Hostname: page-component-cd9895bd7-dk4vv Total loading time: 0 Render date: 2024-12-28T16:43:15.876Z Has data issue: false hasContentIssue false
  • English
  • Français

Alzheimer's Disease: Metabolic Uncoupling of Associative Brain Regions

Published online by Cambridge University Press:  18 September 2015

Stanley I. Rapoport ,
Barry Horwitz ,
James V. Haxby  and
Cheryl L. Grady
Stanley I. Rapoport*
Affiliation:
Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, Maryland
Barry Horwitz
Affiliation:
Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, Maryland
James V. Haxby
Affiliation:
Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, Maryland
Cheryl L. Grady
Affiliation:
Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, Maryland
*
Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD U.S.A. 20892
Rights & Permissions [Opens in a new window]

Abstract:

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

Evidence indicates that Alzheimer's disease (AD) causes functional disconnection of neocortical association areas. In mildly demented AD patients without measurable neocortically-mediated cognitive abnormalities, positron emission tomography demonstrates reduced parietal lobe glucose metabolism and left/right metabolic asymmetries in neocortical association areas. Similar metabolic abnormalities occur in moderately demented patients, but are accompanied by appropriate language and visuospatial discrepancies. Left/right metabolic asymmetries correspond with reduced numbers of partial correlations between metabolic rates in homologous right and left regions, and in the frontal and parietal cortices, indicating metabolic uncoupling among these regions. The affected association regions are those which demonstrate Alzheimer-type neuropathology post-mortem.

Type
Imaging of Demented Subjects
Information
Canadian Journal of Neurological Sciences , Volume 13 , Issue S4 , November 1986 , pp. 540 - 545
Copyright
Copyright © Canadian Neurological Sciences Federation 1986

