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Parkinson Disease: HELP
Articles by Bart F. L. van Nuenen
Based on 8 articles published since 2010
(Why 8 articles?)
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Between 2010 and 2020, B. F. L. van Nuenen wrote the following 8 articles about Parkinson Disease.
 
+ Citations + Abstracts
1 Review Angiogenin variants in Parkinson disease and amyotrophic lateral sclerosis. 2011

van Es, Michael A / Schelhaas, Helenius J / van Vught, Paul W J / Ticozzi, Nicola / Andersen, Peter M / Groen, Ewout J N / Schulte, Claudia / Blauw, Hylke M / Koppers, Max / Diekstra, Frank P / Fumoto, Katsumi / LeClerc, Ashley Lyn / Keagle, Pamela / Bloem, Bastiaan R / Scheffer, Hans / van Nuenen, Bart F L / van Blitterswijk, Marka / van Rheenen, Wouter / Wills, Anne-Marie / Lowe, Patrick P / Hu, Guo-fu / Yu, Wenhao / Kishikawa, Hiroko / Wu, David / Folkerth, Rebecca D / Mariani, Claudio / Goldwurm, Stefano / Pezzoli, Gianni / Van Damme, Philip / Lemmens, Robin / Dahlberg, Caroline / Birve, Anna / Fernández-Santiago, Rubén / Waibel, Stefan / Klein, Christine / Weber, Markus / van der Kooi, Anneke J / de Visser, Marianne / Verbaan, Dagmar / van Hilten, Jacobus J / Heutink, Peter / Hennekam, Eric A M / Cuppen, Edwin / Berg, Daniela / Brown, Robert H / Silani, Vincenzo / Gasser, Thomas / Ludolph, Albert C / Robberecht, Wim / Ophoff, Roel A / Veldink, Jan H / Pasterkamp, R Jeroen / de Bakker, Paul I W / Landers, John E / van de Warrenburg, Bart P / van den Berg, Leonard H. ·Department of Neurology, Rudolf Magnus Institute of Neuroscience, University Medical Center Utrecht, The Netherlands. ·Ann Neurol · Pubmed #22190368.

ABSTRACT: OBJECTIVE: Several studies have suggested an increased frequency of variants in the gene encoding angiogenin (ANG) in patients with amyotrophic lateral sclerosis (ALS). Interestingly, a few ALS patients carrying ANG variants also showed signs of Parkinson disease (PD). Furthermore, relatives of ALS patients have an increased risk to develop PD, and the prevalence of concomitant motor neuron disease in PD is higher than expected based on chance occurrence. We therefore investigated whether ANG variants could predispose to both ALS and PD. METHODS: We reviewed all previous studies on ANG in ALS and performed sequence experiments on additional samples, which allowed us to analyze data from 6,471 ALS patients and 7,668 controls from 15 centers (13 from Europe and 2 from the USA). We sequenced DNA samples from 3,146 PD patients from 6 centers (5 from Europe and 1 from the USA). Statistical analysis was performed using the variable threshold test, and the Mantel-Haenszel procedure was used to estimate odds ratios. RESULTS: Analysis of sequence data from 17,258 individuals demonstrated a significantly higher frequency of ANG variants in both ALS and PD patients compared to control subjects (p = 9.3 × 10(-6) for ALS and p = 4.3 × 10(-5) for PD). The odds ratio for any ANG variant in patients versus controls was 9.2 for ALS and 6.7 for PD. INTERPRETATION: The data from this multicenter study demonstrate that there is a strong association between PD, ALS, and ANG variants. ANG is a genetic link between ALS and PD.

2 Article Intact working memory in non-manifesting LRRK2 carriers--an fMRI study. 2016

Thaler, Avner / Helmich, Rick C / Or-Borichev, Ayelet / van Nuenen, Bart F L / Shapira-Lichter, Irit / Gurevich, Tanya / Orr-Urtreger, Avi / Marder, Karen / Bressman, Susan / Bloem, Bastiaan R / Giladi, Nir / Hendler, Talma / Mirelman, Anat / Anonymous6420847. ·Movement Disorders Unit, Department of Neurology, Tel-Aviv Sourasky Medical Center, 6 Weizman Street, Tel Aviv, 64239, Israel. · Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel. · Functional Brain Center, Wohl Institute for Advanced Imaging, Tel-Aviv Sourasky Medical Center, Tel Aviv, Israel. · Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Centre, Nijmegen, The Netherlands. · Department of Neurology, Catharina Hospital, Eindhoven, The Netherlands. · Genetic Institute, Tel-Aviv Sourasky Medical Center, Tel Aviv, Israel. · Columbia University Medical Center, Columbia University, New-York, NY, USA. · Beth Israel Medical Center, New York, NY, USA. · Sieratzki Chair in Neurology, Tel Aviv University, Tel Aviv, Israel. · Sagol School for Neuroscience, Tel Aviv University, Tel Aviv, Israel. ·Eur J Neurosci · Pubmed #26536050.

