Abstract
The formation and accumulation of neurofibrillary tangles within cortical pyramidal neurones [28], has been considered the major direct cause of nerve cell degeneration. At present the excitement of the work on the structure of betaamyloid protein in senile plaques, and the implications from knowledge of the cDNA sequence of its precursor, has overshadowed the tangle and pyramidal cell. For example, it has been suggested that understanding biochemical changes occurring after the amyloid precursor protein has been synthesized may eventually provide treatment [6]. The disease has also often been approached optimistically as purely a genetic disorder involving chromosome 21, yet research fails to establish this for families where the disease appears late in life (e.g., [19]). It is generally accepted that there is a role for genes and amyloid-related proteins in pathogenesis, but these are unlikely to be the only factors, so a broader view is necessary because it is likely that the clinical syndrome results from a series of different events over a long period [3].
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© 1991 Springer-Verlag Berlin Heidelberg
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Bowen, D.M., Francis, P.T., Lowe, S.L., Pangalos, M.N., Procter, A.W., Steele, J.E. (1991). Alzheimer’s Disease: Role of Energy Metabolism and Treatment of Symptoms. In: Hartmann, A., Kuschinsky, W., Hoyer, S. (eds) Cerebral Ischemia and Dementia. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76208-6_11
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DOI: https://doi.org/10.1007/978-3-642-76208-6_11
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