By Prof. Dr. B. J. Hoffer, L. Olson (auth.), Prof. Dr. Y. Mizuno, Prof. Dr. M. B. H. Youdim, Prof. Dr. D. B. Calne, Dr. R. Horowski, Prof. Dr. W. Poewe, Prof. Dr. P. Riederer (eds.)

Neurodegeneration is without doubt one of the most vital matters of the research now and within the coming twenty first century. Alzheimer's ailment is the prime reason for dementia within the aged humans and Parkinson's disorder is likely one of the significant neurologic issues with the superiority among 1 and 2/1 000 inhabitants in complicated international locations. Many others are struggling with intractable neurodegener­ ative issues reminiscent of amyotrophic lateral sclerosis, Huntington's disorder, or spinocerebellar degeneration. No really powerful therapy is obtainable for any of those neurodegenerative problems with the exception of Parkinson's sickness; even in Parkinson's sickness, nonetheless it truly is most unlikely to decelerate the ailment technique with the at present to be had remedy. it's urgently had to enhance new powerful strategy to halt or decelerate the disorder method in every one of these issues. contemporary enhance within the molecular organic and molecular genetic process has introduced us nice development within the realizing of etiology and pathogenesis of those problems, yet nonetheless it's not recognized how neurons are going to die in those problems. To discover the query, mutual cooperation and alternate of principles among easy scientists and medical peoples are of maximum importance.

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FGF-5 is present in the rat hippocampus and is produced by neurons mainly in the dentate gyrus region. Interestingly, in contrast to some of the other members of the FGF family, FGF-5 is a secreted molecule having a signal sequence at its amino terminal end. This fact makes FGF-5 an interesting candidate as a target-derived neurotrophic factor for the septal cholinergic neurons. g. give trophic support for different cortical neurons including probably the cholinergic interneurons. , 1988). Since CNTF and FGF-2 are normally probably not released the effects of these molecules on lesioned septal neurons reflects the Ubiquitous presence of their receptors on a variety of central neurons.

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J Neurol Neurosurg Psychiatry 50: 345-348 Mann DMA, Yates PO (1983) Pathological basis for neurotransmitter changes in Parkinson's disease. Neuropathol Appl Neurobiol 9: 3-19 Martin WE, Loewenson RB, Resch JA, Baker AB (1973) Parkinson's disease. A clinical analysis of 100 patients. Neurology 23: 783-790 Masters CL, Simms G, Weinmann NA, et al (1985) Amyloid plaque core protein in Alzheimer's disease and Down's syndrome. Proc Natl Acad Sci USA 82: 42454259 Mayeux R, Denaro J, Hemenegilde N, et al (1992) A populationbased investigation of Parkinson'-sdisease with and without dementia.

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