The Heiligendamm Round Table Portant Movement Disorders

Total Page：16

File Type：pdf, Size：1020Kb

parkinson‘s disease is one of the most im- the heiligendamm round table portant movement disorders. it affects large numbers of patients. the burden of disease peter riederer - drug treatment of parkinson‘s disease: how it all started is tremendous. nowadays, numerous drugs are available for its symptomatic treatment. Interdisciplinary the backbone of parkinson‘s disease treat- Working Group for ment, however, is the dopamine replacement Movement Disorders therapy. this treatment concept is a brilliant example of a rational drug development based on neu- ropathology, biochemistry and pharmacology. how did this concept emerge? what were the obstacles? how could they be overcome? who was involved? how did this idea spread? Peter Riederer, one of the world experts of clinical neurochemistry, was there where the dopamine replacement therapy was developed. who could better answer our questions? Dirk Dressler, MD, PhD Head of Movement Disorders Section Department of Neurology, Hannover Medical School Hannover, Germany peter riederer drug treatment of parkinson‘s IAB - Interdisciplinary Working Group for Movement Disorders disease: how it all started Dr. Fereshte Adib Saberi Brahmsallee 21 D-20144 Hamburg, Germany organisation: dirk dressler, MD, PhD peter riederer born in 1942 in königsberg, germany professor riederer grew up in vienna, austria and graduated in 1968 from technical university vienna with a degree in technical chemistry. after a research stay at nuclear research centre seibersdorf, austria from 1968-1970 he received a doctorate in engineering. from 1971-1986 he was head of clinical neurochemistry at the ludwig-boltzmann institutes of neurochemistry and clinical neurobiology in vienna and - at the same time - he was appointed professor at technical university vienna. from 1986-2008 he served as head of clinical neurochemistry at the department of psychiatry of würzburg university. he published extensively on various aspects of clinical neurochemistry. he is one of the world experts of neurochemistry of parkinson‘s disease..

Copy Link

Recommended publications

Peter Riederer
Profiles (List of Publications) February 25, 2016 Peter Riederer 1 1992 (419) Frölich L, Riederer P (1992) Demenz vom Alzheimer-Typ: Biochemische Befunde und ätiologische Hypothesen. Therapiewoche 42 (9):500-505 (420) Riederer P, Lange KW, Kornhuber J, Danielczyk W (1992) Glutamatergic-Dopaminergic Balance in the Brain. Arzneim-Forsch/Drug Res 42 (I):265-268 (421) Gerlach M, Riederer P (1992) Biochemische Grundlagen der Psychosen. In: Der Medizinische Notfall VI. Proceedings, Interdisziplinäres Forum für Med. Fortbildung, Neuhofen/Ybbs, pp 65-71 (422) Riederer P, Laux G, Pöldinger W (1992) Neuro-Psychopharmaka, Bd. 1, SpringerVerlag WienNewYork (423) Berger W, Riederer P (1992) 10.2 Neurotransmitter-Regelkreise. Riederer P, Laux G, Pöldinger (eds) Neuro-Psychopharmaka, Bd. 1. Springer-Verlag WienNewYork, pp 225-271 (424) Müller WE, Riederer P, Kienzel E (1992) 9. Grundlegende Aspekte zur Neurotransmission. Riederer P, Laux G, Pöldinger (eds) Neuro-Psychopharmaka, Bd. 1. Springer-Verlag WienNewYork, pp 222-248 (425) Sofic E, Riederer P, Schmidt B, Fritze J, Kollegger H, Dierks T, Beckmann H (1992) Biogenic amines and metabolites in CSF from patients with HIV infection. Biogenic Amines 8 (5):293-298 (426) Riederer P, Lange KW (1992) Pathogenesis of Parkinson´s disease. Current Opinion in Neurology and Neurosurgery 5:295-300 (427) Gerlach M, Riederer P, Youdim MBH (1992) The molecular pharmacoloy of L-deprenyl. European Journal of Pharmacology - Molecular Pharmacology Section 226:97-108 (428) Hiemke C, Baumann P, Breyer-Pfaff U, Gold R, Klotz U, Müller-Oerlinghausen B, Rao M-L, Riederer P, Wetzel H, Wiedemann K (1992) Drug Monitoring in Psychiatric Patients: Which Approach is Useful to Improve Psychopharmacotherapy? Pharmacopsychiat 25:72-74 2 (429) Youdim MBH, Riederer P (1992) Iron in the Brain, and Parkinson´s Disease.
