Titlebook: Advances in Research on Neurodegeneration; Volume 5 P. Riederer,D. B. Calne,M. B. H. Youdim Conference proceedings 1997 Springer-Verlag Wie

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Developmental and genetic regulation of programmed neuronal deathibility to apoptosis is also regulated by the expression of bcl-2 family proteins. Current research focuses on the significance of these findings for the premature death of adult neurons in human neurodegenerative diseases.

有权威

Assessment of neurotoxicity and “neuroprotection”demonstrated in coronal slice preparations. Taurine affords protection against this neurotoxicity. The possible mechanisms of these effects are considered in terms of the cyclic interrelationships between the different events which can lead to cell death.

愚笨

grenade

Measurement of the dopaminergic degeneration in Parkinson’s disease with [123I]β-CIT and SPECTminals in vivo in the human brain with SPECT. It has been validated that the calculation of a simple ratio of specific/nondisplaceable binding during a period of binding-equilibrium in the striatum about 20 hrs after bolus injection of the tracer gives a strong and reliable index of the binding pote

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百灵鸟

IBZM- and CIT-SPECT of the dopaminergic system in parkinsonism vivo discrimination between IPD and “parkinsonism-plus” syndromes is important. Recently, ligands have become available for imaging the pre- and postsynaptic dopaminergic system by Single Photon Emission Computed Tomography (SPECT). Visualization of postsynaptic D. dopamine receptors using .I-iodob

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synovitis

Contributions of Positron Emission Tomography to elucidating the pathogenesis of Idiopathic Parkinsod evidence that has generated new hypotheses. Progression of the lesion detectable with fluorodopa, in human subjects exposed to MPTP, raises the possibility of a transient environmental event being a cause of progressive neurodegeneration. Studies with fluorodopa in Idiopathic Parkinsonism indicate

小丑

Mechanism of 6-hydroxydopamine neurotoxicityisease. In this article, we highlight the latest findings on the biochemical mechanism of 6-OHDA toxicity. 6-OHDA has two ways of action: it easly forms free radicals and it is a potent inhibitor of the mitochondrial respiratory chain complexes I and IV. The inhibition of respiratory enzymes by 6-OH