rudyvdbrink/CitationDatabase huggingface dataset:
Sleep-wake regulation and the hallmarks of the pathogenesis of Alzheimer's disease.
Sleep, 2019

While efficient treatments for Alzheimer's disease (AD) remain elusive, a growing body of research has highlighted sleep-wake regulation as a potential modifiable factor to delay disease progression. Evidence accumulated in recent years is pointing toward a tight link between sleep-wake disruption and the three main hallmarks of the pathogenesis of AD, i.e. abnormal amyloid-beta (Aβ) and tau proteins accumulation, and neurodegeneration. However, all three hallmarks are rarely considered together in the same study. In this review, we gather and discuss findings in favor of an association between sleep-wake disruption and each AD hallmark in animal models and in humans, with a focus on the preclinical stages of the disease. We emphasize that these relationships are likely bidirectional for each of these hallmarks. Altogether, current findings provide strong support for considering sleep-wake disruption as a true risk factor in the early unfolding of AD, but more research integrating recent technical advances is needed, particularly with respect to tau protein and neurodegeneration. Interventional longitudinal studies among cognitively healthy older individuals should assess the practical use of improving sleep-wake regulation to slow down the progression of AD pathogenesis.
Differential effects of imipramine and phenelzine on corticosteroid receptor gene expression in mouse brain: potential relevance to antidepressant response.
Brain research, 2008

Although glucocorticoid feedback sensitivity of the hypothalamic-pituitary-adrenal (HPA) axis is frequently impaired in depression, atypical depression may exhibit increased feedback sensitivity. Because monoamine oxidase inhibitors (MAOI) are often more effective than tricyclic antidepressants (TCA) for atypical depression, we hypothesized that to normalize HPA function in atypical depression, MAOI would differ from TCA in decreasing rather than increasing feedback sensitivity. Consistent with this hypothesis and prior evidence for opposing effects on HPA feedback in mice, we report contrasting effects of chronic MAOI (phenelzine) and TCA (imipramine) treatment on neural corticosteroid receptor gene expression in adrenalectomized male C57BL/6 mice with fixed glucocorticoid levels. Our findings corroborate prior reports of antidepressant-induced increases in hippocampal mineralocorticoid (MR) and glucocorticoid receptor (GR) expression. However, hippocampal effects were neither sustained nor representative of effects in other brain regions. Imipramine typically increased and phenelzine decreased GR expression in other feedback-related brain regions such as the paraventricular hypothalamus and prefrontal cortex. Imipramine effects were limited to feedback-related regions, whereas phenelzine had additional effects to decrease accumbens GR and central amygdala MR expression. Our results suggest an expansion of the corticosteroid receptor hypothesis of depression to include drug- and brain region-specific actions of antidepressants to decrease as well as increase corticosteroid receptor expression and feedback sensitivity. Our findings further suggest how antidepressants could improve glucocorticoid regulation of HPA activity without also facilitating the adverse effects of glucocorticoids on mood.
Concurrent exergaming and transcranial direct current stimulation to improve balance in people with Parkinson's disease: study protocol for a randomised controlled trial.
Trials, 2018

People with Parkinson's disease (PD) commonly experience postural instability, resulting in poor balance and an increased risk of falls. Exercise-based video gaming (exergaming) is a form of physical training that is delivered through virtual reality technology to facilitate motor learning and is efficacious in improving balance in aged populations. In addition, studies have shown that anodal transcranial direct current stimulation (a-tDCS), when applied to the primary motor cortex, can augment motor learning when combined with physical training. However, no studies have investigated the combined effects of exergaming and tDCS on balance in people with PD.
Capacity to provide informed consent among adults with bipolar disorder.
Journal of affective disorders, 2019

Identifying correlates of capacity to provide informed consent among individuals with bipolar disorder is essential for patient protection. As part of a clinical trial involving approved, standard treatments, we investigated relationships between clinical characteristics and capacity to provide informed consent in adults with bipolar disorder using the MacArthur Competence Assessment Tool for Clinical Research (MacCAT-CR). After administering the MacCAT-CR, continuing participants in the trial were capable of and provided informed consent.
Age differences in DSM-IV borderline personality disorder symptom expression: Results from a national study using item response theory (IRT).
Journal of psychiatric research, 2019

