Monoamine oxidase (MAO) is linked to psychiatric and neurological disorders, because inhibitors of the enzyme are used clinically for treatment of affective disorders and Parkinson’s disease. One of the interesting new aspects of MAO is the occurrence in the human population of deletions of genes coding for one or the other enzyme subtype (A or B). This leads to the possibility of a genetic basis for psychiatric disorders based on MAO. Subjects with deletions of type A or B, and combined deletions, have been described. In the first group of 6 papers in this book, the occurrence and characterization of these phenotypes, as well as the structure of MAO genes, is explored. Advances in the biochemistry of MAO subtypes and their physiological function and localization in brain and periphery is included. Other sections of the book deal with the neuroprotective action of MAO inhibitors and their pharmacology, especially the pharmacology of new MAO-B inhibitors.

This book deals with basic and clinical aspects of monoamine oxidase (MAO) subtypes A and B highlighting its importance in neurological and psychiatric diseases. Consequently the therapeutic actions of MAO-A and -B inhibitors in Parkinson’s disease (PK) and depression are the focus of several chapters. As MAO is the basis of the development of the "oxidative stress hypothesis" of PD, several chapters are devoted to iron and iron-induced oxidative stress in various experimental studies and clinical conditions. Based on these findings, new compounds have been developed which not only block MAO, but are in addition, either inhibitors of acetylcholine esterase or have iron chelating properties. The aspect of "preclinical" and "clinical" neuro protection as well as MAO neuroprotection are additional topics covered in this book. MAO, iron and neuroprotection are seen in the framework of general anti Parkinson’s therapy with chapters on levodopa, dopaminergic receptor agonists and clinical issues.

Expert clinicians and basic scientists with a special interest in Parkinson’s disease review the current state of science and clinical therapeutics of the disease. Therefore these articles represent an authorative review of the current state of knowledge regarding preclinical course and symptomatology, subtypes with their impact on the pathology, genetic alterations, novel mechanisms of neuronal cell death, diagnostic tools and old and novel therapeutic approaches with respect to neuroprotection and neuroregeneration in Parkinson’s disease. Particular emphasis has been placed on a novel antiparkinsonian drug called budipine with various modes of action also influencing altered non dopaminergic systems in Parkinson’s disease. It is evident, that many questions on the cause, course and treatment of Parkinson’s disease are still unanswered and therefore the ideal way to treat a parkinsonian patient remains to be defined.

As human longevity continues to be extended, so will the impact of age-associated dementia on individual lives and society. Alzheimer’s disease as the most common cause of dementia in the elderly remains a sentinal problem and its underlying pathology is still poorly understood. Available therapeutic strategies require considerable refinement and the development of new therapeutic strategies need input from basic research. Thus continued efforts are necessary both to understand basic mechanisms of the condition and to achieve more powerfull therapies. This volume brings together the reports of basic scientists and clinical investigators. The chapters provide a spectrum of information valuable for clinicians and scientists. This issue bridges the gap between laboratory work in basic science and the development of urgently needed therapeutic strategies. Areas presented are the molecular and cellular biology of the disease, pathogenetic mechanisms and potential therapeutic targets, genetics, risk factors, strategies of prevention and treatment as well as practical aspects of medical and social care for patients with Alzheimer’s disease.

This book contains updated reviews and original research work on Down Syndrome focussing on brandnew results in neurobiology, in particular results on gene hunting (subtractive hybridization, differential display) and neurochemistry. The book provides new data such as a subtractive library of Down Syndrome brain showing cDNAs that are overexpressed or downregulated and can be regarded as a source for further research on the preliminary transcriptional data given. A 2D-electrophoretic map of human brain proteins including Down Syndrome brain protein expression established by in-gel-digestion of spots with subsequent MALDI-identification provides the scientific basis for protein work to the neuroscientist. Altogether, the book provides a series of new candidate genes possibly involved in Down Syndrome neurobiology, tools for neuroscience studies on Down Syndrome brain thus serving as a manual and updated views and aspects on Down Syndrome pathobiology.

The Amine Oxidase Workshop was the brain child of Brian Callingham and Keith Tipton. The present book is the proceedings of the fourth in the series and in the past we have dedicated our meeting to individuals who have made significant fundamental contributions to the biochemistry, physiology and pharmacology of this interesting group of enzymes. The present meeting is not an exception because we have gathered here in Wtirzburg to honour an individual whose outstanding work on the autonomic pharmacology has span ned more than 30 years and whose contribution has made a vast impact in our understanding of the kinetic relationship between amine metabolism (that uptake and enzymatic inactivation) and adrenergic neurotransmission. We speak of course of Professor Ullrich Trendelenburg, or Ulli as he likes to be known. Like the amine oxidases, he has a unique place in Pharmacology. Professor Trendelenburg was born on the eve of the new year of 1922 in the city of Rostock in northern Germany, where his father was Professor of Pharmacology at the Faculty of Medicine of Rostock. His father accepted the offer to take over the corresponding chair in Freiburg im Breisgrau (in Southern Germany). As the youngest of four children, Ulli grew up mainly in the garden of the department, in the animal quarters and in the workshop. Of the various coworkers of his father, one he liked especially was Otto Krayer, the young pharmacologist.