[Show full text]
Proteomic Characterization of Synaptosomes from Human Substantia Nigra Indicates Altered Mitochondrial Translation in Parkinson's Disease
UCSF UC San Francisco Previously Published Works Title Proteomic Characterization of Synaptosomes from Human Substantia Nigra Indicates Altered Mitochondrial Translation in Parkinson's Disease. Permalink https://escholarship.org/uc/item/01d6j0mz Journal Cells, 9(12) ISSN 2073-4409 Authors Plum, Sarah Eggers, Britta Helling, Stefan et al. Publication Date 2020-12-02 DOI 10.3390/cells9122580 Peer reviewed eScholarship.org Powered by the California Digital Library University of California cells Article Proteomic Characterization of Synaptosomes from Human Substantia Nigra Indicates Altered Mitochondrial Translation in Parkinson’s Disease 1, 1,2, 1 1,2 3 Sarah Plum y, Britta Eggers y , Stefan Helling , Markus Stepath , Carsten Theiss , Renata E. P. Leite 4,5, Mariana Molina 4, Lea T. Grinberg 4,6, Peter Riederer 7,8, Manfred Gerlach 9, 1,2, 1,2, , Caroline May z and Katrin Marcus * z 1 Medizinisches Proteom-Center, Medical Faculty, Ruhr-University Bochum, 44801 Bochum, Germany; [email protected] (S.P.); [email protected] (B.E.); [email protected] (S.H.); [email protected] (M.S.); [email protected] (C.M.) 2 Medical Proteome Analysis, Center for Proteindiagnostics (PRODI), Ruhr-University Bochum, 44801 Bochum, Germany 3 Department of Cytology, Institute of Anatomy, Ruhr-University Bochum, 44780 Bochum, Germany; [email protected] 4 Department of Pathology, LIM22, University of Sao Paulo Medical School, Sao Paulo 01246-903, Brazil; [email protected] (R.E.P.L.); [email protected] (M.M.); [email protected]
[Show full text]
Treatment for Disease Modification in Chronic Neurodegeneration
cells Review Perspective: Treatment for Disease Modification in Chronic Neurodegeneration Thomas Müller 1,* , Bernhard Klaus Mueller 1 and Peter Riederer 2,3 1 Department of Neurology, St. Joseph Hospital Berlin-Weissensee, Gartenstr. 1, 13088 Berlin, Germany; [email protected] 2 Center of Mental Health, Department of Psychiatry, Psychosomatics and Psychotherapy, University Hospital Würzburg, Margarete-Höppel-Platz 1, 97080 Würzburg, Germany; [email protected] 3 Department of Psychiatry, Southern Denmark University Odense, J.B. Winslows Vey 18, 5000 Odense, Denmark * Correspondence: [email protected] Abstract: Symptomatic treatments are available for Parkinson’s disease and Alzheimer’s disease. An unmet need is cure or disease modification. This review discusses possible reasons for negative clinical study outcomes on disease modification following promising positive findings from experi- mental research. It scrutinizes current research paradigms for disease modification with antibodies against pathological protein enrichment, such as α-synuclein, amyloid or tau, based on post mortem findings. Instead a more uniform regenerative and reparative therapeutic approach for chronic neurodegenerative disease entities is proposed with stimulation of an endogenously existing repair system, which acts independent of specific disease mechanisms. The repulsive guidance molecule A pathway is involved in the regulation of peripheral and central neuronal restoration. Therapeutic antagonism of repulsive guidance molecule A reverses neurodegeneration according to experimental Citation: Müller, T.; Mueller, B.K.; outcomes in numerous disease models in rodents and monkeys. Antibodies against repulsive guid- Riederer, P. Perspective: Treatment for ance molecule A exist. First clinical studies in neurological conditions with an acute onset are under Disease Modification in Chronic Neurodegeneration. Cells 2021, 10, way.
[Show full text]
Association Between a Null Mutation in the Human Ciliary Neurotrophic Factor (CNTF) Gene and Increased Incidence of Psychiatric Diseases?
