Neuroscience Campus Amsterdam

Amsterdam, Netherlands

Neuroscience Campus Amsterdam

Amsterdam, Netherlands
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Piantoni G.,Netherlands Institute for Neuroscience | Poil S.-S.,Center for Neurogenomics and Cognitive Research | Linkenkaer-Hansen K.,Neuroscience Campus Amsterdam | Verweij I.M.,Netherlands Institute for Neuroscience | And 4 more authors.
Journal of Neuroscience | Year: 2013

The characteristic oscillations of the sleeping brain, spindles and slow waves, show trait-like, within-subject stability and a remarkable interindividual variability that correlates with functionally relevant measures such as memory performance and intelligence. Yet, the mechanisms underlying these interindividual differences are largely unknown. Spindles and slow waves are affected by the recent history of learning and neuronal activation, indicating sensitivity to changes in synaptic strength and thus to the connectivity of the neuronal network. Because the structural backbone of this network is formed by white matter tracts, we hypothesized that individual differences in spindles and slow waves depend on the white matter microstructure across a distributed network. We recorded both diffusion-weighted magnetic resonance images and whole-night, high-density electroencephalography and investigated whether individual differences in sleep spindle and slow wave parameters were associated with diffusion tensor imaging metrics; white matter fractional anisotropy and axial diffusivity were quantified using tract-based spatial statistics. Individuals with higher spindle power had higher axial diffusivity in the forceps minor, the anterior corpus callosum, fascicles in the temporal lobe, and the tracts within and surrounding the thalamus. Individuals with a steeper rising slope of the slow wave had higher axial diffusivity in the temporal fascicle and frontally located white matter tracts (forceps minor, anterior corpus callosum). These results indicate that the profiles of sleep oscillations reflect not only the dynamics of the neuronal network at the synaptic level, but also the localized microstructural properties of its structural backbone, the white matter tracts. © 2013 the authors.


Vriend C.,VU University Amsterdam | Pattij T.,VUmc | Van Der Werf Y.D.,VUmc | Van Der Werf Y.D.,Royal Netherlands Academy of Arts and science | And 4 more authors.
Neuroscience and Biobehavioral Reviews | Year: 2014

Depression and impulse control disorders (ICD) are two common neuropsychiatric features in Parkinson's disease (PD). Studies have revealed that both phenomena are associated with aberrations in ventral striatal dopamine signaling and concomitant dysfunction of the reward-related (limbic) cortico-striatal-thalamocortical (CSTC) circuit. Depression in PD seems associated with decreased activity in the limbic CSTC circuit, whereas ICD seem associated with increased limbic CSTC circuit activity, usually after commencing dopamine replacement therapy (DRT). Not all DRT using PD patients, however, develop symptoms of ICD, suggesting an additional underlying neurobiological susceptibility. Furthermore, the symptoms of depression and ICD frequently coincide even though they are related to seemingly contrasting limbic CSTC circuit activation states. The aim of this review is to provide an overview of the currently available literature on the neurobiology of PD-related depression and ICD and discusses possible susceptibility factors. Finally, we propose a neurobiological model that identifies ventral striatal dopaminergic denervation as a common underlying neurobiological substrate of depression and ICD and subsequent dysfunction of reward and motivation-related brain areas. © 2013 Elsevier Ltd.


Van Hemmen J.,Netherlands Institute for Neuroscience | Veltman D.J.,VU University Amsterdam | Hoekzema E.,Netherlands Institute for Neuroscience | Cohen-Kettenis P.T.,Neuroscience Campus Amsterdam | And 3 more authors.
Cerebral Cortex | Year: 2016

