associated differentially methylated regions (DMRs) may elucidate the pathways defining differential risk and resilience of PTSD. Here we aimed to identify epigenetic differences associated with PTSD. DNA methylation data profiled from blood samples using the MethylationEPIC BeadChip were used to perform a DMR analysis in 187 PTSD cases and 367 trauma-exposed controls from the Grady Trauma Project (GTP). DMRs were assessed with R package bumphunter. We identified two regions that associate with PTSD after multiple test correction. These regions were in the gene body of HLA-DPB1 and in the promoter of SPATC1L. The DMR in HLA-DPB1 was associated with PTSD in an independent cohort. Both DMRs included CpGs whose methylation associated with nearby sequence variation (meQTL) and that associated with expression of their respective genes (eQTM). This study supports an emerging literature linking PTSD risk to genetic and epigenetic variation in the HLA region.
An unusual cause of stroke in a 55-year-old woman.
The International journal of neuroscience, 2014

A 55-year-old woman presented with acute onset ataxia and right-sided dysmetria. Magnetic resonance imaging (MRI) confirmed clinical suspicion of stroke. She was found to have middiastolic murmur which led to urgent echocardiogram demonstrating left atrial myxoma. She underwent prompt surgical resection. Cardiac myxoma is a very rare cause of stroke. The presentation can be varied and diagnosis can be often missed. Early surgical intervention is a definitive treatment. Our case is unique and underlines importance of eliciting accurate physical signs at bedside.
The pathophysiology of SARS-CoV-2: A suggested model and therapeutic approach.
Life sciences, 2020

In this paper, a model is proposed of the pathophysiological processes of COVID-19 starting from the infection of human type II alveolar epithelial cells (pneumocytes) by SARS-CoV-2 and culminating in the development of ARDS. The innate immune response to infection of type II alveolar epithelial cells leads both to their death by apoptosis and pyroptosis and to alveolar macrophage activation. Activated macrophages secrete proinflammatory cytokines and chemokines and tend to polarise into the inflammatory M1 phenotype. These changes are associated with activation of vascular endothelial cells and thence the recruitment of highly toxic neutrophils and inflammatory activated platelets into the alveolar space. Activated vascular endothelial cells become a source of proinflammatory cytokines and reactive oxygen species (ROS) and contribute to the development of coagulopathy, systemic sepsis, a cytokine storm and ARDS. Pulmonary activated platelets are also an important source of proinflammatory cytokines and ROS, as well as exacerbating pulmonary neutrophil-mediated inflammatory responses and contributing to systemic sepsis by binding to neutrophils to form platelet-neutrophil complexes (PNCs). PNC formation increases neutrophil recruitment, activation priming and extraversion of these immune cells into inflamed pulmonary tissue, thereby contributing to ARDS. Sequestered PNCs cause the development of a procoagulant and proinflammatory environment. The contribution to ARDS of increased extracellular histone levels, circulating mitochondrial DNA, the chromatin protein HMGB1, decreased neutrophil apoptosis, impaired macrophage efferocytosis, the cytokine storm, the toll-like receptor radical cycle, pyroptosis, necroinflammation, lymphopenia and a high Th17 to regulatory T lymphocyte ratio are detailed.
Expansion of a Specific Plasmodium falciparum PfMDR1 Haplotype in Southeast Asia with Increased Substrate Transport.
mBio, 2020

Artemisinin-based combination therapies (ACTs) have been vital in reducing malaria mortality rates since the 2000s. Their efficacy, however, is threatened by the emergence and spread of artemisinin resistance in Southeast Asia. The
Feline cognitive dysfunction as a model for Alzheimer's disease in the research of CBD as a potential treatment-a narrative review.
Journal of cannabis research, 2020

With the improvement in modern medicine, the world's human and feline (Felis catus, the domestic cat) population is aging. As the population grows older, there is an increase of age-related diseases, such as Alzheimer's disease in humans and feline cognitive dysfunction in felines, which shares many similarities with Alzheimer's disease. They both result in cognitive decline and lack effective treatments. In light of their pathological similarities, both occur at old age, and as domestic cats share the human environment and risk factors (cats are considered an indicator to the effect of environmental contaminants on humans as they share exposures and diseases), cats have the potential to be a spontaneous model for Alzheimer's disease. Classic animal models in many cases fail to predict the results in humans, and a natural model can lead to better prediction of results, thus being both time and cost-effective. The feline disease can be researched in trials that could be simultaneously clinical trials for cats and preclinical trials for humans, also referred to as reverse translational medicine. As both maladies lack effective medical intervention, new potential treatments are merited. Cannabidiol (CBD) is a promising agent that may improve the life of these patients, as it was shown to potentially treat several of the pathologies found in both conditions. yet there is a need for further research in order to establish the benefits and safety of CBD to both human and feline patients.
Chronic cannabidiol (CBD) treatment did not exhibit beneficial effects in 4-month-old male TAU58/2 transgenic mice.
Pharmacology, biochemistry, and behavior, 2020

Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive cognitive decline, motor impairments, and accumulation of hallmark proteins, amyloid-beta (Aβ) and tau. Traditionally, transgenic mouse models for AD have focused on Aβ pathology, however, recently a number of tauopathy transgenic models have been developed, including the TAU58/2 transgenic model. Cannabidiol (CBD), a non-toxic constituent of the Cannabis sativa plant, has been shown to prevent and reverse cognitive deficits in Aβ transgenic mouse models of AD. Importantly, the therapeutic properties of CBD on the behavioural phenotype of tauopathy mouse models have not been investigated. We assessed the impact of chronic CBD treatment (i.e. 50 mg/kg CBD i.p. administration starting 3 weeks prior to behavioural assessments) on disease-relevant behaviours of 4-month-old TAU58/2 transgenic males in paradigms for anxiety, motor functions, and cognition. TAU58/2 transgenic males demonstrated reduced body weight, anxiety and impaired motor functions. Furthermore, they demonstrated increased freezing in fear conditioning compared to wild type-like animals. Interestingly, both sociability and social recognition memory were intact in AD transgenic mice. Chronic CBD treatment did not affect behavioural changes in transgenic males. In summary, 4-month-old TAU58/2 transgenic males exhibited no deficits in social recognition memory, suggesting that motor deficits and changes in anxiety at this age do not impact on social domains. The moderate increase in fear-associated memory needs further investigation but could be related to differences in fear extinction. Future investigations will need to clarify CBD's therapeutic potential for reversing motor deficits in TAU58/2 transgenic mice by considering alternative CBD treatment designs including changed CBD dosing.
Macrocyclization of a Ligand Targeting a Toxic RNA Dramatically Improves Potency.
Chembiochem : a European journal of chemical biology, 2020

RNA molecules both contribute to and are causative of many human diseases. One method to perturb RNA function is to target its structure with small molecules. However, discovering bioactive ligands for RNA targets is challenging. Here, we show that the bioactivity of a linear dimeric ligand that inactivates the RNA trinucleotide repeat expansion that causes myotonic dystrophy type 1 [DM1; r(CUG)
Presence of Genetic Variants Among Young Men With Severe COVID-19.
JAMA, 2020

Severe coronavirus disease 2019 (COVID-19) can occur in younger, predominantly male, patients without preexisting medical conditions. Some individuals may have primary immunodeficiencies that predispose to severe infections caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).
Sustained Hypoxia Reduces GABAergic Modulation on NTS Neurons Sending Projections to Ventral Medulla of Rats.
Neuroscience, 2021

Peripheral chemoreflex is activated during short-term sustained hypoxia (SH), and the first synapse of these afferents is located in Nucleus Tractus Solitarius(NTS). NTS neurons projecting to the ventral lateral medulla (NTS-VLM) are part of the respiratory pathways of the chemoreflex. SH increases the magnitude of basal respiratory parameters in rats from Wistar-Hannover strain. In this study, we hypothesized that the observed changes in the respiratory pattern in response to SH were due to changes in the GABAergic modulation of the synaptic transmission of NTS-VLM neurons. We used an electrophysiological approach to record the synaptic activity of NTS neurons labeled with a retrograde tracer previously microinjected into VLM of Wistar-Hannover rats submitted to 24 h SH. The data are showing that: (a) the amplitude of evoked inhibitory currents in NTS-VLM neurons of SH rats was reduced and not accompanied by any change in rise-time and decay-time; (b) the 1/CV
Moderators of the effect of psychosocial interventions on fatigue in women with breast cancer and men with prostate cancer: Individual patient data meta-analyses.
Psycho-oncology, 2020

Psychosocial interventions can reduce cancer-related fatigue effectively. However, it is still unclear if intervention effects differ across subgroups of patients. These meta-analyses aimed at evaluating moderator effects of (a) sociodemographic characteristics, (b) clinical characteristics, (c) baseline levels of fatigue and other symptoms, and (d) intervention-related characteristics on the effect of psychosocial interventions on cancer-related fatigue in patients with non-metastatic breast and prostate cancer.
Long-term seizure and psychosocial outcome in childhood epilepsy of unknown cause.
Acta neurologica Scandinavica, 2021

The purpose was to investigate long-term prognosis of epilepsy of unknown cause with onset between ages 2 and 16 in children without any major disability, by evaluation of a previously described prognostic model and long-term follow-up of a study on the impact of duration of initial antiseizure medication (ASM) treatment.
Gastrointestinal Disorders and Risk of First-Ever Ischemic Stroke.
Stroke, 2020

Recent studies suggest that alteration of the normal gut microbiome contributes to atherosclerotic burden and cardiovascular disease. While many gastrointestinal diseases are known to cause disruption of the normal gut microbiome in humans, the clinical impact of gastrointestinal diseases on subsequent cerebrovascular disease remains unknown. We conducted an exploratory analysis evaluating the relationship between gastrointestinal diseases and ischemic stroke.
Publisher Correction: Inhibitory circuit gating of auditory critical-period plasticity.
Nature neuroscience, 2018

