Skip to main content
Hauptrubriken
CME Facharzt-Training Webinare Zeitschriften Bücher e.Medpedia Podcast
Service
Jobbörse Info & Hilfe
Fachgebiete
Anästhesiologie Allgemeinmedizin Arbeitsmedizin Augenheilkunde Chirurgie Dermatologie Gynäkologie und Geburtshilfe HNO Innere Medizin Kardiologie Neurologie Onkologie und Hämatologie Orthopädie und Unfallchirurgie Pädiatrie Pathologie Psychiatrie Radiologie Rechtsmedizin Urologie Zahnmedizin
Themen
Typ-2-Diabetes und Adipositas Klimawandel und Gesundheit Neues aus dem Markt COVID-19 Praxis und Beruf Seltene Erkrankungen GOÄ & EBM Panorama
Sammlungen
Kasuistiken Algorithmen & Infografiken Blickdiagnosen Arthropedia FlapFinder (für Dermatochirurgen) Videos Kongressberichterstattung Medizin für Apothekerinnen und Apotheker Für Ärztinnen und Ärzte in Weiterbildung Für Medizinstudierende
Erweiterte Suche
Anmelden
nach oben
European Journal of Nuclear Medicine and Molecular Imaging
Erschienen in: European Journal of Nuclear Medicine and Molecular Imaging 4/2005

01.04.2005 | Review Article

Brain glucose metabolism in the early and specific diagnosis of Alzheimer’s disease

FDG-PET studies in MCI and AD

verfasst von: Lisa Mosconi

Erschienen in: European Journal of Nuclear Medicine and Molecular Imaging | Ausgabe 4/2005

Einloggen, um Zugang zu erhalten

Abstract

The demographics of aging suggest a great need for the early diagnosis of dementia and the development of preventive strategies. Neuropathology and structural MRI studies have pointed to the medial temporal lobe (MTL) as the brain region earliest affected in Alzheimer’s disease (AD). MRI findings provide strong evidence that in mild cognitive impairments (MCI), AD-related volume losses can be reproducibly detected in the hippocampus, the entorhinal cortex (EC) and, to a lesser extent, the parahippocampal gyrus; they also indicate that lateral temporal lobe changes are becoming increasingly useful in predicting the transition to dementia. Fluoro-2-deoxy-D-glucose positron emission tomography (FDG-PET) imaging has revealed glucose metabolic reductions in the parieto-temporal, frontal and posterior cingulate cortices to be the hallmark of AD. Overall, the pattern of cortical metabolic changes has been useful for the prediction of future AD as well as in distinguishing AD from other neurodegenerative diseases. FDG-PET on average achieves 90% sensitivity in identifying AD, although specificity in differentiating AD from other dementias is lower. Moreover, recent MRI-guided FDG-PET studies have shown that MTL hypometabolism is the most specific and sensitive measure for the identification of MCI, while the utility of cortical deficits is controversial. This review highlights cross-sectional, prediction and longitudinal FDG-PET studies and attempts to put into perspective the value of FDG-PET in diagnosing AD-like changes, particularly at an early stage, and in providing diagnostic specificity. The examination of MTL structures, which has so far been exclusive to MRI protocols, is then examined as a possible strategy to improve diagnostic specificity. All told, there is considerable promise that early and specific diagnosis is feasible through a combination of imaging modalities.
Fußnoten
1
MEDLINE (PubMed) database search for literature published between 1989 and present (November 2004). The search strategy involved the combined concepts of AD and FDG-PET, and the search was limited to articles in the English language that involved human subjects. Investigations that did not involve FDG PET were excluded. (Keywords: FDG-PET or PET or positron emission tomography, mild cognitive impairment, cognitively impaired not demented, Alzheimer’s disease, differential diagnosis, diagnostic accuracy.)
 
2
Sensitivity = number of decliners correctly identified/total number of decliners; specificity = number of non-decliners correctly identified/total number of non-decliners; accuracy = number of total cases correctly identified/total number of cases.
 