ELSEVIER Neuroscience Letters 203 (1996) 109-110 Association between a null mutation in the human ciliary neurotrophic factor (CNTF) gene and increased incidence of psychiatric diseases? Johannes Thome a,*, Johannes Kornhuber a, Alessandra Baumer b, Michael R6sler a, Helmut Beckmann a, Peter Riederer a aDepartment of Psychiatry, University of Wfirzburg, Fiichsleinstrafle 15, 97080 Wfirzburg, Germany blnstitute of Human Genetics, University of Wfirzburg, Am Hubland, 97074 Wiirzburg, Germany Received 16 October 1995; revised version received 6 December 1995; accepted 6 December 1995 Abstract We report a possible association between a null mutation in the human ciliary neurotrophic factor (CNTF) gene and psychiatric dis- eases. Prior findings that the mutant allele frequency is not significantly elevated in patients suffering from neurological diseases are confirmed. The frequency of the mutant allele was higher among psychiatric patients (0.192, n = 297) than among healthy controls and neurological patients (0.142, n = 267). This difference (one-tailed 2 x 2 chi-square test, P < 0.05) might be evidence that disturbances in the neurotrophic factor system could play a crucial role in the etiopathogenesis of psychiatric disorders, mainly psychoses. Keywords: Ciliary neurotrophic factor; Genetics; Mutation; Neurodevelopment; Neurotrophic factor; Psychiatry; Psychoses Neurodevelopmental deficits, disturbances of the quency in a Caucasian population was determined for the cell migration and dysconnections of neuronal and glial first time. structures are currently discussed as possible pathome- Inpatients (208 neurological: 112 female, 96 male; chanisms for psychiatric disorders, mainly endogenous and 297 psychiatric: 155 female, 142 male) suffering psychoses including schizophrenia [2,3,9] and manic- from various diseases, as well as 59 age- and sex-matched depressive disorders, severe brain diseases with until now healthy subjects (31 female, 28 male) were examined unknown pathogenesis and putative genetic and environ- (mean age __.
[Show full text]
The Diabetic Brain and Cognition
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by SZTE Publicatio Repozitórium - SZTE - Repository of Publications J Neural Transm DOI 10.1007/s00702-017-1763-2 NEUROLOGY AND PRECLINICAL NEUROLOGICAL STUDIES - REVIEW ARTICLE The diabetic brain and cognition 1 16 2 3 Peter Riederer • Amos D. Korczyn • Sameh S. Ali • Ovidiu Bajenaru • 4 5 7 Mun Seong Choi • Michael Chopp • Vesna Dermanovic-Dobrota • 8,9,10 11 13,14,15 Edna Gru¨nblatt • Kurt A. Jellinger • Mohammad Amjad Kamal • 12 17 19 Warda Kamal • Jerzy Leszek • Tanja Maria Sheldrick-Michel • 20 18 6 21 Gohar Mushtaq • Bernard Meglic • Rachel Natovich • Zvezdan Pirtosek • 22 23 24 Martin Rakusa • Melita Salkovic-Petrisic • Reinhold Schmidt • 25 26 27 Angelika Schmitt • G. Ramachandra Sridhar • La´szlo´ Ve´csei • 28 29 5,29 6 Zyta Beata Wojszel • Hakan Yaman • Zheng G. Zhang • Tali Cukierman-Yaffe Received: 1 June 2017 / Accepted: 13 July 2017 Ó Springer-Verlag GmbH Austria 2017 Abstract The prevalence of both Alzheimer’s disease (AD) Congress on Vascular Disorders and on literature search and vascular dementia (VaD) is increasing with the aging of using PUBMED, it can be concluded that T2DM is a risk the population. Studies from the last several years have factor for both, AD and VaD, based on a pathology of glu- shown that people with diabetes have an increased risk for cose utilization. This pathology is the consequence of a dementia and cognitive impairment. Therefore, the authors disturbance of insulin-related mechanisms leading to brain of this consensus review tried to elaborate on the role of insulin resistance.
