Marcel M. Verbeek

ORCID: 0000-0003-4635-7876
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About
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Research Areas
  • Alzheimer's disease research and treatments
  • Dementia and Cognitive Impairment Research
  • Parkinson's Disease Mechanisms and Treatments
  • Intracerebral and Subarachnoid Hemorrhage Research
  • Metabolism and Genetic Disorders
  • Neurological disorders and treatments
  • Amyloidosis: Diagnosis, Treatment, Outcomes
  • Cerebrovascular and genetic disorders
  • Neurological Disease Mechanisms and Treatments
  • S100 Proteins and Annexins
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Amino Acid Enzymes and Metabolism
  • Mitochondrial Function and Pathology
  • Genetic Neurodegenerative Diseases
  • Neurological diseases and metabolism
  • Diet and metabolism studies
  • Amyotrophic Lateral Sclerosis Research
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Prion Diseases and Protein Misfolding
  • Sleep and related disorders
  • Nuclear Receptors and Signaling
  • Proteoglycans and glycosaminoglycans research
  • Neurological Disorders and Treatments
  • Heat shock proteins research
  • Multiple Sclerosis Research Studies

Radboud University Nijmegen
2016-2025

Radboud University Medical Center
2016-2025

University Medical Center
2012-2024

University Hospital and Clinics
2021-2024

Radboud Institute for Molecular Life Sciences
2021-2024

Max Planck Institute of Psychiatry
2024

Nia Association
2022

ID Genomics (United States)
2022

Erasmus MC
2021

Medisch Centrum Haaglanden
2021

Neurofilament light protein (NfL) is elevated in cerebrospinal fluid (CSF) of a number neurological conditions compared with healthy controls (HC) and candidate biomarker for neuroaxonal damage. The influence age sex largely unknown, levels across disorders have not been systematically to date.

10.1001/jamaneurol.2019.1534 article EN JAMA Neurology 2019-06-17

<b>Objective: </b> To determine the optimal timing of somatosensory evoked potential (SSEP) recordings and additional value clinical biochemical variables for prediction poor outcome in patients who remain comatose after cardiopulmonary resuscitation (CPR). <b>Methods: A prospective cohort study was conducted 32 intensive care units including adult still unconscious 24 hours CPR. Clinical, neurophysiologic, were recorded 24, 48, 72 CPR related to death or persisting unconsciousness 1 month....

10.1212/01.wnl.0000191308.22233.88 article EN Neurology 2006-01-10

Biochemical markers have a central position in the diagnosis and management of patients clinical medicine, also research drug development, for brain disorders, such as Alzheimer's disease. The enzyme-linked immunosorbent assay (ELISA) is frequently used measurement low-abundance biomarkers. However, quality ELISA methods varies, which may introduce both systematic random errors. This urges need more rigorous control performance, regardless its use setting, routine, or development. aim method...

10.3389/fneur.2015.00179 article EN cc-by Frontiers in Neurology 2015-08-19

<b><i>Objective:</i></b> To study the ability of glial (glial fibrillary acidic protein [GFAP] and S100b) neuronal (neuron specific enolase [NSE]) levels in peripheral blood to predict outcome after severe traumatic brain injury. <b><i>Methods:</i></b> Eighty-five patients with injury (admission Glasgow Coma Score [GCS] ≤ 8) were included. Blood samples taken at time hospital admission analyzed for S100b, GFAP, NSE. Data collected included demographic clinical variables. Outcome was assessed...

10.1212/01.wnl.0000120550.00643.dc article EN Neurology 2004-04-27

Background The cerebrospinal fluid (CSF) biomarkers amyloid β (Aβ)‐42, total‐tau (T‐tau), and phosphorylated‐tau (P‐tau) demonstrate good diagnostic accuracy for Alzheimer's disease (AD). However, there are large variations in biomarker measurements between studies, within laboratories. Association has initiated a global quality control program to estimate monitor variability of measurements, quantify batch‐to‐batch assay variations, identify sources variability. In this article, we present...

10.1016/j.jalz.2011.05.2243 article EN Alzheimer s & Dementia 2011-07-01

Glucose transporter-1 deficiency syndrome is caused by mutations in the SLC2A1 gene majority of patients and results impaired glucose transport into brain. From 2004–2008, 132 requests for mutational analysis were studied automated Sanger sequencing multiplex ligation-dependent probe amplification. Mutations detected 54 (41%) subsequently three clinically affected family members. In these 57 we identified 49 different mutations, including six multiple exon deletions, known 37 novel (13...