Limited literature suggests that there may be age-related differences in borderline personality disorder (BPD) symptom expression. The present study used item response theory (IRT) methods to examine whether there are age differences in the likelihood of endorsing DSM-IV symptoms of BPD, when equating for levels of BPD symptom severity. Data were drawn from a nationally representative survey of adults in the US (n = 34,653), the second wave of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC). We found that 7 out of the 9 DSM-IV symptoms of BPD were age invariant. However, there were statistically and clinically significant differences between the oldest and youngest age groups in two BPD symptoms: oldest adult women were less likely to report suicidal/self-harm behavior than the youngest adult women across levels of BPD severity and unstable/intense interpersonal relationships discriminated BPD severity better in the youngest age group compared to the oldest age group in both genders. Overall, our findings indicate substantial age-related differences in BPD symptom expression. Mental health care providers should be alert to these two age-related differences in BPD symptom expression when making assessment and treatment decisions across adult age groups.
The Complex Relationships between Sex and the Brain.
The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry, 2020

In the past decennia, our understanding of the sexual differentiation of the mammalian brain has dramatically changed. The simple model according to which testosterone masculinizes the brain of males away from a default female form, was replaced with a complex scenario, according to which sex effects on the brain of both females and males are exerted by genetic, hormonal, and environmental factors. These factors act via multiple partly independent mechanisms that may vary according to internal and external factors. These observations led to the "mosaic" hypothesis-the expectation of high variability in the degree of "maleness"/"femaleness" of different features within a single brain. Here, we briefly review animal data that form the basis of current understanding of sexual differentiation; present, in this context, the results of co-analyses of human brain measures obtained by magnetic resonance imaging or postmortem; discuss criticisms and controversies of the mosaic hypothesis and implications for research; and conclude that co-analysis of several (preferably, many) features and going back from the group level to that of the individual would advance our understanding of the relations between sex and the brain in health and disease.
Homeostatic Plasticity Scales Dendritic Spine Volumes and Changes the Threshold and Specificity of Hebbian Plasticity.
iScience, 2018

Information is encoded in neural networks through changes in synaptic weights. Synaptic learning rules involve a combination of rapid Hebbian plasticity and slower homeostatic synaptic plasticity that regulates neuronal activity through global synaptic scaling. Hebbian and homeostatic plasticity have been extensively investigated, whereas much less is known about their interaction. Here we investigated structural and functional consequences of homeostatic plasticity at dendritic spines of mouse hippocampal neurons. We found that prolonged activity blockade induced spine growth, paralleling synaptic strength increases. Following activity blockade, glutamate uncaging-mediated stimulation at single spines led to size-dependent structural potentiation: smaller spines underwent robust growth, whereas larger spines remained unchanged. Moreover, spines near the stimulated spine exhibited volume changes following homeostatic plasticity, indicating that there was a breakdown of input specificity following homeostatic plasticity. Overall, these findings demonstrate that Hebbian and homeostatic plasticity interact to shape neural connectivity through non-uniform structural plasticity at inputs.
Autacoid 14S,21R-dihydroxy-docosahexaenoic acid counteracts diabetic impairment of macrophage prohealing functions.
The American journal of pathology, 2011

