Ciba Foundation Symposium 126 - Selective Neuronal Death

Parkinson's ailment, Alzheimer's disorder, and motor neuron illness proportion an important universal characteristic: selective demise of neurons in limited areas of the mind. This overseas symposium, held through the Ciba starting place in 1986, is the 1st to compile neurophysiologists engaged on neuronal demise and neuropathologists facing human degenerative mind affliction. contributors describe the reasons and series of occasions resulting in neuronal loss of life and speak about what should be performed to avoid it. one of the subject matters lined are contemporary advances within the knowing of brokers corresponding to trophic components, excitotoxins and poisons which are identified to be eager about neuronal demise; examples of neuronal demise in the course of general improvement; and the position performed via endocrine mechanisms and neuronal job. additionally considers trophic elements controlling the survival of neuronal transplants and the healing clients for tissue transplantation.


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In contrast to Alzheimer’s disease, and even motor neuron disease, Parkinson’s disease does not appear to occur in a familial fashion, suggesting that the pathogenesis of Parkinson’s disease may be completely different. Marsden: The final pathogenesis might well be similar. There is much speculation that Parkinson’s disease may be due to failure of protective mechanisms against free radicals and other reactive species, perhaps generated from the neurotoxic action of some exogenous agent(s). Bradley: Isn’t the frequency of dominantly inherited Parkinson’s disease about lo%, similar to Alzheimer’s disease and ALS?

My third worry about ageing is that in the material studied there has been no screening of the ‘normal’ brains for Lewy bodies. Yet about 10% of those over the age of 65 years have Lewy bodies in the substantia nigra (see Quinn et al 1986), which would distort all counts of nigral cells and measurements of striatal dopamine in later life. D o we really know that the substantia nigra ages in normal circumstances? Agid: This also raises the question of how we define pathology. D o we define it as the association of: (1) clinical signs, (2) histopathological abnormalities and (3) specific neuronal losses?

J Neuropathol Exp Neurol 40:667-675 Kemper TL 1983 Organization of the neuropathology of the amygdala in Alzheimer’s disease. Biological aspects of Alzheimer’s disease. Cold Spring Harbor Laboratory, Cold Spring Harbor, NY (Banbury Rep 15) p 31-35 Kidd M 1963 Paired helical filaments in electron microscopy of Alzheimer’s disease. Nature (Lond) 197:192-193 Kitt CA, Price DL, Struble RG et a1 1984 Evidence for cholinergic neurites in senile plaques. Science (Wash DC) 226: 1443-1445 Kitt CA, Struble RG, Cork LC et a1 1985 Catecholaminergic neurites in senile plaques in prefrontal cortex of aged nonhuman primates.

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