ABSTRACT: Cognitive impairments are prevalent in patients with Parkinson's disease. Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are the most common cause of genetic Parkinsonism. Non-manifesting carriers of the G2019S mutation in the LRRK2 gene were found to have lower executive functions as measured by the Stroop task. This exploratory study aimed to assess whether the cognitive impairment in non-manifesting carriers is specific for executive functions or includes other cognitive domains such as working memory. We recruited 77 non-manifesting first-degree relatives of Parkinson's disease patients (38 carriers). A block-design fMRI N-back task, with 0-back, 2-back and 3-back conditions, was used in order to assess working memory. Participants were well matched on the Montreal Cognitive Assessment, University of Pennsylvania Smell Identification Test, Unified Parkinson's Disease Rating Scale part III, digit span, age, gender and Beck Depression Inventory. The task achieved the overall expected effect in both groups with longer reaction times and lower accuracy rates with increasing task demands. However, no whole-brain or region-of-interest between-groups differences were found on any of the task conditions. These results indicate that non-manifesting carriers of the G2019S mutation in the LRRK2 gene have a specific cognitive profile with executive functions, as assessed by the Stroop task, demonstrating significant impairment but with working memory, as assessed with the N-back task, remaining relatively intact. These finding shed light on the pre-motor cognitive changes in this unique 'at risk' population and should enable more focused cognitive assessments of these cohorts.

3 Article Reorganization of corticostriatal circuits in healthy G2019S LRRK2 carriers. 2015

Helmich, Rick C / Thaler, Avner / van Nuenen, Bart F L / Gurevich, Tanya / Mirelman, Anat / Marder, Karen S / Bressman, Susan / Orr-Urtreger, Avi / Giladi, Nir / Bloem, Bastiaan R / Toni, Ivan / Anonymous2510816. ·From the Centre for Cognitive Neuroimaging (R.C.H., I.T.), Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen · Department of Neurology (R.C.H., B.R.B.), Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, the Netherlands · Movement Disorders Unit, Department of Neurology (A.T., T.G., A.M., N.G.), and Genetic Institute (A.O.-U.), Tel Aviv Sourasky Medical Center · Sackler School of Medicine (A.T., T.G., A.O.-U., N.G.), Tel Aviv University, Israel · Department of Neurology (B.F.L.v.N.), Catharina Hospital, Eindhoven, the Netherlands · Columbia University (K.S.M.), Columbia University Medical Center, New York · and Beth Israel Medical Center (S.B.), New York, NY. ·Neurology · Pubmed #25540317.

ABSTRACT: OBJECTIVE: We investigated system-level corticostriatal changes in a human model of premotor Parkinson disease (PD), i.e., healthy carriers of the G2019S LRRK2 mutation that is associated with a markedly increased, age-dependent risk of developing PD. METHODS: We compared 37 asymptomatic LRRK2 G2019S mutation carriers (age range 30-78 years) with 32 matched, asymptomatic nonmutation carriers (age range 30-74 years). Using fMRI, we tested the hypothesis that corticostriatal connectivity in premotor PD shifts from severely affected to less affected striatal subregions, as shown previously in symptomatic PD. Specifically, we predicted that in premotor PD, the shift in corticostriatal connectivity would follow the same gradient of striatal dopamine depletion known from overt PD, with the dorsoposterior putamen being more affected than the ventroanterior putamen. RESULTS: The known parallel topology of corticostriatal loops was preserved in each group, but the topography of putamen connectivity shifted. In LRRK2 G2019S mutation carriers, the right inferior parietal cortex had reduced functional connectivity with the dorsoposterior putamen but increased connectivity with the ventroanterior putamen, as compared with noncarriers. This shift in functional connectivity increased with age in LRRK2 G2019S mutation carriers. CONCLUSIONS: Asymptomatic LRRK2 G2019S mutation carriers show a reorganization of corticostriatal circuits that mirrors findings in idiopathic PD. These changes may reflect premotor basal ganglia dysfunction or circuit-level compensatory changes.