Sex hormones, androgens in particular, are hypothesized to play a key role in the sexual differentiation of the human brain. However, possible direct effects of the sex chromosomes, that is, XX or XY, have not been well studied in humans. Individuals with complete androgen insensitivity syndrome (CAIS), who have a 46,XY karyotype but a female phenotype due to a complete androgen resistance, enable us to study the separate effects of gonadal hormones versus sex chromosomes on neural sex differences. Therefore, in the present study, we compared 46,XY men (n = 30) and 46,XX women (n = 29) to 46,XY individuals with CAIS (n = 21) on a mental rotation task using functional magnetic resonance imaging. Previously reported sex differences in neural activation during mental rotation were replicated in the control groups, with control men showing more activation in the inferior parietal lobe than control women. Individuals with CAIS showed a female-like neural activation pattern in the parietal lobe, indicating feminization of the brain in CAIS. Furthermore, this first neuroimaging study in individuals with CAIS provides evidence that sex differences in regional brain function during mental rotation are most likely not directly driven by genetic sex, but rather reflect gonadal hormone exposure. © 2014 The Author. Published by Oxford University Press. All rights reserved.


Wolf N.I.,VU University Amsterdam | Salomons G.S.,VU University Amsterdam | Rodenburg R.J.,Radboud University Nijmegen | Pouwels P.J.W.,Neuroscience Campus Amsterdam | And 8 more authors.
Annals of Neurology | Year: 2014

Hypomyelinating disorders of the central nervous system are still a diagnostic challenge, as many patients remain without genetic diagnosis. Using magnetic resonance imaging (MRI) pattern recognition and whole exome sequencing, we could ascertain compound heterozygous mutations in RARS in 4 patients with hypomyelination. Clinical features included severe spasticity and nystagmus. RARS encodes the cytoplasmic arginyl-tRNA synthetase, an enzyme essential for RNA translation. This protein is among the subunits of the multisynthetase complex, which emerges as a key player in myelination. Ann Neurol 2014;76:134-139 © 2014 American Neurological Association.


Schomaker J.,VU University Amsterdam | Berendse H.W.,VU University Amsterdam | Foncke E.M.J.,VU University Amsterdam | van der Werf Y.D.,Neuroscience Campus Amsterdam | And 4 more authors.
Neuropsychologia | Year: 2014

Parkinson[U+05F3]s disease (PD) is characterized by a degeneration of nigrostriatal dopaminergic cells, resulting in dopamine depletion. This depletion is counteracted through dopamine replacement therapy (DRT). Dopamine has been suggested to affect novelty processing and memory, which suggests that these processes are also implicated in PD and that DRT could affect them. Objective: To investigate word learning and novelty processing in patients with PD as indexed by the P2 and P3 event-related potential components, and the role of DRT in these processes. Methods: 21 patients with PD and 21 matched healthy controls were included. Patients with PD were tested on and off DRT in two sessions in a counterbalanced design, and healthy controls were tested twice without intervention. Electroencephalogram (EEG) was measured while participants performed a word learning Von Restorff task. Results: Healthy controls showed the typical Von Restorff effect, with better memory for words that were presented in novel fonts, than for words presented in standard font. Surprisingly, this effect was reversed in the patients with PD. In line with the behavioral findings, the P3 was larger for novel than for standard font words in healthy controls, but not in patients with PD. For both groups the P2 and P3 event-related components were larger for recalled versus forgotten words. DRT did not affect these processes. Conclusions: Learning of novel information is compromised in patients with PD. Likewise, the P2 and P3 components that predict successful memory encoding are reduced in PD patients. This was true both on and off DRT, suggesting that these findings reflect abnormalities in learning and memory in PD that are not resolved by dopaminergic medication. © 2014 Elsevier Ltd.