In the version of this article initially published online, the wrong version of Fig. 5 was used. There were errors in the statistical comparison brackets in Fig. 5c and the left-hand error bar in Fig. 5f. The errors have been corrected in the print, PDF and HTML versions of this article. In the version of this article initially published online and in print, the wrong version of Fig. 3h was used. There was a slight error in the alignment of the traces in the top right panel. The error has been corrected in the PDF and HTML versions of this article. The original and corrected figures are shown in the accompanying Publisher Correction.
Immunosuppression-related neurological disorders in kidney transplantation.
Journal of nephrology, 2021

A large number of neurological disorders can affect renal transplant recipients, potentially leading to disabling or life-threatening complications. Prevention, early diagnosis and appropriate management of these conditions are critical to avoid irreversible lesions. A pivotal role in the pathogenesis of common post-transplant neurological disorders is played by immunosuppressive therapy. The most frequently administered regimen consists of triple immunosuppression, which comprises a calcineurin inhibitor (CNI), a purine synthesis inhibitor and glucocorticoids. Some of these immunosuppressive drugs may lead to neurological signs and symptoms through direct neurotoxic effects, and all of them may be responsible for the development of tumors or opportunistic infections. In this review, after a brief summary of neurotoxic pathogenetic mechanisms encompassing recent advances in the field, we focus on the clinical presentation of more common and severe immunosuppression-related neurological complications, classifying them by characteristics of urgency and anatomic site. Our goal is to provide a general framework that addresses such clinical issues with a multidisciplinary approach, as these conditions require.
Neuroprotective Effects of Anti-proBDNF in a Rat Photothrombotic Ischemic Model.
Neuroscience, 2020

Up-regulation of proBDNF in ischemic brain and the detrimental role of proBDNF on cellular survival has already been established. We propose that the up-regulated proBDNF may trigger the harmful events and evoke a secondary ischemic damage after ischemia. This study aimed to establish the neuroprotective effects of anti-proBDNF antibody in a rat photothrombotic ischemic model. Photothrombotic ischemic model was performed on Sprague Dawley rats and anti-proBDNF antibodies were administered intraperitoneally to the ischemic rats at a dose of 5 mg/kg after 6 hours (6 h) and on 3 days (3d) after ischemia. Behavioural tests were performed for sensorimotor functional analyses. Animals were euthanized at 7d for histochemical and biochemical studies. We observed higher proBDNF expression around the ischemic infarct. Higher level of apoptosis and inflammation was evident at 7d after ischemia on brain sections. Interestingly, the anti-proBDNF treatment instigated significant reduction of the infarction size as detected by Haematoxylin and Eosin (H&E) staining. Similar reduction of apoptotic signaling proteins in western blot and immunostaining after anti-proBDNF treatment was found. Up-regulation of synaptic protein expression was also observed after this treatment. Significant sensorimotor functional improvements were also noticed at 7d after anti-proBDNF treatment. We conclude that anti-proBDNF treatment is anti-apoptotic and anti-inflammatory, and plays advantageous role in promoting cellular growth and improving sensorimotor function after ischemic insult. Taken together, our study suggests that this anti-proBDNF treatment can be considered as a therapeutic approach for ischemic recovery.
The inferior intercavernous sinus: An anatomical study with application to trans-sphenoidal approaches to the pituitary gland.
Clinical neurology and neurosurgery, 2020

The inferior intercavernous sinus is located below the pituitary gland in the sella turcica. Its presence has been controversial among anatomists because it is not always found on radiological imaging or during cadaveric dissections; however, it is becoming a better-known structure in the neurosurgical and radiological fields, specifically with respect to transsphenoidal surgery. Therefore, the present study was performed to better elucidate this structure at the skull base.
The arrow of time: Advancing insights into action control from the arrow version of the Eriksen flanker task.
Attention, perception & psychophysics, 2021

Since its introduction by B. A. Eriksen and C. W. Eriksen (Perception & Psychophysics, 16, 143-49, 1974), the flanker task has emerged as one of the most important experimental tasks in the history of cognitive psychology. The impact of a seemingly simple task design involving a target stimulus flanked on each side by a few task-irrelevant stimuli is astounding. It has inspired research across the fields of cognitive neuroscience, psychophysiology, neurology, psychiatry, and sports science. In our tribute to Charles W. ("Erik") Eriksen, we (1) review the seminal papers originating from his lab in the 1970s that launched the paradigmatic task and laid the foundation for studies of action control, (2) describe the inception of the arrow version of the Eriksen flanker task, (3) articulate the conceptual and neural models of action control that emerged from studies of the arrows flanker task, and (4) illustrate the influential role of the arrows flanker task in disclosing developmental trends in action control, fundamental deficits in action control due to neuropsychiatric disorders, and enhanced action control among elite athletes.