Impaired macrophage functions imposed by diabetic complications and the suppressed formation of 14S,21R-dihydroxydocosa-4Z,7Z,10Z,12E,16Z,19Z-hexaenoic acid (14S,21R-diHDHA) in wounds contribute significantly to deficient wound healing in diabetics, but how are macrophage functions and 14S,21R-diHDHA formation associated? We studied 14S,21R-diHDHA generation from macrophages using liquid chromatography/mass spectrometry. The role in macrophage-mediated wound healing functions was determined using a murine splinted excisional wound healing model and in vitro assays. 14S,21R-diHDHA acts as a macrophage-generated autacoid, and its attenuated formation in macrophages of diabetic db/db mice was accompanied by impairment of macrophage prohealing functions. 14S,21R-diHDHA restored db/db macrophage-impaired prohealing functions by promoting wound re-epithelialization, formulation of granulation tissue, and vascularization. Additionally, 12/15-lipoxygenase-deficient macrophages, which are unable to produce 14S,21R-diHDHA, exhibited impaired prohealing functions, which also were restored by 14S,21R-diHDHA treatment. The molecular mechanism for 14S,21R-diHDHA-induced recovery of impaired prohealing functions of db/db macrophages involves enhancing their secretion of vascular endothelial growth factor and platelet-derived growth factor BB, decreasing hyperglycemia-induced generation of reactive oxygen species, and increasing IL-10 expression under inflammatory stimulation. Taken together, these results indicate that deficiency of 14S,21R-diHDHA formation by diabetic macrophages contributes to their impaired prohealing functions. Our findings provide mechanistic insights into wound healing in diabetics and suggest the possibility of using autologous macrophages/monocytes, treated with 14S,21R-diHDHA, or related compounds, to promote diabetes-impaired wound healing.
The role of granulocyte-colony stimulating factor (G-CSF) in the healthy brain: a characterization of G-CSF-deficient mice.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009

Granulocyte-colony stimulating factor (G-CSF) is a hematopoietic growth factor that controls proliferation and differentiation of neural stem cells. Although recent studies have begun to explore G-CSF-related mechanisms of action in various disease models, little is known about its function in the healthy brain. In the present study, the effect of G-CSF deficiency on memory formation and motor skills was investigated. The impact of G-CSF deficiency on the structural integrity of the hippocampus was evaluated by analyzing the generation of doublecortin-expressing cells, the amount of bromodeoxyurine-labeled cells, the dendritic complexity in hippocampal neurons, the binding densities of NMDA and GABA(A) receptors and the induction of long-term potentiation (LTP). G-CSF deficiency caused a disruption in memory formation and in the development of motor skills. These impairments were associated with reduced ligand binding densities of NMDA receptors in hippocampal subfields CA3 and the dentate gyrus. The reduced excitation was potentiated by increased ligand binding densities of GABA(A) receptors resulting in a relative shift in favor of inhibition and impaired behavioral performance. These alterations were accompanied by impaired induction of LTP in the CA1 region. Moreover, G-CSF deficiency led to decreased dendritic complexity in hippocampal neurons in the dentate gyrus and the CA1 region. G-CSF deficiency also caused a reduction of neuronal precursor cells in the dentate gyrus. These findings confirm G-CSF as an essential neurotrophic factor, and point to a role in the proliferation, differentiation and functional integration of neural cells necessary for the structural and functional integrity of the hippocampal formation.
Functional role of striatal A2A, D2, and mGlu5 receptor interactions in regulating striatopallidal GABA neuronal transmission.
Journal of neurochemistry, 2016

In this study, the functional role of individual striatal receptors for adenosine (A2AR), dopamine (D2R), and the metabotropic glutamate receptor mGlu5R in regulating rat basal ganglia activity was characterized in vivo using dual-probe microdialysis in freely moving rats. In particular, intrastriatal perfusion with the D2R agonist quinpirole (10 μM, 60 min) decreased ipsilateral pallidal GABA and glutamate levels, whereas intrastriatal CGS21680 (A2AR agonist; 1 μM, 60 min) was ineffective on either pallidal GABA and glutamate levels or the quinpirole-induced effects. Intrastriatal perfusion with the mGlu5R agonist (RS)-2-chloro-5-hydroxyphenylglycine (600 μM, 60 min), by itself ineffective on pallidal GABA and glutamate levels, partially counteracted the effects of quinpirole. When combined with CGS21680 (1 μM, 60 min), (RS)-2-chloro-5-hydroxyphenylglycine (CHPG; 600 μM, 60 min) fully counteracted the quinpirole (10 μM, 60 min)-induced reduction in ipsilateral pallidal GABA and glutamate levels. These effects were fully counteracted by local perfusion with the mGlu5R antagonist MPEP (300 μM) or the A2AR antagonist ZM 241385 (100 nM). These results suggest that A2ARs and mGlu5Rs interact synergistically in modulating the D2R-mediated control of striatopallidal GABA neurons. Using dual-probe microdialysis, we characterized the functional role of striatal adenosine A2A receptor (A2AR), dopamine D2 receptor (D2R), and metabotropic glutamate receptor 5 (mGluR5) interactions in regulating rat basal ganglia activity. The results suggest the possible usefulness of using an A2AR antagonist and mGluR5 antagonist combination in the treatment of Parkinson's disease to increase the inhibitory D2 signaling on striatopallidal GABA neurons.
Achievement of optimal medical therapy goals for U.S. adults with coronary artery disease: results from the REGARDS Study (REasons for Geographic And Racial Differences in Stroke).
Journal of the American College of Cardiology, 2014