Van Rooden S.,Leiden University | Goos J.D.C.,Neuroscience Campus Amsterdam | Van Opstal A.M.,Leiden University | Versluis M.J.,Leiden University | And 9 more authors.
Radiology | Year: 2014

Purpose: To assess the prevalence and number of cortical microinfarcts in patients with Alzheimer disease (AD) by using a 7-T magnetic resonance (MR) imaging system, to assess the independent association of cortical microinfarcts with cognitive dysfunction, and to investigate potential confounding effects of the coexisting presence of cerebral amyloid angiopathy (CAA). Materials and Methods: The local institutional review board approved this study. In all cases, informed consent was obtained. High-spatialresolution fluid-attenuated inversion recovery and T2*-weighted images were acquired in 14 AD patients and 18 control subjects to assess the presence of microinfarcts and microbleeds. Presence of CAA was assessed according to the Boston criteria. Image analysis was performed independently by two reviewers. Mann-Whitney U test was performed to assess differences in number of microinfarcts between groups. Negative binomial regression models were used to assess the association between diagnosis of AD and diagnosis of CAA and number of microinfarcts, between diagnosis of AD and number of microbleeds and number of microinfarcts, and between cognitive function and number of microinfarcts, all corrected for age and sex. Results: Interobserver agreement was excellent for detecting microinfarcts (k = 0.91) (P < .001). Patients with AD demonstrated higher number (P = .005) of microinfarcts (mean, 7.2) compared with control subjects (mean, 1.8). Negative binomial regression models showed an independent association between AD and number of microinfarcts (P = .006) and a trend for CAA and microinfarcts (P = .052). A negative correlation was found between cognitive function and the number of microinfarcts (P = .009). Conclusion: Patients with AD show more microinfarcts than do control subjects, the number of microinfarcts correlates with global cognitive performance, and the presence of microinfarcts was mainly AD rather than CAA related. © RSNA, 2013.


Vriend C.,VUmc | Vriend C.,VU University Amsterdam | Raijmakers P.,VU University Amsterdam | Veltman D.J.,VUmc | And 8 more authors.
Journal of Neurology, Neurosurgery and Psychiatry | Year: 2014

Background Depression is a common neuropsychiatric symptom in Parkinson's disease (PD). In previous research, PD-related depression was associated with striatal dopaminergic deficits, presumably due to degeneration of brainstem dopaminergic projections. Segregated areas of the striatum are crucially involved in various parallelly arranged cortical-striatal-thalamocortical circuits and serve functions in, among others, motor control or emotion. This suggests regional specificity of dopaminergic deficits in the striatum in motor and depressive symptoms in PD. Methods In this cross-sectional retrospective study, we correlated severity scores of depressive and motor symptoms in 100 non-demented PD patients (median Hoehn and Yahr stage: 2) with dopamine loss in specific regions of the striatum as measured by [123I]FP-CIT SPECT tracer binding to the dopamine transporter (DaT). Results Depressive symptoms were related to lower DaT binding in the right caudate nucleus, while motor symptoms were associated with decreased DaT binding in the right putamen. This double dissociation was most pronounced in early-stage PD patients. Conclusions These results suggest that depressive symptoms in PD are associated with dopamine loss in the caudate nucleus, possibly related to degeneration of dopaminergic projections from the ventral tegmental area, while motor symptoms are associated with low dopamine signalling to the putamen and loss of nigrostriatal projections. This is consistent with the neuroanatomy of partially segregated cortical-striatalthalamocortical circuits and supports the role of dysfunctional associative and motivational circuits in PD-related depression.


Geytenbeek J.J.M.,VU University Amsterdam | Vermeulen R.J.,Neuroscience Campus Amsterdam | Vermeulen R.J.,VU University Amsterdam | Becher J.G.,VU University Amsterdam | And 2 more authors.
Developmental Medicine and Child Neurology | Year: 2015

