M Minnerop

Publications (11)32.4 Total impact

• Article: [MSA-QoL: disease-specific questionnaire to assess health-related quality of life in multiple system atrophy : Validation of the German translation].

  F Krismer, S Duerr, M Minnerop, T Klockgether, M Stamelou, K M Eggert, W H Oertel, A Schrag, W Poewe, G K Wenning
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  ABSTRACT: Multiple system atrophy (MSA) is a rapidly progressive neurodegenerative disorder which causes early sustained disability and quality of life impairment. Recently, a self-reported questionnaire focusing on MSA-specific symptoms (Multiple System Atrophy Quality of Life questionnaire, MSA-QoL) was developed in the English language. This article reports the validation of the German translation of the MSA-QoL. Translation of the MSA-QoL was implemented in a 3-tiered approach including a forward translation, a back translation and an independent review. For the validation study 38 consecutive patients with MSA according to the consensus criteria were recruited by the participating centers in a German-Austrian cohort. Data were analyzed using standard psychometric procedures. As determined by the independent review, the German translation of the MSA-QoL was classified as fully equivalent to the English version. The validation study confirmed good psychometric properties of the rating scale. The German translation of the MSA-QoL was shown to be a reliable patient-reported rating scale to determine health-related quality of life in MSA patients.
  Der Nervenarzt 06/2013; 84(6):709-14. · 0.68 Impact Factor
• Article: [The genetics of spinocerebellar ataxias.]

  H Jacobi, M Minnerop, T Klockgether
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  ABSTRACT: Spinocerebellar ataxias are genetically heterogeneous autosomal dominant ataxia disorders. To date more than 30 different subtypes are known. In Germany particularly SCA1, SCA2, SCA3 and SCA6 are prevalent, as well as the less frequent subtypes SCA5, SCA14, SCA15, SCA17 and SCA28. Genetic causes range from coding repeat expansions (polyglutamine diseases), to non-coding expansions as well as conventional mutations. In some subtypes the genetic background is currently unknown. Age of onset, typical clinical findings and geographic distribution may help to reach a correct diagnosis; however a definitive diagnosis requires molecular genetic testing.
  Der Nervenarzt 01/2013; · 0.68 Impact Factor
• Article: Sporadic adult onset ataxia of unknown etiology

  M. Abele, M. Minnerop, H. Urbach, K. Specht, T. Klockgether
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  ABSTRACT: Background The sporadic adult onset ataxias of unknown etiology (SAOA) denote the non-hereditary degenerative adult onset ataxias that are distinct from multiple system atrophy (MSA). Objective To define and characterize the clinical phenotype of sporadic adult onset ataxia of unknown etiology (SAOA). Design A survey of clinical features, nerve conduction and evoked potentials, autonomic tests, and magnetic resonance imaging (MRI)-based brain morphometry was conducted in patients with SAOA. Patients Study subjects were a consecutive sample of 27 patients (11 male, 16 female) who met the diagnostic criteria for SAOA (age 55 ± 13 years; age at disease onset 47 ± 14 years; disease duration 8 ± 7 years). Results All patients presented with a cerebellar syndrome. The most frequent extracerebellar symptoms were decreased vibration sense in 70% and decreased or absent ankle reflexes in 33% of the patients. Nerve conduction studies revealed a polyneuropathy in 26% of the patients. Somatosensory evoked potentials were abnormal in 44%, and central motor conduction time in 17% of patients. Autonomic testing revealed an affected autonomic nervous system in 58% of patients. Voxel-based brain morphometry showed a predominant reduction of gray matter in the cerebellum which was significantly correlated with disease stages. A loss of white matter was found in both middle cerebellar peduncles and the outer edge of the pons. Conclusions The data show that SAOA is a predominantly, but not exclusively cerebellar disorder. Clinical, electrophysiological, and imaging findings showed some similarities with multiple system atrophy which raises the question of an overlap of these two disorders.
  Journal of Neurology 04/2012; 254(10):1384-1389. · 3.47 Impact Factor
• Article: Sporadic adult onset ataxia of unknown etiology : a clinical, electrophysiological and imaging study.

