Abstract
In normoglycemic patients with either incipient early-onset or incipient late-onset dementia of the Alzheimer type (DAT), the predominant disturbance consists of a significant reduction in cerebral glucose utilization. Cerebral blood flow and oxygen consumption is changed only in late-onset dementia types and is most severely decreased in advanced late-onset dementia (Hoyer et al.,1991). Reductions in resting state regional brain metabolism are roughly proportional to the severity of dementia. These reductions are greater in association than in primary sensory and motor neocortical regions and correlate with the distribution of neuropathology and cell loss after death (for review, see Rapoport, 1991).
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References
Backstrom, J.R., Miller, C.A., and Takes, Z.A., 1992, Characterization of neutral proteinases from Alzheimer-affected and control brain specimens: identification of calcium-dependent metalloproteinases from the hippocampus, J. Neurochem. 58: 983–992.
Baskin, D.G., Porte, D., Jr, Guest, K., and Dorsa, M., 1983, Regional concentration of insulin in the rat brain, Endocrinology 112: 898–903.
Benzi, G., Pastoris, O., Fenton, S., and Villa, R.F., 1987, Modifications in cerebral lipid metabolism by severe glucose deprivation during aging, Neurobiol. Aging 8: 457–463.
Brooksbank, B.W.L., and Martinez, M., 1989, Lipid abnormalities in the brain in adult Down’s syndrome and Alzheimer’s disease, Mol. Chem. Neuropathol. 11: 157–185.
Hoyer, S., and Nitsch, R., 1989, Cerebral excess release of neurotransmitter amino acids subsequent to reduced cerebral glucose metabolism in early-onset dementia of Alzheimer type, J. Neural Transm. 75: 227–232.
Hoyer, S., Nitsch, R., and Oesterreich, K., 1991, Predominant abnormality in cerebral glucose utilization in late-onset dementia of the Alzheimer type: a cross-sectional comparison against advanced late-onset and incipient early-onset cases, J. Neural Transm. (P-D Sect) 3: 1–14.
Hoyer, S., Prem, L., Sorbi S., and Amaducci, L., 1993, Stimulation of glycolytic key enzymes in cerebral cortex by insulin, NeuroReport 4: 991–993.
Iwangoff, P., Armbruster, R., Enz, A., Meier-Ruge,W., and Sandoz, P., 1980, Glycolytic enzymes from human autoptic brain cortex: normally aged and demented cases, in: “Biochemistry of Dementia”, P.J. Roberts, ed., Wiley, Chichester.
Junod, A., Lambert, A.E., Stauffacher, W., and Renold, A.E., 1968, Diabetogenic action of streptozotocin: relationship of dose to metabolic response, J. Clin. Invest. 48: 2129–2139.
Kadowaki, T., Kasuga, M., Akanuma, Y., Ezaki, O., and Takaku, F., 1984, Decreased autophosphorylation of the insulin receptor-kinase in streptozotocin diabetic rats, J. Biol. Chem. 259: 14208–14216.
Liguri, G., Taddei, N., Nassi, P., Latorraca, S., Nediani, C., and Sorbi, S., 1990, Changes in Nat, K*–ATPase, Ca’ -ATPase and some soluble enzymes related to energy metabolism in brains of patients with Alzheimer’s disease, Neurosci. Lett. 112: 338–342.
Nitsch, R., and Hoyer, S., 1991, Local action of the diabetogenic drug, streptozotocin, on glucose and energy metabolism in rat brain cortex, Neurosci. Lett. 128: 199–202.
Nitsch, R.M., Blusztajn, J.K., Pittas, A.G., Slack, B.E., Growdon, J.H., and Wurtman, R.J., 1992, Evidence for a membrane defect in Alzheimer disease brain, Proc. Natl. Acad. Sci. USA 89: 1671–1675.
Padmini, S., and Rao, P.S., 1991, Enhanced ß-oxidative utilization of [1!`C] palmitate during active myelinogenesis in developing rat brain under nutritional stress, Lipids 26: 83–85.
Perry, E.K., Perry, R.H., Tomlinson, B.E., Blessed, G., and Gibson, P.H., 1980, Coenzyme A-acetylating enzymes in Alzheimer’s disease: possible cholinergic ‘compartment’ of pyruvate dehydrogenase, Neurosci. Lett. 18: 105–110.
Plaschke, K., and Hoyer, S., 1993, Action of the diabetogenic drug streptozotocin on glycolytic and glycogenolytic metabolism in adult rat brain cortex and hippocampus, Int. J. Dev. Neurosci. 11: 477–483
Rapoport, S.I., 1991, Positron emission tomography in Alzheimer’s disease in relation to disease pathogenesis: a critical review, Cerebrovasc. Brain Metab. Rev. 3: 297–335.
Saito, K.-I., Elce, J.S., Hamos, J.E., and Nixon, R.A., 1993, Widespread activation of calcium-activated neutral proteinase (calpain) in the brain in Alzheimer disease, a potential molecular basis for neuronal degeneration, Proc. Natl. Acad. Sci. USA 90: 2628–2632.
Siesj6, B.K., 1978, “Brain Energy Metabolism”, Wiley, Chichester.
Unger, J.W., Livingston, J.N., and Moss, A.M., 1991, Insulin receptors in the central nervous system: localization, signalling mechanisms and functional aspects, Prog. Neurobiol. 36: 343–362.
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Müller, D., Plaschke, K., Hoyer, S. (1995). Intracerebroventricular Injection of Streptozotocin — An Animal Model for Sporadic Alzheimer’s Disease?. In: Hanin, I., Yoshida, M., Fisher, A. (eds) Alzheimer’s and Parkinson’s Diseases. Advances in Behavioral Biology, vol 44. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9145-7_58
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DOI: https://doi.org/10.1007/978-1-4757-9145-7_58
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