Literatur
1.
Schoenberg BS. Epidemiology of Alzheimer’s disease and other dementing disorders. J Chronic Dis 1986;39:1095–104.
2.
Fratiglioni L, Grut M, Forsell Y, Viitanen M, Grafstrom M, Holmen K, et al. Prevalence of Alzheimer’s disease and other dementias in an elderly urban population: relationship with age sex, and education. Neurology 1991;41:1886–92.
3.
Brookmeyer R, Gray S, Kawas C. Projections of Alzheimer’s disease in the United States and the public health impact of delaying disease onset. Am J Public Health 1998;88:1337–42.
4.
Larrabee GJ, Crook TH. Estimated prevalence of age-associated memory impairment derived from standardized tests of memory function. Int Psychogeriatr 1994;6:95–104.
5.
Petersen RC, Smith GE, Waring SC, Ivnik RJ, Tangalos EG, Kokmen E. Mild cognitive impairment: clinical characterization and outcome. Arch Neurol 1999;56:303–8.CrossRefPubMed
6.
McKhann G, Drachman D, Folstein M, Katzman R, Price D, Stadlan EM. Clinical diagnosis of Alzheimer’s disease: report of the NINCDS-ADRDA work group under the auspices of Department of Health & Human Services Task Force on Alzheimer’s disease. Neurology 1984;34:939–44.PubMed
7.
Folstein M. The mini-mental state examination. In: Crook T, Ferris SH, Bartus R, editors. Assessment in geriatric psychopharmacology. New Canaan: Mark Powley Associates; 1983. p 47–51.
8.
American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, DC: American Psychiatric Association; 1994.
9.
Knopman DS, DeKosky ST, Cummings JL, Chui H, Corey-Bloom J, Relkin N, et al. Practice parameter: diagnosis of dementia (an evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2001;56:1143–53.PubMed
10.
Ritchie K, Lovestone S. The dementias. Lancet 2002;360:1759–66.
11.
Petersen RC, Stevens JC, Ganguli M, Tangalos EG, Cummings JL, DeKosky ST. Practice parameter: early detection of dementia: mild cognitive impairment (an evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2001;56:1133–42.PubMed
12.
Petersen RC, Doody R, Kurz A, Mohs RC, Morris JC, Rabins PV, et al. Current concepts in mild cognitive impairment. Arch Neurol 2001;58:1985–92.CrossRefPubMed
13.
DeCarli C. Mild cognitive impairment: prevalence, prognosis, aetiology, and treatment. Lancet Neurol 2003;2:15–21.
14.
Mattis S. Dementia rating scale professional manual. Odess (FL): Psychological Assessment Resources; 1988.
15.
Reisberg B, Ferris SH, de Leon MJ, Crook T. The global deterioration scale for assessment of primary degenerative dementia. Am J Psychiatry 1982;139:1136–9.
16.
Ball MJ, Hachinski V, Fox A, Kirshen AJ, Fisman M, Blume W, et al. A new definition of Alzheimer’s disease: a hippocampal dementia. Lancet 1985;1:14–6.
17.
Insausti R, Tunon T, Sobreviela T, Insausti AM, Gonzalo LM. The human entorhinal cortex: a cytoarchitectonic analysis. J Comp Neurol 1995;355:171–98.
18.
Amaral DG, Insausti R. Hippocampal formation. In: Paxinos G, editor. The human nervous system. San Diego: Academic; 1990. p. 711–55.
19.
Squire LR, Knowlton BJ. Memory, hippocampus, and brain systems. Cogn Neurosci 1995;825–37.
20.
Braak H, Braak E. Neuropathological stageing of Alzheimer-related changes. Acta Neuropathol 1991;82:239–59.PubMed
21.
Mesulam MM. Neuroplasticity failure in Alzheimer’s disease: bridging the gap between plaques and tangles. Neuron 1999;24:521–9.
22.
Price JL, Morris JC. Tangles and plaques in nondemented aging and “preclinical” Alzheimer’s disease. Ann Neurol 1999;45:358–68.CrossRefPubMed
23.
Trojanowski JQ, Schmidt ML, Shin R-W, Bramblett GT, Rao D, Lee VMY. Altered tau and neurofilament proteins in neuro-degenerative diseases: diagnostic implication for Alzheimer’s disease and Lewy body dementias. Brain Pathol 1993;3:45–54.