  M Abele, M Minnerop, H Urbach, K Specht, T Klockgether
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  ABSTRACT: The sporadic adult onset ataxias of unknown etiology (SAOA) denote the non-hereditary degenerative adult onset ataxias that are distinct from multiple system atrophy (MSA). To define and characterize the clinical phenotype of sporadic adult onset ataxia of unknown etiology (SAOA). A survey of clinical features, nerve conduction and evoked potentials, autonomic tests, and magnetic resonance imaging (MRI)-based brain morphometry was conducted in patients with SAOA. Study subjects were a consecutive sample of 27 patients (11 male, 16 female) who met the diagnostic criteria for SAOA (age 55 +/- 13 years; age at disease onset 47 +/- 14 years; disease duration 8 +/- 7 years). All patients presented with a cerebellar syndrome. The most frequent extracerebellar symptoms were decreased vibration sense in 70% and decreased or absent ankle reflexes in 33% of the patients. Nerve conduction studies revealed a polyneuropathy in 26% of the patients. Somatosensory evoked potentials were abnormal in 44%, and central motor conduction time in 17% of patients. Autonomic testing revealed an affected autonomic nervous system in 58% of patients. Voxel-based brain morphometry showed a predominant reduction of gray matter in the cerebellum which was significantly correlated with disease stages. A loss of white matter was found in both middle cerebellar peduncles and the outer edge of the pons. The data show that SAOA is a predominantly, but not exclusively cerebellar disorder. Clinical, electrophysiological, and imaging findings showed some similarities with multiple system atrophy which raises the question of an overlap of these two disorders.
  Journal of Neurology 11/2007; 254(10):1384-9. · 3.47 Impact Factor
• Article: Voxel-based morphometry and voxel-based relaxometry in multiple system atrophy-a comparison between clinical subtypes and correlations with clinical parameters.

  M Minnerop, K Specht, J Ruhlmann, N Schimke, M Abele, A Weyer, U Wüllner, T Klockgether
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  ABSTRACT: Multiple system atrophy (MSA) is a neurodegenerative disease affecting basal ganglia, brainstem, cerebellum, and intermediolateral cell columns of the spinal cord. Clinically, a cerebellar (MSA-C) and a parkinsonian variant of MSA (MSA-P) are distinguished. We used voxel-based morphometry (VBM) and voxel-based relaxometry (VBR) in 48 MSA patients (32 MSA-C, 16 MSA-P) and 46 controls. In MSA-C, VBM revealed gray matter loss in cerebellum, right thalamus, both putamina and several cortical regions including insular cortex. Gray matter loss in the cerebellum and insular cortex was correlated with disease duration and severity. There was white matter loss in the brainstem, which was correlated with disease duration and severity. VBR analysis in MSA-C showed decreased relaxation rate R2 in cerebellum, pontine brainstem and cortical regions including insular cortex. In MSA-P, gray matter was reduced in cerebellum, dorsal midbrain, both putamina, and several cortical regions including insular cortex. A correlation with disease duration and severity was detected only for some small cortical areas. Direct comparison of MSA-C and MSA-P showed differences only in infratentorial brain regions where structural abnormalities were more pronounced in MSA-C than in MSA-P. In MSA-C, there was a stronger reduction of gray matter in the basal parts of the cerebellum, of white matter in the brainstem and of the relaxation rate R2 in the cerebellum and brainstem.
  NeuroImage 08/2007; 36(4):1086-95. · 5.89 Impact Factor
• Article: PET-Imaging of a4ß2* nicotinic acetylcholine receptors in the central and peripheral nervous system

  U. Wüllner, J. Bucerius, D. Gündisch, M. Minnerop, F. Jessen, A. Joe, T. Klockgether, H. Herzog, J. Schmaljohann
  Aktuelle Neurologie - AKTUEL NEUROL. 01/2006; 33.
• Article: A simple and fast method for the preparation of n.c.a. 2-[18F]F-A85380 for human use.

  J Schmaljohann, D Gündisch, M Minnerop, A Joe, J Bucerius, C Dittmar, F Jessen, S Guhlke, U Wüllner
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  ABSTRACT: 2-[18F]F-A85380 is the first subtype selective PET-radiotracer to visualize the distribution of alpha4beta2 nicotinic acetylcholine receptors in human brain in vivo. We investigated a fast and safe automated production of 2-[18F]F-A85380 by purification of the BOC-protected intermediate product with a combination of solid phase extraction cartridges. After deprotection, adjustment of the pH and sterile filtration n.c.a. 2-[18F]F-A85380 was applicable for the use in human studies with a high specific activity and an overall radiochemical yield of 55% in 35 minutes.
  Applied Radiation and Isotopes 11/2005; 63(4):433-5. · 1.17 Impact Factor
• Article: Putamen dopamine transporter and glucose metabolism are reduced in SCA17.

  M Minnerop, A Joe, Martin Lutz, P Bauer, H Urbach, C Helmstaedter, M Reinhardt, T Klockgether, U Wüllner
  Annals of Neurology 10/2005; 58(3):490-1. · 11.09 Impact Factor
• Source

  Available from: nih.gov

  Article: Dopamine transporter SPECT in patients with mitochondrial disorders.