Aim: To assess spoken language comprehension in non-speaking children with severe cerebral palsy (CP) and to explore possible associations with motor type and disability. Method: Eighty-seven non-speaking children (44 males, 43 females, mean age 6y 8mo, SD 2y 1mo) with spastic (54%) or dyskinetic (46%) CP (Gross Motor Function Classification System [GMFCS] levels IV [39%] and V [61%]) underwent spoken language comprehension assessment with the computer-based instrument for low motor language testing (C-BiLLT), a new and validated diagnostic instrument. A multiple linear regression model was used to investigate which variables explained the variation in C-BiLLT scores. Associations between spoken language comprehension abilities (expressed in z-score or age-equivalent score) and motor type of CP, GMFCS and Manual Ability Classification System (MACS) levels, gestational age, and epilepsy were analysed with Fisher's exact test. A p-value <0.05 was considered statistically significant. Results: Chronological age, motor type, and GMFCS classification explained 33% (R=0.577, R2=0.33) of the variance in spoken language comprehension. Of the children aged younger than 6 years 6 months, 52.4% of the children with dyskinetic CP attained comprehension scores within the average range (z-score ≥-1.6) as opposed to none of the children with spastic CP. Of the children aged older than 6 years 6 months, 32% of the children with dyskinetic CP reached the highest achievable age-equivalent score compared to 4% of the children with spastic CP. No significant difference in disability was found between CP-related variables (MACS levels, gestational age, epilepsy), with the exception of GMFCS which showed a significant difference in children aged younger than 6 years 6 months (p=0.043). Interpretation: Despite communication disabilities in children with severe CP, particularly in dyskinetic CP, spoken language comprehension may show no or only moderate delay. These findings emphasize the importance of introducing alternative and/or augmentative communication devices from early childhood. © 2014 Mac Keith Press.


Vriend C.,VU University Amsterdam | Gerrits N.J.H.M.,VU University Amsterdam | Berendse H.W.,Neuroscience Campus Amsterdam | Berendse H.W.,VU University Amsterdam | And 4 more authors.
Neurobiology of Aging | Year: 2015

Behavioral impairments in response inhibition and initiation are common in Parkinson's disease (PD) and are associated with reduced impulse control. No prior study, however, has investigated the functional correlates of response inhibition in de novo PD. Twenty-one de novo PD patients and 37 matched healthy controls performed a stop-signal task during functional magnetic resonance imaging. The results showed that PD patients, compared with healthy controls, were slower on response initiation but not inhibition. Task-related activation of the response inhibition network, including the inferior frontal gyrus, was reduced in PD patients, and the activity in the inferior frontal gyrus correlated negatively with motor symptom severity. These findings show that de novo PD patients exhibit functional deficits in the response inhibition network, which are partly related to disease pathology and already evident before commencing dopamine replacement therapy. This study provides insights into the neural underpinnings of impulse control deficits, relevant for the study of the neural vulnerability factors involved in the development of impulse control disorders in PD. © 2015 Elsevier Inc.


van Mierlo T.J.,VU University Amsterdam | Chung C.,VU University Amsterdam | Foncke E.M.,VU University Amsterdam | Berendse H.W.,VU University Amsterdam | van den Heuvel O.A.,Neuroscience Campus Amsterdam
Movement Disorders | Year: 2015

Depression and anxiety are common in Parkinson's disease (PD), and are among the non-motor symptoms that interfere with quality of life dramatically. Motor, cognitive, and affective features overlap in PD, hampering diagnosis. To shed more light on the contribution of structural brain changes to the presence of PD-related depressive symptoms, we conducted a Voxel-Based Morphometry (VBM) study. We hypothesized that depressive symptoms in PD are related to regional gray matter (GM) volume loss within the limbic circuit. We analyzed the T1-weigthed magnetic resonance imaging (MRI) images of 67 PD patients with a mean disease duration of 2.95 (±3.39) years. Scores on the Beck Depression Inventory (BDI) and GM probability maps were analyzed by regression analysis to study the association between GM volume and severity of depressive symptoms. Results are reported at both the uncorrected and the family-wise error (FWE) corrected level for multiple comparisons. The BDI scores correlated negatively with bilateral hippocampus and right amygdala volume and positively with the volume of the anterior cingulate cortex. These findings confirm the hypothesized involvement of the limbic circuit in PD-related depressive symptoms. We speculate that non-dopaminergic changes are essential in the pathophysiology of depressive symptoms in PD, because our findings suggest the involvement of extra-striatal brain regions. © 2015 International Parkinson and Movement Disorder Society.

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