[Show full text]
Print Special Issue Flyer
IMPACT FACTOR 4.879 an Open Access Journal by MDPI In Honor of the 80th Birthday of Professor Peter Riederer Guest Editors: Message from the Guest Editors Prof. Dr. Lars Tönges Dear Colleagues, Department of Neurology, Ruhr- Universität Bochum, Bochum, This issue is dedicated to the 80th birthday of Professor Dr Germany Peter Riederer. [email protected] He is one the most influential experimental researchers in Prof. Dr. Thomas Müller the field of neurochemistry in psychiatry and neurology. St. Joseph Hospital Berlin- His life time achievement is characterised by the Weißensee, Department of Neurology, Berlin, Germany continuous successful approach to combine clinical and experimental research. [email protected] This honorary issue in “Biomolecules” reflects this scientific Prof. Dr. Wilfried Kuhn Leopoldina Hospital Schweinfurt, principle and includes experimental findings and outcomes Schweinfurt, Germany of clinical studies. [email protected] The editors wish Professor Riederer many further fruitful future years and thank him for his continuous support over the years. Deadline for manuscript submissions: Prof. Dr. Lars Tönges 31 December 2021 Prof. Dr. Thomas Müller Prof. Dr. Wilfried Kuhn Guest Editors mdpi.com/si/84176 SpeciaIslsue IMPACT FACTOR 4.879 an Open Access Journal by MDPI Editor-in-Chief Message from the Editor-in-Chief Dr. Vladimir N. Uversky Biomolecules is a multidisciplinary open-access journal Department of Molecular that reports on all aspects of research related to biogenic Medicine, USF Health Byrd substances, from small molecules to complex polymers. Alzheimer’s Research Institute, Morsani College of Medicine, We invite manuscripts of high scientific quality that pertain University of South Florida, 12901 to the diverse aspects relevant to organic molecules, Bruce B.
[Show full text]
Proteomic Characterization of Synaptosomes from Human Substantia Nigra Indicates Altered Mitochondrial Translation in Parkinson’S Disease
cells Article Proteomic Characterization of Synaptosomes from Human Substantia Nigra Indicates Altered Mitochondrial Translation in Parkinson’s Disease 1, 1,2, 1 1,2 3 Sarah Plum y, Britta Eggers y , Stefan Helling , Markus Stepath , Carsten Theiss , Renata E. P. Leite 4,5, Mariana Molina 4, Lea T. Grinberg 4,6, Peter Riederer 7,8, Manfred Gerlach 9, 1,2, 1,2, , Caroline May z and Katrin Marcus * z 1 Medizinisches Proteom-Center, Medical Faculty, Ruhr-University Bochum, 44801 Bochum, Germany; [email protected] (S.P.); [email protected] (B.E.); [email protected] (S.H.); [email protected] (M.S.); [email protected] (C.M.) 2 Medical Proteome Analysis, Center for Proteindiagnostics (PRODI), Ruhr-University Bochum, 44801 Bochum, Germany 3 Department of Cytology, Institute of Anatomy, Ruhr-University Bochum, 44780 Bochum, Germany; [email protected] 4 Department of Pathology, LIM22, University of Sao Paulo Medical School, Sao Paulo 01246-903, Brazil; [email protected] (R.E.P.L.); [email protected] (M.M.); [email protected] (L.T.G.) 5 Division of Geriatrics, LIM 66, University of Sao Paulo Medical School, Sao Paulo 01246-903, Brazil 6 Department of Neurology, Memory and Aging Center, University of California, San Francisco, CA 94158, USA 7 Center of Mental Health, Clinic and Policlinic for Psychiatry, Psychosomatics and Psychotherapy, University Hospital Wuerzburg, Margarete-Höppel-Platz 1, 97080 Wuerzburg, Germany; [email protected] 8 Psychiatry Department of Clinical Research, University of Southern Denmark Odense University Hospital, Winslows Vey 18, 5000 Odense, Denmark 9 Center of Mental Health, Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University Hospital of Wuerzburg, University of Wuerzburg, 97080 Wuerzburg, Germany; [email protected] * Correspondence: [email protected]; Tel.: +49-234-32-18106 These authors contributed equally to this work.