24.
Braak H, Braak E. Development of Alzheimer-related neurofibrillary changes in the neocortex inversely recapitulates cortical myelogenesis. Acta Neuropathol 1996;92:197–201.CrossRefPubMed
25.
Delacourte A, David JP, Sergeant N, Buee L, Wattez A, Vermersch P, et al. The biochemical pathway of neurofibrillary degeneration in aging and Alzheimer’s disease. Neurology 1999;52:1158–65.
26.
Gomez-Isla T, Price JL, McKeel DW Jr, Morris JC, Growdon JH, Hyman BT. Profound loss of layer II entorhinal cortex neurons occurs in very mild Alzheimer’s disease. J Neurosci 1996;16:4491–4500.
27.
Trojanowski JQ, Clark CM, Arai H, Lee VMY. Elevated levels of tau in cerebrospinal fluid: implications for the antemorten diagnosis of Alzheimer’s disease. Alzheimers Dis Rev 1996;1:77–83.
28.
St.George-Hyslop P. Molecular genetics of Alzheimer’s disease. Biol Psychiatry 2000;47:183–99.
29.
Selkoe DJ. Alzheimer’s disease: genotypes, phenotype, and treatments. Science 1997;275:630–1.
30.
Arriagada PV, Marzloff K, Hyman BT. Distribution of Alzheimer-type pathologic changes in nondemented elderly individuals matches the pattern in Alzheimer’s disease. Neurology 1992;42:1681–8.
31.
Giannakopoulos P, Hof PR, Mottier S, Michel JP, Bouras C. Neuropathological changes in the cerebral cortex of 1258 cases from a geriatric hospital: retrospective clinicopathological evaluation of a 10-year autopsy population. Acta Neuropathol 1994;87:456–68.
32.
Ulrich J. Alzheimer changes in nondemented patients younger than sixty-five: possible early stages of Alzheimer’s disease and senile dementia of Alzheimer type. Ann Neurol 1985;17:273–7.
33.
Hulette CM, Welsh-Bohmer KA, Saunders AM, Mash DC, McIntyre LM. Neuropathological and neuropsychological changes in “normal” aging: evidence for preclinical Alzheimer disease in cognitively normal individuals. J Neuropathol Exp Neurol 1998;57:1168–74.
34.
Mark RJ, Pang Z, Geddes JW, Uchida K, Mattson MP. Amyloid β-peptide impairs glucose transport in hippocampal and cortical neurons: involvement of membrane lipid peroxidation. J Neurosci 1997;17:1046–54.
35.
Copani A, Koh JY, Cotman CW. Beta-amyloid increases neuronal susceptibility to injury by glucose deprivation. Neuroreport 1991;2:763–5.
36.
Hyman BT, Van Hoesen GW, Damasio AR, Barnes CL. Alzheimer’s disease: cell-specific pathology isolates the hippocampal formation. Science 1984;225:1168–70.
37.
Davies DC, Horwood N, Isaacs SL, Mann DMA. The effect of age and Alzheimer’s disease on pyramidal neuron density in the individual fields of the hippocampal formation. Acta Neuropathol 1992;83:510–7.
38.
Bobinski MJ, Wegiel J, Wisniewski HM, Tarnawski B, Bobinski M, Reisberg B, et al. Neurofibrillary pathology—correlation with hippocampal formation atrophy in Alzheimer disease. Neurobiol Aging 1996;17:909–9.
39.
Price JL, McKeel J, Morris JC. Synaptic loss and pathological change in older adults—aging versus disease?. Neurobiol Aging 2001;22:351–2.
40.
Price JL, Ko AI, Wade MJ, Tsou SK, McKeel DW, Morris JC. Neuron number in the entorhinal cortex and CA1 in preclinical Alzheimer disease. Arch Neurol 2001;58:1395–1402.
41.
Kril JJ, Patel S, Harding AJ, Halliday GM. Neuron loss from the hippocampus of Alzheimer’s disease exceeds extracellular neurofibrillary tangle formation. Acta Neuropathol 2002;103:370–6.CrossRefPubMed
42.
Bobinski M, de Leon MJ, Wegiel J, De Santi S, Convit A, Saint Louis LA, et al. The histological validation of post mortem magnetic resonance imaging-determined hippocampal volume in Alzheimer’s disease. Neuroscience 2000;95:721–5.
43.