In a nonclinical trial setting, we sought to determine the proportion of individuals with coronary artery disease (CAD) with optimal risk factor levels based on the COURAGE (Clinical Outcomes Utilizing Revascularization and Aggressive DruG Evaluation) trial.
An attachment theoretical perspective for the neural representation of close others.
Social cognitive and affective neuroscience, 2019

Recent investigations in neuroscience elucidate the neural basis of close other cognitive representations, which serve functions central to our health and happiness. Yet, there are persistent barriers to this research, including disparate research methods and the absence of a common theoretical background. The present review connects neuroimaging and attachment theory within a novel social, cognitive and affective framework. We apply attachment theory to understand why we would expect cognitive representations of close others to be different from other social neural representations. Developing reliable markers of attachment is a critical step in mapping close other neural representations. We then examine existing neuroimaging literature on close other representations, highlighting the recruitment of neural systems supporting reward, motivation and distress alleviation, in addition to the mirror neuron system, default network and salience network. We then review the methodologies of past studies, revealing a diverse array of self-report measures assessing `closeness' and social cognitive tasks that, taken together, preclude meaningful synthesis of findings. Lastly, we discuss specific behavioral measures of attachment and closeness with recommendations for the field. This attachment framework integrates brain and behavioral sciences and unites theoretical principles with empirical methods to further our understanding of how the brain represents close others.
Network medicine links SARS-CoV-2/COVID-19 infection to brain microvascular injury and neuroinflammation in dementia-like cognitive impairment.
Alzheimer's research & therapy, 2021

Dementia-like cognitive impairment is an increasingly reported complication of SARS-CoV-2 infection. However, the underlying mechanisms responsible for this complication remain unclear. A better understanding of causative processes by which COVID-19 may lead to cognitive impairment is essential for developing preventive and therapeutic interventions.
High-saturated fat-sucrose feeding affects lactation energetics in control mice and mice selectively bred for high wheel-running behavior.
American journal of physiology. Regulatory, integrative and comparative physiology, 2013

Feeding a diet high in fat and sucrose (HFS) during pregnancy and lactation is known to increase susceptibility to develop metabolic derangements later in life. A trait for increased behavioral activity may oppose these effects, since this would drain energy from milk produced to be made available to the offspring. To investigate these interactions, we assessed several components of behavioral energetics during lactation in control mice (C) and in mice of two lines selectively bred for high wheel-running activity (S1, S2) subjected to a HFS diet or a low-fat (LF) diet. Energy intake, litter growth, and milk energy output at peak lactation (MEO; assessed by subtracting maternal metabolic rate from energy intake) were elevated in HFS-feeding dams across all lines compared with the LF condition, an effect that was particularly evident in the S dams. This effect was not preceded by improved lactation behaviors assessed between postnatal days 1 and 7 (PND 1-7). In fact, S1 dams had less high-quality nursing, and S2 dams showed poorer pup retrieval than C dams during PND 1-7, and S dams had generally higher levels of physical activity at peak lactation. These data demonstrate that HFS feeding increases MEO underlying increased litter and pup growth, particularly in mice with a trait for increased behavioral physical activity.
Exploring the putative role of kallikrein-6, calpain-1 and cathepsin-D in the proteolytic degradation of α-synuclein in multiple system atrophy.
Neuropathology and applied neurobiology, 2019