4 Article A voxel-based morphometry and diffusion tensor imaging analysis of asymptomatic Parkinson's disease-related G2019S LRRK2 mutation carriers. 2014

Thaler, Avner / Artzi, Moran / Mirelman, Anat / Jacob, Yael / Helmich, Rick C / van Nuenen, Bart F L / Gurevich, Tanya / Orr-Urtreger, Avi / Marder, Karen / Bressman, Susan / Bloem, Bastiaan R / Hendler, Talma / Giladi, Nir / Ben Bashat, Dafna / Anonymous3410783. ·Movement Disorders Unit, Department of Neurology, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; Sackler School of Medicine, Sagol School for Neuroscience, Tel Aviv University, Tel Aviv, Israel. ·Mov Disord · Pubmed #24482120.

ABSTRACT: BACKGROUND: Patients with Parkinson's disease have reduced gray matter volume and fractional anisotropy in both cortical and sub-cortical structures, yet changes in the pre-motor phase of the disease are unknown. METHODS: A comprehensive imaging study using voxel-based morphometry and diffusion tensor imaging tract-based spatial statistics analysis was performed on 64 Ashkenazi Jewish asymptomatic first degree relatives of patients with Parkinson's disease (30 mutation carriers), who carry the G2019S mutation in the leucine-rich repeat kinase 2 (LRRK2) gene. RESULTS: No between-group differences in gray matter volume could be noted in either whole-brain or volume-of-interest analysis. Diffusion tensor imaging analysis did not identify group differences in white matter areas, and volume-of-interest analysis identified no differences in diffusivity parameters in Parkinson's disease-related structures. CONCLUSIONS: G2019S carriers do not manifest changes in gray matter volume or diffusivity parameters in Parkinson's disease-related structures prior to the appearance of motor symptoms.

5 Article Neural correlates of executive functions in healthy G2019S LRRK2 mutation carriers. 2013

Thaler, Avner / Mirelman, Anat / Helmich, Rick C / van Nuenen, Bart F L / Rosenberg-Katz, Keren / Gurevich, Tanya / Orr-Urtreger, Avi / Marder, Karen / Bressman, Susan / Bloem, Bastiaan R / Giladi, Nir / Hendler, Talma / Anonymous3700748. ·Movement Disorders Unit, Department of Neurology, Tel-Aviv Sourasky Medical Center, Israel; Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel. Electronic address: avnerth@gmail.com. ·Cortex · Pubmed #23357204.

ABSTRACT: INTRODUCTION: The G2019S mutation in the leucine rich repeat kinase 2 (LRRK2) gene is prevalent among Ashkenazi Jewish patients with Parkinson's disease (PD). Cognitive deficits are common in early stage PD. We aimed to characterize the effect of the G2019S mutation on neural mechanisms of executive function processing by testing whether healthy mutation carriers who are an "at risk" population for the future development of PD differed from non-carriers on an functional magnetic resonance imaging (fMRI) Stroop interference task. METHODS: Cognitive performance and task related cerebral activity were measured in 40 healthy first-degree relatives of Ashkenazi PD patients (19 carriers and 21 non-carriers of the G2019S mutation). Both regional differences in neural activity and seed region driven functional connectivity methods were performed using fMRI. RESULTS: Compared to non-carriers, mutation carriers had greater baseline deactivation and increased task related activity in the right inferior parietal lobe, right precuneus and right fusiform gyrus. Whole brain functional connectivity analysis revealed stronger coupling between these regions and both basal ganglia structures as well as cortical regions in the carrier group. Non-manifesting G2019S mutation carriers and non-carriers performed similarly on the task and on all other assessed measures, so behavioral differences in task performance and baseline cognitive functions cannot explain the observed imaging differences. CONCLUSIONS: G2019S carriers, at risk for developing PD, had similar behavioral performance as non-carriers during the Stroop task, but increased activity in brain regions that have previously been found to be part of the ventral attention system together with stronger coupling between task related areas and structures that make up the ventral and dorsal attention system as well as the basal ganglia-thalamocortical network. This suggests a neural compensatory mechanism that enables intact cognitive performance in asymptomatic mutation carriers.