[Show full text]
(WFSBP) Guidelines for the Biological Treatment of Alzheimer Disease
The World Journal of Biological Psychiatry, 2011; 12: 2–32 GUIDELINES World Federation of Societies of Biological Psychiatry (WFSBP) Guidelines for the Biological Treatment of Alzheimer’ s disease and other dementias RALF IHL 1 , LUTZ FR Ö LICH 2 , BENGT WINBLAD 3 , LON SCHNEIDER 4 , ALISTAIR BURNS 5 , HANS-J Ü RGEN M Ö LLER 6 & WFSBP TASK FORCE ON TREATMENT GUIDELINES FOR ALZHEIMER’S DISEASE AND ∗ OTHER DEMENTIAS 1 Alexian Hospital Krefeld and Department of Psychiatry, University of Duesseldorf, Germany, 2 Division of Geriatric Psychiatry Central Institute of Mental Health Mannheim University of Heidelberg, Mannheim, Germany, 3 Karolinska Institute, Neurotec, Huddinge, Sweden, 4 University of Southern California Keck School of Medicine, Los Angeles, CA, USA, 5 Psychiatry Research Group, University of Manchester, Manchester, UK, and 6 Department of Psychiatry and Psychotherapy, University of Munich, Munich, Germany Abstract Objectives. To deﬁ ne a practice guideline for biological treatment of dementia and to make transparent the development of the guideline connecting the original data with the resulting recommendations. Methods. This guideline includes pharma- cologic treatment considerations for patients with Alzheimer’s disease, vascular dementia, DLB, and fronto-temporal dementia. Studies were selected that represent double-blind placebo-controlled trials of at least 3 months duration in patients with a diagnosis of dementia according to accepted international diagnostic criteria (for example the NINCDS/ ADRDA or NINDS/AIREN criteria). Moreover, to be included studies had to fulﬁ ll a restrictive set of methodological criteria. Original studies and not meta-analyses determined the evaluation and the development of recommendations. Results. Antidementia pharmaceuticals neither cure nor arrest the disease.
[Show full text]
Differential Effects of Neuromelanin and Synthetic Dopamine Melanin On
Aus der Klinik und Poliklinik für Psychiatrie und Psychotherapie der Universität Würzburg Direcktor: Professor Dr. med. Dr. h. c. Helmut Beckmann Differential effects of neuromelanin and synthetic dopamine melanin on cell lines Inaugural – Dissertation zur Erlangung der Doktorwürde der Medizinischen Fakultät der Bayerischen Julius-Maximilians-Unversität zu Würzburg vorgelegt von Jie Li aus Tianjin, China Würzburg, November 2004 Referent: Prof. Dipl.-Ing. Dr. techn. Peter Riederer Koreferent: Prof. Dr. W. Roggendorf Dekan: Prof. Dr. med. Georg Ertl Tag der mündlichen Prüfung: 03, 06, 2005 Die Promovendin ist Ärztin Content 1. Introduction.................................................................................................................1 1.1 About Parkinson’s Disease……………………………………………………. 1 1.2 Etiopathogenesis of PD………………………………….………..……………3 1.3 Pathological anatomy of PD ………………………………………….……….5 1.4 Pathogenesis of PD……………………………………………………….……7 1.5 Hypothesis and aims of this project……………………………………..……19 2. Materials and Methods……………………………………………………………..20 2.1 Cell culture as a model of nigral pigmented neurons…………………………..20 2.2 General cell culture methods…………………………………………………...21 2.3 Preparation of melanin pigment..........................................................................23 2.4 Treatment of cells................................................................................................24 2.5 Electron photography………………………………………………………..…25 2.6 Measurement of experimental endpoints……………………………………....26 2.7 Apoptosis
[Show full text]
Research Collection
Research Collection Journal Article Chronic monoamine oxidase-B inhibitor treatment blocks monoamine oxidase-A enzyme activity Author(s): Bartl, Jasmin; Müller, Thomas; Grünblatt, Edna; Gerlach, Manfred; Riederer, Peter Publication Date: 2014-04 Permanent Link: https://doi.org/10.3929/ethz-b-000082695 Originally published in: Journal of Neural Transmission 121(4), http://doi.org/10.1007/s00702-013-1120-z Rights / License: In Copyright - Non-Commercial Use Permitted This page was generated automatically upon download from the ETH Zurich Research Collection. For more information please consult the Terms of use. ETH Library J Neural Transm (2014) 121:379–383 DOI 10.1007/s00702-013-1120-z NEUROLOGY AND PRECLINICAL NEUROLOGICAL STUDIES - SHORT COMMUNICATION Chronic monoamine oxidase-B inhibitor treatment blocks monoamine oxidase-A enzyme activity Jasmin Bartl • Thomas Mu¨ller • Edna Gru¨nblatt • Manfred Gerlach • Peter Riederer Received: 28 September 2013 / Accepted: 8 November 2013 / Published online: 23 November 2013 Ó Springer-Verlag Wien 2013 Abstract Patients with Parkinson’s disease receive common in patients with Parkinson’s disease (PD) selective irreversible monoamine oxidase (MAO)-B inhib- (Deftereos et al. 2012). Two isoforms of the enzyme, itors, but their effects on MAO-A activity are not known MAO-A and MAO-B, are known according to MAO (EC during long-term application. We determined MAO-A 1.4.3.4) substrate and inhibitor speciﬁcities (Johnston inhibition in plasma samples from patients with MAO-B 1968). MAO-A is primarily located in the periphery with inhibitor intake or without MAO-B inhibitor treatment and approximately 80 % of total MAO activity in the gastro- from healthy controls.