Jack CR Jr, Dickson DW, Parisi JE, Xu YC, Cha RH, O’Brien PC, et al. Antemortem MRI findings correlate with hippocampal neuropathology in typical aging and dementia. Neurology 2002;58:750–7.PubMed
44.
Mosconi L, De Santi S, Rusinek H, Convit A, de Leon MJ. Magnetic resonance and PET studies in the early diagnosis of Alzheimer’s disease. Expert Rev Neurother 2004;4:831–49.
45.
de Leon MJ, George AE, Stylopoulos LA, Smith G, Miller DC. Early marker for Alzheimer’s disease: the atrophic hippocampus. Lancet 1989;2:672–3.
46.
Fox NC, Freeborough PA. Brain atrophy progression measured from registered serial MRI: validation and aplication to Alzheimer’s disease. J Magn Reson Imaging 1997;7:1069–75.
47.
Fox NC, Warrington EK, Freeborough PA, Hartikainen P, Kennedy AM, Stevens JM, et al. Presymptomatic hippocampal atrophy in Alzheimer’s disease: a longitudinal MRI study. Brain 1996;119:2001–7.
48.
Press GA, Amaral DG, Squire LR. Hippocampal abnormalities in amnesic patients revealed by high-resolution magnetic resonance imaging. Nature 1989;341:54–7.
49.
Kesslak JP, Nalcioglu O, Cotman CW. Quantification of magnetic resonance scans for hippocampal and parahippocampal atrophy in Alzheimer’s disease. Neurology 1991;41:51–4.
50.
Jack CR Jr, Petersen RC, O’Brien PC, Tangalos EG. MR-based hippocampal volumetry in the diagnosis of Alzheimer’s disease. Neurology 1992;42:183–8.PubMed
51.
Killiany RJ, Moss MB, Albert MS, Sandor T, Tieman J, Jolesz F. Temporal lobe regions on magnetic resonance imaging identify patients with early Alzheimer’s disease. Arch Neurol 1993;50:949–54.
52.
Convit A, de Leon MJ, Tarshish C, De Santi S, Kluger A, Rusinek H, et al. Hippocampal volume losses in minimally impaired elderly. Lancet 1995;345:266.
53.
Detoledo-Morrell L, Sullivan MP, Morrell F, Wilson RS, Bennett DA, Spencer S. Alzheimer’s disease: in vivo detection of differential vulnerability of brain regions. Neurobiol Aging 1997;18:463–8.
54.
Jack CR Jr, Petersen RC, Xu YC, Waring SC, O’Brien PC, Tangalos EG, et al. Medial temporal atrophy on MRI in normal aging and very mild Alzheimer’s disease. Neurology 1997;49:786–94.
55.
Convit A, de Leon MJ, Tarshish C, De Santi S, Tsui W, Rusinek H, et al. Specific hippocampal volume reductions in individuals at risk for Alzheimer’s disease. Neurobiol Aging 1997;18:131–8.
56.
de Leon MJ, George AE, Golomb J, Tarshish C, Convit A, Kluger A, et al. Frequency of hippocampal formation atrophy in normal aging and Alzheimer’s disease. Neurobiol Aging 1997;18:1–11.
57.
de Leon MJ, Golomb J, George AE, Convit A, Tarshish CY, McRae T, et al. The radiologic prediction of Alzheimer’s disease: the atrophic hippocampal formation. Am J Neuroradiol 1993;14:897–906.
58.
Kaye JA, Swihart T, Howieson D, Dame A, Moore MM, Karnos T, et al. Volume loss of the hippocampus and temporal lobe in healthy elderly persons destined to develop dementia. Neurology 1997;48:1297–1304.
59.
Jack CR Jr, Petersen RC, Xu YC, O’Brien PC, Smith GE, Ivnik RJ, et al. Prediction of AD with MRI-based hippocampal volume in mild cognitive impairment. Neurology 1999;52:1397–1403.
60.
Visser PJ, Scheltens P, Verby FRJ, Schmand B, Launer LJ, Jolles J, et al. Medial temporal lobe atrophy and memory dysfunction as predictors for dementia in subjects with mild cognitive impairment. J Neurol 1999;246:477–85.
61.
Convit A, de Asis J, de Leon MJ, Tarshish C, De Santi S, Rusinek H. Atrophy of the medial occipitotemporal, inferior, and middle temporal gyri in non-demented elderly predict decline to Alzheimer’s disease. Neurobiol Aging 2000;21:19–26.
62.