There is evidence that accumulation of α-synuclein (α-syn) in Parkinson's disease (PD) and dementia with Lewy bodies (DLB) results from impaired removal of α-syn rather than its overproduction. Kallikrein-6 (KLK6), calpain-1 (CAPN1) and cathepsin-D (CTSD) are among a small number of proteases that cleave α-syn and are dysregulated in PD and DLB. Our aim in this study was to determine whether protease activity is altered in another α-synucleinopathy, multiple system atrophy (MSA), and might thereby modulate the regional distribution of α-syn accumulation.
Dynamic Network Communication in the Human Functional Connectome Predicts Perceptual Variability in Visual Illusion.
Cerebral cortex (New York, N.Y. : 1991), 2018

Ubiquitous variability between individuals in visual perception is difficult to standardize and has thus essentially been ignored. Here we construct a quantitative psychophysical measure of illusory rotary motion based on the Pinna-Brelstaff figure (PBF) in 73 healthy volunteers and investigate the neural circuit mechanisms underlying perceptual variation using functional magnetic resonance imaging (fMRI). We acquired fMRI data from a subset of 42 subjects during spontaneous and 3 stimulus conditions: expanding PBF, expanding modified-PBF (illusion-free) and expanding modified-PBF with physical rotation. Brain-wide graph analysis of stimulus-evoked functional connectivity patterns yielded a functionally segregated architecture containing 3 discrete hierarchical networks, commonly shared between rest and stimulation conditions. Strikingly, communication efficiency and strength between 2 networks predominantly located in visual areas robustly predicted individual perceptual differences solely in the illusory stimulus condition. These unprecedented findings demonstrate that stimulus-dependent, not spontaneous, dynamic functional integration between distributed brain networks contributes to perceptual variability in humans.
Regulation of subcellular dendritic synapse specificity by axon guidance cues.
eLife, 2019

Neural circuit assembly occurs with subcellular precision, yet the mechanisms underlying this precision remain largely unknown. Subcellular synaptic specificity could be achieved by molecularly distinct subcellular domains that locally regulate synapse formation, or by axon guidance cues restricting access to one of several acceptable targets. We address these models using two
TMS-Induced Central Motor Conduction Time at the Non-Infarcted Hemisphere Is Associated with Spontaneous Motor Recovery of the Paretic Upper Limb after Severe Stroke.
Brain sciences, 2021

Stroke affects the neuronal networks of the non-infarcted hemisphere. The central motor conduction time (CMCT) induced by transcranial magnetic stimulation (TMS) could be used to determine the conduction time of the corticospinal tract of the non-infarcted hemisphere after a stroke.
Visuomotor Correlates of Conflict Expectation in the Context of Motor Decisions.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2018

Many behaviors require choosing between conflicting options competing against each other in visuomotor areas. Such choices can benefit from top-down control processes engaging frontal areas in advance of conflict when it is anticipated. Yet, very little is known about how this proactive control system shapes the visuomotor competition. Here, we used electroencephalography in human subjects (male and female) to identify the visual and motor correlates of conflict expectation in a version of the Eriksen Flanker task that required left or right responses according to the direction of a central target arrow surrounded by congruent or incongruent (conflicting) flankers. Visual conflict was either highly expected (it occurred in 80% of trials; mostly incongruent blocks) or very unlikely (20% of trials; mostly congruent blocks). We evaluated selective attention in the visual cortex by recording target- and flanker-related steady-state visual-evoked potentials (SSVEPs) and probed action selection by measuring response-locked potentials (RLPs) in the motor cortex. Conflict expectation enhanced accuracy in incongruent trials, but this improvement occurred at the cost of speed in congruent trials. Intriguingly, this behavioral adjustment occurred while visuomotor activity was less finely tuned: target-related SSVEPs were smaller while flanker-related SSVEPs were higher in mostly incongruent blocks than in mostly congruent blocks, and incongruent trials were associated with larger RLPs in the ipsilateral (nonselected) motor cortex. Hence, our data suggest that conflict expectation recruits control processes that augment the tolerance for inappropriate visuomotor activations (rather than processes that downregulate their amplitude), allowing for overflow activity to occur without having it turn into the selection of an incorrect response.