[Show full text]
Parkinson's Disease and Depression
590 Journal of Neurology, Neurosurgery, and Psychiatry 1997;63:590–596 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.63.5.590 on 1 November 1997. Downloaded from Parkinson’s disease and depression: evidence for an alteration of the basal limbic system detected by transcranial sonography Thomas Becker, Georg Becker, Jochen Seufert, Erich Hofmann, Klaus W Lange, Markus Naumann, Alfred Lindner, Heinz Reichmann, Peter Riederer, Helmut Beckmann, Karlheinz Reiners Abstract disease.1 The average prevalence of depression Objectives—Depression is a frequent in Parkinson’s disease is around 40% with a symptom in Parkinson’s disease. Compel- range from 4%-70%.2 Although it is evident ling evidence suggests a role of the brain- that the degree of impairment and psychologi- stem in the control of mood and cognition. cal and social factors inﬂuence the mood of In patients with unipolar depression tran- patients with Parkinson’s disease3 there are scranial sonography (TS) studies have several lines of evidence pointing towards shown structural alteration of the mesen- organic factors in the pathogenesis of depres- cephalic brainstem raphe which could sion in the disease.4–16 Transcranial sonography suggest an involvement of the basal limbic (TS) is a valuable tool in visualising both nor- system in the pathogenesis of primary mal and diseased brain parenchyma, and mood disorders. The objective of the brainstem anatomy can be reliably Department of present study was to evaluate whether a depicted.17–23 In a TS study in patients with Psychiatry, University similar alteration could be found in de- Parkinson’s disease the substantia nigra was of Würzburg, pressed patients with Parkinson’s disease found to be hyperechogenic, which is thought Füchsleinstrasse 15, 24 D-97080 Würzburg, using TS.
[Show full text]
Neuropsychiatric Disorders: an Integrative Approach
review articles, many from colleagues and collaborators of BOOK REVIEW Professor Riederer. Researchers from all over the world have contributed. The articles are divided into 5 sections: “Basic Neuropsychiatric Disorders: An Neuroscience,” “Parkinson’s Disease and Allied Conditions,” Integrative Approach “Alzheimer’s Disease and Related Disorders,” “Biological Psy- chiatry,” and “Other Disorders.” Thirty-one articles represent M. Gerlach, J. Deckert, K. Double, and E. Koutsilieri, eds. New original research and are presented in the format of the Journal York: SpringerWien; 2007, 341 pages, 109 figures, $229.00. of Neural Transmission. Graphs, tables, and figures are clearly he Journal of Neural Transmission is a very well-respected presented and labeled. A partial list of methodologies repre- Tpeer-reviewed journal in the field of neuroscience. This sented includes research on postmortem human or animal 2007 supplement volume, entitled Neuropsychiatric Disorders: brains, cultured animal or human neuronal cell lines, clinical An Integrative Approach, is a Festschrift in honor of Professor trials in humans, knockdown animals, therapeutic drug mon- Peter Riederer, Editor-in-Chief of the Journal, who retired in itoring, and stem cells. April 2007. Dr. Riederer was Professor of Clinical Neuro- Eight review articles are sprinkled throughout the volume, chemistry in the Clinic for Psychiatry and Psychotherapy at unfortunately not clearly marked as such, though the titles of the University of Wu¨rzburg, Germany, and is an enormously some suggest their nature. Topics range from an extensive influential neurochemist, who authored more than 900 papers review of the therapeutic potential of small inhibitory ribonu- and book chapters and helped launch the careers of many cleic acid in the gene therapy of neurodegenerative disorders successful scientists.
[Show full text]