OXIDATIVE ENERGY-METABOLISM IN ALZHEIMER BRAIN - STUDIES IN EARLY-ONSET AND LATE-ONSET CASES

被引:138
作者
HOYER, S
机构
[1] Brain Metabolism Group, Department of Pathochemistry and General Neurochemistry, University of Heidelberg, Heidelberg, D-6900
关键词
DEMENTIA OF ALZHEIMER TYPE; BRAIN; GLUCOSE METABOLISM; ENERGY FORMATION; ENERGY DEFICIT;
D O I
10.1007/BF03159971
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Reduction of the cerebral metabolic rate of glucose is one of the most predominant abnormalities generally found in the Alzheimer brain, whereas the cerebral metabolic rate of oxygen is only slightly diminished or not at all the beginning of this dementive disorder. This metabolic abnormality may induce severe functional disturbances, obviously preceding morphobiological changes. From the cerebral metabolic rates of oxidized glucose and oxygen, the cerebral ATP formation rate was calculated in incipient early-onset, incipient late-onset and stable advanced dementia of Alzheimer type. A reduction of ATP formation was found from at least 7% in incipient early-onset, to around 20% in incipient late-onset DAT, and from 35% to more than 50% in stable advanced dementia. This approximation was adjusted to findings demonstrating diminished activities of enzymes active in glucose metabolism and formation of oxidation equivalents for ATP production from substrates other than glucose. A reduction for energy formation to the same range was found, as was also recently reported, in vivo in Alzheimer patients. From this rather theoretical point of view, a permanent loss of energy by at least 7-20% in incipient and progressively advancing dementia of the Alzheimer type may be assumed, with an increasing tendency in stable advanced dementia to around 50% energy loss. This energy deficit may have drastic impacts on brain function.
引用
收藏
页码:207 / 224
页数:18
相关论文
共 70 条
[1]   OXIDATION OF UNIFORMLY LABELLED ALBUMIN-BOUND PALMITIC ACID TO CO2 BY PERFUSED CAT BRAIN [J].
ALLWEIS, C ;
LANDAU, T ;
ABELES, M ;
MAGNES, J .
JOURNAL OF NEUROCHEMISTRY, 1966, 13 (09) :795-&
[2]  
ARAI H, 1985, Neuroscience Research, V2, P486, DOI 10.1016/0168-0102(85)90020-3
[3]   INDUCTION OF ALZHEIMER ANTIGENS BY AN UNCOUPLER OF OXIDATIVE-PHOSPHORYLATION [J].
BLASS, JP ;
BAKER, AC ;
KO, LW ;
BLACK, RS .
ARCHIVES OF NEUROLOGY, 1990, 47 (08) :864-869
[4]  
BLASS JP, 1979, BRAIN ACETYLCHOLINE, P89
[5]  
BOWEN DM, 1979, LANCET, V1, P11
[6]   INVIVO P-31 NMR PROFILES OF ALZHEIMERS-DISEASE AND MULTIPLE SUBCORTICAL INFARCT DEMENTIA [J].
BROWN, GG ;
LEVINE, SR ;
GORELL, JM ;
PETTEGREW, JW ;
GDOWSKI, JW ;
BUERI, JA ;
HELPERN, JA ;
WELCH, KMA .
NEUROLOGY, 1989, 39 (11) :1423-1427
[7]   PHOSPHORYLATION-MEDIATED CHANGES IN PYRUVATE-DEHYDROGENASE ACTIVITY INFLUENCE PYRUVATE-SUPPORTED CALCIUM ACCUMULATION BY BRAIN MITOCHONDRIA [J].
BROWNING, M ;
BAUDRY, M ;
BENNETT, WF ;
LYNCH, G .
JOURNAL OF NEUROCHEMISTRY, 1981, 36 (06) :1932-1940
[8]  
CHASE TN, 1983, AGING-US, V22, P143
[9]   INSITU HYBRIDIZATION OF NUCLEUS BASALIS NEURONS SHOWS INCREASED BETA-AMYLOID MESSENGER-RNA IN ALZHEIMER-DISEASE [J].
COHEN, ML ;
GOLDE, TE ;
USIAK, MF ;
YOUNKIN, LH ;
YOUNKIN, SG .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1988, 85 (04) :1227-1231
[10]   EFFECTS OF HYPOXIA AND NORMOCARBIA ON CEREBRAL BLOOD FLOW AND METABOLISM IN CONSCIOUS MAN [J].
COHEN, PJ ;
ALEXANDER, SC ;
SMITH, TC ;
REIVICH, M ;
WOLLMAN, H .
JOURNAL OF APPLIED PHYSIOLOGY, 1967, 23 (02) :183-+