10.1093/brain/awp336 article EN Brain 2010-02-02
Niklas Mattsson Ulf Andréasson Staffan Persson María C. Carrillo Steven Collins and 95 more Sonia Chalbot Neal E. Cutler Diane Dufour‐Rainfray Anne M. Fagan Niels H. H. Heegaard Ging‐Yuek Robin Hsiung Bradley T. Hyman Khalid Iqbal D. Richard Lachno Alberto Lleó Piotr Lewczuk José Luís Molinuevo Piero Parchi Axel Regeniter Robert A. Rissman Hanna Rosenmann Giuseppe Sancesario Johannes Schröder Leslie M. Shaw Charlotte E. Teunissen John Q. Trojanowski Hugo Vanderstichele Manu Vandijck Marcel M. Verbeek Henrik Zetterberg Kaj Blennow Stephan A. Käser Aladro José A. Rojo Marilyn Albert Daniel Alcolea Ulf Andréasson Anna Antonell Hiroyuki Arai Silvana Archetti Eva Lagberg Arkblad Inês Baldeiras Aleš Bartoš Dev Batish Aurélie Bedel Danièle Bentué‐Ferrer Flora Berisha Sergio Bernardini Marinus A. Blankenstein Kaj Blennow Olivier Bousiges Michael C. Camuso Maria Carrillo Tiziana Casoli Sebastiano Cavallaro Sonia Chalbot Steven Collins Odete Cruz e Silva Neal E. Cutler I. Cuvelier Odile Delaroche Diane Dufour‐Rainfray Roy B. Dyer Sebastiaan Engelborghs Anne M. Fagan Anne Fogli Orestes Vicente Forlenza Nick C. Fox Giovanni B. Frisoni Daniela Galimberti Elisabetta Galloni Silvana Maria Gritti Karen H. Gylys Harald Hampel Sabine Haustein Theresa Heath Niels H. H. Heegaard Michael T. Heneka Sanna‐Kaisa Herukka David M. Holtzman Ging‐Yuek Robin Hsiung Christian Humpel Bradley T. Hyman Takeshi Iwatsubo Khalid Iqbal Claude Jardel Mathias Jucker Elisabeth Kapaki Stephan A. Käser Daniel Kidd Péter Klivényi Ryozo Kuwano D. Richard Lachno Foudil Lamari Jean Laplanche Jordan Laser Sylvian Lehmann Piotr Lewczuk Qiao‐Xin Li Alberto Lleó Walter Maetzler

Abstract Background The cerebrospinal fluid (CSF) biomarkers amyloid beta 1–42, total tau, and phosphorylated tau are used increasingly for Alzheimer's disease (AD) research patient management. However, there large variations in biomarker measurements among within laboratories. Methods Data from the first nine rounds of Association quality control program was to define extent sources analytical variability. In each round, three CSF samples prepared at Clinical Neurochemistry Laboratory...

10.1016/j.jalz.2013.01.010 article EN Alzheimer s & Dementia 2013-05-01

Increasing evidence suggests a relationship between poor sleep and the risk of developing Alzheimer disease. A previous study found an effect on β-amyloid (Aβ), which is key protein in disease pathology.To determine 1 night total deprivation cerebrospinal fluid Aβ42 levels healthy middle-aged men.The Alzheimer, Wakefulness, Amyloid Kinetics (AWAKE) at Radboud Center, randomized clinical trial that took place June 1, 2012, October 2012. Participants were cognitively normal men (40-60 years...

10.1001/jamaneurol.2014.1173 article EN JAMA Neurology 2014-06-02

This study was designed to establish the reliability of neurologic examination, neuron-specific enolase (NSE), and median nerve somatosensory-evoked potentials (SEPs) predict poor outcome in patients treated with mild hypothermia after cardiopulmonary resuscitation (CPR).This multicenter prospective cohort included adult comatose admitted intensive care unit (ICU) CPR (32-34°C). False-positive rates (FPRs 1 - specificity) their 95% confidence intervals (CIs) were calculated for pupillary...

10.1002/ana.22632 article EN Annals of Neurology 2011-09-12

Objective Sporadic inclusion body myositis (sIBM) is an inflammatory myopathy characterized by both degenerative and autoimmune features. In contrast to other myopathies, myositis‐specific autoantibodies had not been found in sIBM patients until recently. We used human skeletal muscle extracts as a source of antigens detect characterize the corresponding antigen. Methods Autoantibodies were detected immunoblotting. The target antigen was immunoaffinity‐purified from mass spectrometry. A cDNA...

10.1002/ana.23822 article EN Annals of Neurology 2012-11-29

To examine neurofilament (Nf) concentrations according to symptom onset and clinical diagnostic certainty categories of amyotrophic lateral sclerosis (ALS).We measured Nf light chain (NfL) phosphorylated heavy (pNfH) CSF NfL serum levels in patients with ALS first ≤6 months (n = 54) or >6 135) from sampling, other neurologic diseases, differential diagnoses a motor neuron disease (MND mimics), MND variants determine the accuracy early onset. Samples were received multicentric analyzed by...

10.1212/wnl.0000000000004761 article EN Neurology 2017-12-06

The small heat shock protein family (sHsp) comprises molecular chaperones able to interact with incorrectly folded proteins. Alzheimer's disease (AD) is characterized by pathological lesions such as senile plaques (SPs), cerebral amyloid angiopathy (CAA) and neurofibrillary tangles (NFTs), predominantly consisting of the proteins amyloid‐β (Aβ) tau respectively. aim this study was investigate association Hsp20, HspB2, αB‐crystallin Hsp27 AD brains. For purpose, a panel well‐characterized...

10.1111/j.1365-2990.2006.00689.x article EN Neuropathology and Applied Neurobiology 2006-02-22

<b>Objective:</b> To describe the current treatment; clinical, biochemical, and molecular findings; clinical follow-up of patients with aromatic l-amino acid decarboxylase (AADC) deficiency. <b>Method:</b> Clinical biochemical data 78 AADC deficiency were tabulated in a database pediatric neurotransmitter disorders (JAKE). A total 46 have been previously reported; 32 are described for first time. <b>Results:</b> In 96% AADC-deficient patients, symptoms (hypotonia 95%, oculogyric crises 86%,...

10.1212/wnl.0b013e3181e620ae article EN Neurology 2010-05-27

Tyrosine hydroxylase deficiency is an autosomal recessive disorder resulting from cerebral catecholamine deficiency. has been reported in fewer than 40 patients worldwide. To recapitulate all available evidence on clinical phenotypes and rational diagnostic therapeutic approaches for this devastating, but treatable, neurometabolic disorder, we studied 36 with tyrosine reviewed the literature. Based presenting neurological features, can be divided two phenotypes: infantile onset, progressive,...

10.1093/brain/awq087 article EN Brain 2010-04-29
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