  M Minnerop, C Kornblum, A Y Joe, K Tatsch, W S Kunz, T Klockgether, U Wüllner, M J Reinhardt
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  ABSTRACT: Mitochondrial disorders may affect basal ganglia function. In addition, decreased activity of complex I of the mitochondrial electron transport chain has been linked to the pathogenesis of dopaminergic cell loss in Parkinson's disease. Objective : To investigate the dopaminergic system in patients with known mitochondrial disorders and complex I deficiency. Dopamine transporter density was studied in 10 female patients with mitochondrial complex I deficiency by (123)I-FP-CIT (N-beta-fluoropropyl-2beta-carbomethyl-3beta-(4-iodophenyl)-nortropane) SPECT. No differences in (123)I-FP-CIT striatal binding ratios were observed and no correlation of the degree of complex I deficiency and striatal binding ratios could be detected. These data argue against the possibility that mitochondrial complex I deficiency by itself is sufficient to elicit dopaminergic cell loss.
  Journal of Neurology Neurosurgery &amp Psychiatry 02/2005; 76(1):118-20. · 4.76 Impact Factor
• Article: Imaging of central nAChReceptors with 2-[18F]F-A85380: optimized synthesis and in vitro evaluation in Alzheimer's disease.

  J Schmaljohann, M Minnerop, P Karwath, D Gündisch, P Falkai, S Guhlke, U Wüllner
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  ABSTRACT: In vivo labeling of the nicotinic acetylcholine receptors (nAChR) could be a useful tool for early diagnosis of neurodegenerative disorders. 2-[18F]F-A85380 (2-[18F]Fluoro-3-[2(S)-2-azetidinylmethoxy]pyridine), a ligand with high affinity to the beta2 subunit of the nAChRs, has been shown to label neurons in the nAChR-rich thalamus, cortex and striatum in baboons. We report an optimized synthesis resulting in an uncorrected yield of 58% in 45 min (precursor 2), enabling efficient production intended for clinical use. Incubation of normal rat brain sections with 2-[18F]F-A85380 with subsequent autoradiographic analyses showed the expected distribution in nAChR areas. In human brain sections of Alzheimer's disease (AD) a decrease of 2-[18F]F-A85380 uptake to 36% of the control group was measured in the thalamus and also in the occipital cortex. These findings suggest that 2-[18F]F-A85380 is a promising PET-ligand in the diagnosis of AD.
  Applied Radiation and Isotopes 01/2005; 61(6):1235-40. · 1.17 Impact Factor
• Article: Imaging of central nAChReceptors with 2-[ 18F]FA85380: optimized synthesis and in vitro evaluation in Alzheimer's disease

  J. Schmaljohann, M. Minnerop, P. Karwath, D. Gündisch, P. Falkai, S. Guhlke, U. Wüllner
  [show abstract] [hide abstract]
  ABSTRACT: In vivo labeling of the nicotinic acetylcholine receptors (nAChR) could be a useful tool for early diagnosis of neurodegenerative disorders. 2-[18F]F-A85380 (2-[18F]Fluoro-3-[2(S)-2-azetidinylmethoxy]pyridine), a ligand with high affinity to the β2 subunit of the nAChRs, has been shown to label neurons in the nAChR-rich thalamus, cortex and striatum in baboons. We report an optimized synthesis resulting in an uncorrected yield of 58% in 45min (precursor 2), enabling efficient production intended for clinical use. Incubation of normal rat brain sections with 2-[18F]F-A85380 with subsequent autoradiographic analyses showed the expected distribution in nAChR areas. In human brain sections of Alzheimer's disease (AD) a decrease of 2-[18F]F-A85380 uptake to 36% of the control group was measured in the thalamus and also in the occipital cortex. These findings suggest that 2-[18F]F-A85380 is a promising PET-ligand in the diagnosis of AD.
  Applied Radiation and Isotopes - APPL RADIAT ISOTOPES. 01/2004; 61(6):1235-1240.
• Article: Cerebral white matter affection in myotonic dystrophy type 1 and 2 - a diffusion-tensor-imaging study at 3T

  M Minnerop, J. C. Schoene-Bake, S. Mirbach, C Helmstaedter, B Weber, Marc Tittgemeyer, T Klockgether, C Kornblum
  Neuromuscular Disorders, v.18, 9-10, 797-797.
• Article: In vivo detection of neuropathological differences between Multiple System Atrophy (MSA) and Sporadic Adult Onset Ataxias of Unknown Aetiology (SAOA) using MR-Morphometry

  M Minnerop, Jan-Christoph Schoene-Bake, S. Roske, U. Wuellner, M Abele, Katrin Amunts, Marc Tittgemeyer, Bernd Weber, Thomas Klockgether
  Acta Neuropathologica, v.118, 452-452 (2009).