References

1.Brun, A, Gustafson, L.Distribution of cerebral degeneration in Alzheimer’s disease. A clinico-pathological study. Arch Psychiat Nervenkr 1976; 223: 15–33.CrossRefGoogle ScholarPubMed
2.Ball, MJ, Fisman, M, Hachinski, V, et al. A new definition of Alzheimer’s disease: a hippocampal dementia. Lancet Jan., 1985; 14–16.CrossRefGoogle ScholarPubMed
3.Pearson, RCA, Esiri, MM, Hiorns, RW, et al. Anatomical correlates of the distribution of the pathological changes in the neocortex in Alzheimer’s disease. Proc Natl Acad Sci 1985; 82: 4531–4534.CrossRefGoogle Scholar
4.Haxby, JV, Duara, R, Grady, CL, et al. Relations between neuropsychological and cerebral metabolic asymmetries in early Alzheimer’s disease. J Cerebr Blood Flow Metab 1985; 5: 193–200.CrossRefGoogle ScholarPubMed
5.Haxby, JV, Grady, CL, Duara, R, et al. Neocortical metabolic abnormalities precede non memory cognitive deficits in early Alz-heimer’s-type dementia. Arch Neurol 1986; 43: 882–885.CrossRefGoogle Scholar
6.Grady, CL, Haxby, J, Sundaram, M, et al. Longitudinal relations between cognitive and cerebral metabolic deficits in Alzheimer’s disease (AD). J Clin Exp Neuropsychol 1985; 7: 622.Google Scholar
7.Huang, S-C, Phelps, ME, Hoffman, EJ.et al. Noninvasive determination of local cerebral metabolic rate of glucose in man. Am J Physiol 1980; 238: E69–E82.Google ScholarPubMed
8.Pandya, DN, Seltzer, B.Assocation areas of the cerebral cortex. Trends Neurosci 1982; 5: 386–390.CrossRefGoogle Scholar
9.Van Hoesen, GW.The parahippocampal gyrus. New observations regarding its cortical connections in the monkey. Trends Neurosci 1982; 5: 345–350.CrossRefGoogle Scholar
10.Schwartz, ML, Goldman-Rakic, PS.Callosal and intrahemispheric connectivity of the prefrontal association cortex in Rhesus monkey: relation between intraparietal and principal sulcal cortex. J Comp Neurol 1984; 226: 403–420.CrossRefGoogle ScholarPubMed
11.Goldman, PS, Nauta, WJH.Columnar distribution of cortico-cortical fibers in the frontal association, limbic, and motor cortex of the developing Rhesus monkey. Brain Res 1977; 122: 393–413.CrossRefGoogle ScholarPubMed
12.Duara, R, Grady, C, Haxby, J, et al. Positron emission tomography in Alzheimer’s disease. Neurol 1986; 36: 879–887.CrossRefGoogle ScholarPubMed
13.McKhann, G, Drachman, D, Folstein, M, et al. Clinical diagnosis of Alzheimer’s disease: Report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer’s disease. Neurol 1984; 34: 939–944.CrossRefGoogle ScholarPubMed
14.Fostein, MF, Folstein, SE, McHugh, PR.“Mini-Mental State”. A practical method for grading the cognitive state of patients for the clinician. J Phychiat Res 1975; 12: 189–198.Google Scholar
15.Friedland, RP, Budinger, TF, Koss, E, et al. Alzheimer’s disease: anterior-posterior and lateral hemispheric alterations in cortical glucose utilization. Neurosci Lett 1985; 53: 235–240.CrossRefGoogle ScholarPubMed
16.Foster, NL, Chase, TN, Mansi, L, et al. Cortical abnormalities in Alzheimer’s disease. Ann Neurol 1984; 16: 649–654.CrossRefGoogle ScholarPubMed
17.Grady, CL, Haxby, JV, Schlageter, NL, et al. Stability of metabolic and neuropsychological asymmetries in dementia of the Alzheimer type. Neurol (in press).Google Scholar
18.Horwitz, B, Grady, CL, Schlageter, NL, et al. Intercorrelations of regional cerebral metabolic rates in Alzheimer’s disease. Brain Res (in press).Google Scholar
19.Horwitz, B, Duara, R, Rapoport, SI.Age differences in intercorrelations between regional cerebral metabolic rates for glucose. Ann Neurol 1986; 19: 60–67.CrossRefGoogle ScholarPubMed
20.Arendt, T, Bifl, V, Tennstedt, A, et al. Neuronal loss in different parts of the nucleus basalis is related to neuritic plaque formation in cortical target areas in Alzheimer’s disease. Neurosci 1985; 14, 1–14.CrossRefGoogle ScholarPubMed
21.Soncrant, TT, Horwitz, B, Sato, S, et al. Left-right regional functional interactions are disrupted by corpus callosotomy in the rat. Abstr Soc Neurosci 1986; 12: 177.Google Scholar
22.Metter, EJ, Riege, WH, Kameyama, M, et al. Cerebral metabolic relationships for selected brain regions in Alzheimer’s, Huntington’s, and Parkinson’s diseases. J Cerebr Blood Flow Metab 1984; 4: 500–506.CrossRefGoogle ScholarPubMed
23.Hyman, BT, Hoesen, GWB, Damasio, AR, et al. Alzheimer’s disease: cell-specific pathology isolates the hippocampal formation. Science 1984; 225: 1168–1170.CrossRefGoogle ScholarPubMed
24.Rogers, J, Morrison, JH.Quantitative morphology and regional and laminar distributions of senile plaques in Alzheimer’s disease. J Neurosci 1985; 5: 2801–2808.CrossRefGoogle ScholarPubMed
25.Terry, RD, Peck, A, DeTeresa, R, et al. Some morphometric aspects of the brain in senile dementia of the Alzheimer type. Ann Neurol 1981; 10: 184–192.CrossRefGoogle ScholarPubMed
26.Duyckaerts, C, Hauw, JJ, Piette, F, et al. Cortical atrophy in senile dementia of the Alzheimer type is mainly due to a decrease in cortical length. Acta Neuropath (Berl) 1985; 66: 72–74.Google Scholar
27.Gajdusek, DC.Hypothesis: Interference with axonal transport of neurofilament as a common pathogenetic mechanism in certain diseases of the central nervous system. New Eng J Med 1985; 312: 714–719.CrossRefGoogle ScholarPubMed