6 Article Compensatory activity in the extrastriate body area of Parkinson's disease patients. 2012

van Nuenen, Bart F L / Helmich, Rick C / Buenen, Noud / van de Warrenburg, Bart P C / Bloem, Bastiaan R / Toni, Ivan. ·Radboud University Nijmegen Medical Center, Donders Institute for Brain, Cognition and Behaviour, Department of Neurology, 6500 HB Nijmegen, The Netherlands. ·J Neurosci · Pubmed #22787040.

ABSTRACT: Compensatory mechanisms are a crucial component of the cerebral changes triggered by neurodegenerative disorders. Identifying such compensatory mechanisms requires at least two complementary approaches: localizing candidate areas using functional imaging, and showing that interference with these areas has behavioral consequences. Building on recent imaging evidence, we use this approach to test whether a visual region in the human occipito-temporal cortex-the extrastriate body area-compensates for altered dorsal premotor activity in Parkinson's disease (PD) during motor-related processes. We separately inhibited the extrastriate body area and dorsal premotor cortex in 11 PD patients and 12 healthy subjects, using continuous theta burst stimulation. Our goal was to test whether these areas are involved in motor compensatory processes. We used motor imagery to isolate a fundamental element of motor planning, namely subjects' ability to incorporate the current state of their body into a motor plan (mental hand rotation). We quantified this ability through a posture congruency effect (i.e., the improvement in subjects' performance when their current body posture is congruent to the imagined movement). Following inhibition of the right extrastriate body area, the posture congruency effect was lost in PD patients, but not in healthy subjects. In contrast, inhibition of the left dorsal premotor cortex reduced the posture congruency effect in healthy subjects, but not in PD patients. These findings suggest that the right extrastriate body area plays a compensatory role in PD by supporting a function that is no longer performed by the dorsal premotor cortex.

7 Article "On" state freezing of gait in Parkinson disease: a paradoxical levodopa-induced complication. 2012

Espay, A J / Fasano, A / van Nuenen, B F L / Payne, M M / Snijders, A H / Bloem, B R. ·UC Neuroscience Institute, Department of Neurology, Gardner Family Center for Parkinson’s Disease and MovementDisorders, University of Cincinnati, Cincinnati, OH, USA. alberto.espay@uc.edu ·Neurology · Pubmed #22262741.

ABSTRACT: OBJECTIVE: To describe the phenotype of levodopa-induced "on" freezing of gait (FOG) in Parkinson disease (PD). METHODS: We present a diagnostic approach to separate "on" FOG (deterioration during the "on state") from other FOG forms. Four patients with PD with suspected "on" FOG were examined in the "off state" (>12 hours after last medication intake), "on state" (peak effect of usual medication), and "supra-on" state (after intake of at least twice the usual dose). RESULTS: Patients showed clear "on" FOG, which worsened in a dose-dependent fashion from the "on" to the "supra-on" state. Two patients also demonstrated FOG during the "off state," of lesser magnitude than during "on." In addition, levodopa produced motor blocks in hand and feet movements, while other parkinsonian features improved. None of the patients had cognitive impairment or a predating "off" FOG. CONCLUSIONS: True "on" FOG exists as a rare phenotype in PD, unassociated with cognitive impairment or a predating "off" FOG. Distinguishing the different FOG subtypes requires a comprehensive motor assessment in at least 3 medication states.

8 Minor Serum angiogenin levels are elevated in ALS, but not Parkinson's disease. 2014

van Es, Michael A / Veldink, Jan H / Schelhaas, Helenius J / Bloem, Bastiaan R / Sodaar, Peter / van Nuenen, Bart F L / Verbeek, Marcel / van de Warrenburg, Bart P / van den Berg, Leonard H. ·Department of Neurology, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, The Netherlands. · Department of Neurology, Radboud University Medical Center, Donders Institute for Brain, Cognition and Behaviour, Center for Neuroscience, Nijmegen, The Netherlands. · Department of Neurology, Radboud University Medical Center, Donders Institute for Brain, Cognition and Behaviour, Center for Neuroscience, Nijmegen, The Netherlands Department of Neurology, Catharina Hospital, Eindhoven, The Netherlands. · Department of Neurology, Radboud University Medical Center, Donders Institute for Brain, Cognition and Behaviour, Center for Neuroscience, Nijmegen, The Netherlands Department of Laboratory Medicine, Radboud University Medical Center, Nijmegen, The Netherlands. ·J Neurol Neurosurg Psychiatry · Pubmed #24876190.

ABSTRACT: -- No abstract --