Abstract
Since ancient times, a creative tension has existed between two viewpoints on illness. One, associated with the Platonic physicians of the island of Cnos, looks on diseases as specific entities which can be classified like plants. From this viewpoint, the specific patient in the examining room is a more or less close copy of an idealized patient. In modern times, this view was developed with particular strength by Sydenham in London in the 1600s. The second viewpoint, associated with the Hippocratic physicians of the island of Cos, views illness as occurring when an organism can no longer remain in balance with the challenges of its environment. In modern times, this view was put forward with particular clarity by Claude Bernard in Paris in the 1800s. He emphasized that an illness occurs when living organisms cannot maintain their “milieu interne” in the face of the challenges of their environment.
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Adolfsson, R. Gottfries C.G., Oreland, L., et al., Increased activity of brain and platelet monoamine oxidase in dementia of the Alzheimer type, Life Sci. 27:1029.
Ali, G., Wasco, W., Cai, X. et al, 1994, Isolation, characterization, and mapping of the dihyrodlipoyl succinyltransferase [E2k] of human α-ketoglutarate dehyrogenase complex, Somat. Cell Mol Genet. 20:99.
Beal, M.F., 1992, Does impairment of energy metabolism result in excitotoxic neuronal death in neurodegenerative diseases? Ann. Neural. 31:119.
Bick, K., Amaducci, L., and Pepeu, G., 1987, The early story of Alzheimer’s disease. Livinia Press, Padua.
Blass, J.P., 1993a, Pathophysiology of the Alzheimer’s syndrome, Neurology 43 (suppl 4):S25.
Blass, J.P., 1993b, The cultured fibroblast model, J. Neural. Trans. (Suppl) 44:87.
Blass, J.P., Baker, A.C., Ko, L. et al, 1991, Expression of Alzheimer antigens in cultured skin fibroblasts, Arch. Neurol. 48:709.
Blass, J.P., and Gibson, G.E., 1991, The role of oxidative abnormalities in the pathophysiology of Alzheimer’s Disease, Rev. Neurol. (Paris) 147:513.
Blass, J.P., and Gibson, G.E., 1993, Nonneural markers in Alzheimer disease, Alz. Dis. Assoc. Dis. 6:205.
Blass, P., Hoyer, S., and Nitsch, R., 1992, In reply, Arch. Neurol. 49:800.
Blass, J.P., Milne, J.A., and Rodnight, R., 1977, Newer concepts of psychiatric diagnosis and biochemical research on mental illness. Lancet 1:738.
Blass, J.P., and Poirier, J., 1995, Pathophysiology of the Alzheimer’s Syndrome, In press.
Blass, J.P., Sheu, K.-F.R., and Cederbaum, J.M., 1988, Energy metabolism in disorders of the nervous system, Rev. Neurol. (Paris) 144:543.
Butterworth, R.F., and Besnard, A.M., 1990, Thiamine-dependent enzyme changes in temporal cortex of patients with Alzheimer’s disease, Metab. Brain Dis. 4:179.
Cai, X., Sabo, P., Ali, G. et al, 1994, A pseudogene of dihyrdrolipoyl succinyltransferase (E2k) found by PCR amplification and direct sequencing in rodent-human cell hybrid DNAs. Somat. Cell Mol. Genet. 20:339.
Cheng, B., and Mattson, M.P., 1992, Glucose deprivation elicits neurofibrillary tangle-likeantigenic changes in hippocampal neurons: Prevention by NGF and bFGF, Exp. Neurol. 117:114.
Endoh, M., Pulsinelli, W.A., and Wagner, J.A., 1994, Transient global ischemia induces dynamic changes in the expression of bFGF and the FGF receptor, Brain Res. 22:76.
Fillit, H., Ding, W.H., Buee, L. et al, 1991, Elevated circulating tumor necrosis factor levels in Alzheimer’s disease. Neurosci Lett 129:318.
Gabuzda, D., Busciglio, J., Chen, L.B. et al, 1994, Inhibition of eneergy metabolism alters the processing of amyloid precursor protein and induces a potentially amyloidogenic derivative, J. Biol. Chem. 269:13628.
Garrod, A.E., 1923, Inborn Errors of Metabolism, Oxford, London.
Gibson, G.E., and Blass, J.P., 1982, Metabolism and neurotransmission, in: Handbook of Neurochemistry, A. Lajtha, ed., vol. 3, 2nd ed., Plenum Press, N.Y.
Gibson, G.E., Blass, J.P., Huang, H.-M. et al, 1991, The cellular basis of delerium and its relevance to age-related disorders including Alzheimer’s disease, Int. Psychogeriatrics 3:373.
