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.
Innehållsförteckning
Levodopa in the treatment of Parkinson’s disease.- Changing dopamine agonist treatment in Parkinson’s disease: experiences with switching to pramipexole.- The DONPAD-study — Treatment of dementia in patients with Parkinson’s disease with donepezil.- PD-related psychosis: pathophysiology with therapeutical strategies.- Antioxidant capacity in postmortem brain tissues of Parkinson’s and Alzheimer’s diseases.- Apoptosis inhibition in T cells triggers the expression of proinflammatory cytokines — implications for the CNS.- Molecular mechanism of the relation of monoamine oxidase B and its inhibitors to Parkinson’s disease: possible implications of glial cells.- Involvement of type A monoamine oxidase in neurodegeneration: regulation of mitochondrial signaling leading to cell death or neuroprotection.- The relationship of early studies of monoamine oxidase to present concepts.- Isatin, an endogenous MAO inhibitor, and a rat model of Parkinson’s disease induced by the Japanese encephalitis virus.- Isatin interaction with glyceraldehyde-3-phosphate dehydrogenase, a putative target of neuroprotective drugs: partial agonism with deprenyl.- Inhibition of amine oxidases by the histamine-1 receptor antagonist hydroxyzine.- Neuroprotection for Parkinson’s disease.- Marker for a preclinical diagnosis of Parkinson’s disease as a basis for neuroprotection.- Assessing neuroprotection in Parkinson’s disease: from the animal models to molecular neuroimaging in vivo.- Deprenyl: from chemical synthesis to neuroprotection.- The use of rasagiline in Parkinson’s disease.- Novel neuroprotective neurotrophic NAP analogs targeting metal toxicity and oxidative stress: potential candidates for the control of neurodegenerative diseases.- Acute and chronic effects ofdevelopmental iron deficiency on m RNA expression patterns in the brain.- Long lasting effects of infancy iron deficiency — Preliminary results.- Altered regulation of iron transport and storage in Parkinson’s disease.- Iron dyshomeostasis in Parkinson’s disease.- Cerebral oligemia and iron influence in cerebral structures — element of Morbus Parkinson Models?.- Impact of selenium, iron, copper and zinc in on/off Parkinson’s patients on L-dopa therapy.- Metal specificity of an iron-responsive element in Alzheimer’s APP m RNA 5?untranslated region, tolerance of SH-SY5Y and H4 neural cells to desferrioxamine, clioquinol, VK-28, and a piperazine chelator.- Green tea catechins as brain-permeable, non toxic iron chelators to “iron out iron” from the brain.
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