Gibson, G.E., Pulsinelli, W.A., and Blass, J.P., 1981, Brain dysfunction in mild to moderate hypoxia, Am. J. Med. 70:1247.
Gibson, G.E., Sheu, K.-F.R., Blass, J.P. et al, 1988, Reduced activities of thiamine-dependent enzymes in the brains and peripheral tissues of patients with Alzheimer’s Disease, Arch. Neurol. 45:836.
Henneberry, R.A., 1989, The role of energy in the toxicity of excitatory amino acids, Neurobiol. Aging 10:611.
Hirsch, J.A., and Gibson, G.E., 1984, Selective alterations of neurotransmitter release by low oxygen in vitro, Neurochem. Res. 9:1039.
Huang, H.-M., and Gibson, G.E., 1993, Altered β-receptor stimulated cAMP formation in cultured skin fibroblasts from Alzheimer donors, J. Biol. Chem. 268:14616.
Ko, L., Sheu, K.-F.R., and Blass, J.P., 1993, Chemical neuroanatomy of energy metabolism: immunohistochemical studies in relation to selective vulnerability, J. Neurochem. 61: S70.
Makar, T.K., Cooper, A.J.L., Tofel-Grehl, B., et al, 1995, Carnitine, carnitine acetyltransferase, and glutathione in Alzheimer brain, Neurochem. Res. 20:705.
Mattson, M.P., Cheng, B., Culwell, A.R. et al, 1993, Evidence for excitoprotective and intraneuronal calcium regulating for secreted forms of the β-amyloid precursor protein. Neuron 10:246.
Mattson, M.P., and Goodman, Y., 1995, Different amyloidogenic peptides share a similar mechanism of neurotoxicity involving reactive oxygen species and calcium. Brain Res. 676:219–224.
McGeer, P.L., McGeer, E., Kawamata, T. et al, 1991, Reactions of the immune system in chronic degenerative neurological diseases, Can. J. Neurol. Sci. 18 (suppl 3): 376.
Nakano, K., Takase, C., Sakamoto, T. et al, 1994, Isolation, characterization, and structural organization of the gene and pseudogene for the dihyrolipoylamide succinyltransferase component of the 2-oxoglutarate dehydrogenase complex, Eur. J. Biochem. 224:179.
Paoletti, F., and Mocali, A., 1991, Enhanced proteolytic activities in cultured fibroblasts of Alzheimer patients are revealed by peculiar transketolase alterations, J. Neurol. Sci. 105:211.
Parker, W.D., Filley, C.M., and Parks, J.K., 1990, Cytochrome oxidase deficiency in Alzheimer’s disease, Neurology 40: 1302.
Rogers, J., Cooper, N.R., Webster, S. et al, 1992, Complement activation by β-amyloid in Alzheimer’s disease, Proc. Nad. Acad. Sci. (USA) 89:10016.
Roses, A.D., 1995, Alzheimer’s disease as a model of molecular gerontology, J. NIH Res. 7:51.
Sheu, K.-F.R., Clarke, D.D., Kim, Y.T. et al, 1988, Studies of the transketolase abnormality in Alzheimer’s disease, Arch. Neurol. 45:841.
Sheu, K.-F.R., Cooper, A.J.L., Lindsay, J.G., et al, 1994, Abnormality of the β-ketoglutarate dehydrogenase complex in fibroblasts from familial Alzheimer’s Disease, Ann. Neurol. 35:312.
Sims, N.R., Finegan, J.M., and Blass, J.P., 1987, Altered metabolic properties of cultured skin fibroblasts in Alzheimer’s disease, Ann. Neurol. 21:451.
Van Zuylen, A.J., Bosman, G.J.C.G.M., Ruitenbeek, W., et al, 1992, No evidence for reduced thrombocyte cytochrome oxidase activity in Alzheimer’s Disease, Neurology 42:1246.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1996 Springer Science+Business Media New York
About this chapter
Cite this chapter
Blass, J.P., Sheu, KF.R., Tanzi, R.E. (1996). α-Ketoglutarate Dehydrogenase in Alzheimer’s Disease. In: Fiskum, G. (eds) Neurodegenerative Diseases. GWUMC Department of Biochemistry and Molecular Biology Annual Spring Symposia. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0209-2_24
Download citation
DOI: https://doi.org/10.1007/978-1-4899-0209-2_24
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4899-0211-5
Online ISBN: 978-1-4899-0209-2
eBook Packages: Springer Book Archive