Jack CR, Peterson RC, Xu Y, O’Brien PC, Smith GE, Ivnik RJ. Rates of hippocampal atrophy correlate with change in clinical status in aging and AD. Neurology 2000;55:484–9.
63.
Jack CRJ, Shiung MM, Gunther JL, O’Brien PC, Weigand SD, Knopman DS, et al. Comparison of different MRI brain atrophy measures with clinical disease progression in AD. Neurology 2004;62:591–600.
64.
Harris MI, Hadden WC, Knowler WC, Bennett PH. Prevalence of diabetes and impaired glucose tolerance and plasma glucose levels in U.S. population aged 20–74 yr. Diabetes 1987;36:523–34.
65.
Fox NC, Warrington EK, Rossor MN. Serial magnetic resonance imaging of cerebral atrophy in preclinical Alzheimer’s disease. Lancet 1999;353:2125.
66.
Dickerson BC, Goncharova I, Sullivan MP, Forchetti C, Wilson RS, Bennett DA, et al. MRI-derived entorhinal and hippocampal atrophy in incipient and very mild Alzheimer’s disease. Neurobiol Aging 2001;22:747–54.
67.
Kohler S, Black SE, Sinden M, Szekely C, Kidron D, Parker JL, et al. Memory impairments associated with hippocampal versus parahippocampal-gyrus atrophy: an MR volumetry study in Alzheimer’s disease. Neuropsychologia 1998;36:901–14.
68.
Bobinski M, de Leon MJ, Convit A, De Santi S, Wegiel J, Tarshish CY, et al. MRI of entorhinal cortex in mild Alzheimer’s disease. Lancet 1999;353:38–40.
69.
Erkinjuntti T, Lee DH, Gao F, Steenhuis R, Eliasziw M, Fry R, et al. Temporal lobe atrophy on magnetic resonance imaging in the diagnosis of early Alzheimer’s disease. Arch Neurol 1993;50:305–10.
70.
Juottonen K, Laakso MP, Insausti R, Lehtovirta M, Pitkanen A, Partanen K, et al. Volumes of the entorhinal and perirhinal cortices in Alzheimer’s disease. Neurobiol Aging 1998;19:15–22.
71.
Killiany RJ, Hyman BT, Gomez-Isla T, Moss MB, Kikinis R, Jolesz F, et al. MRI measures of entorhinal cortex vs hippocampus in preclinical AD. Neurology 2002;58:1188–96.
72.
De Lacoste M-C, White CHI. The role of cortical connectivity in Alzheimer’s disease pathogenesis: a review and model system. Neurobiol Aging 1993;14:1–16.
73.
Simpson IA, Chundu KR, Davies-Hill T, Honer WG, Davies P. Decreased concentrations of GLUT1 and GLUT3 glucose transporters in the brains of patients with Alzheimer’s disease. Ann Neurol 1994;35:546–51.
74.
Kalaria RN, Gravina SA, Schmidley JW, Perry G, Harik SI. The glucose transporter of the human brain and blood–brain barrier. Ann Neurol 1988;24:757–64.
75.
Magistretti PJ, Pellerin L, Rothman DL, Shulman RG. Energy on demand. Science 1999;283:496–7.CrossRefPubMed
76.
Marcus DL, de Leon MJ, Goldman J, Logan J, Christman DR, Wolf AP, et al. Altered glucose metabolism in microvessels from patients with Alzheimer’s disease. Ann Neurol 1989;26:91–4.
77.
Hoyer S, Muller D, Plaschke K. Desensitization of brain insulin receptor: effect on glucose/energy and related metabolism. J Neural Transm 1994;44(Suppl):259–68.
78.
Vanhanen M, Soininen H. Glucose intolerance, cognitive impairment and Alzheimer’s disease. Curr Opin Neurol 1998;11:673–7.
79.
de Leon MJ, Ferris SH, George A, Reisberg B, Christman DR, Kricheff II, et al. Computed tomography and positron emission transaxial tomography evaluations of normal aging and Alzheimer’s disease. J Cereb Blood Flow Metab 1983;3:391–4.
80.
Foster NL, Chase TN, Mansi L, Brooks R, Fedio P, Patronas NJ, et al. Cortical abnormalities in Alzheimer’s disease. Ann Neurol 1984;16:649–54.
81.
Friedland RP, Brun A, Budinger TF. Pathological and positron emission tomographic correlations in Alzheimer’s disease. Lancet 1985;26:228.
82.
Koss E, Friedland RP, Ober BA, Jagust WJ. Differences in lateral hemispheric asymmetries of glucose utilization between early- and late-onset Alzheimer-type dementia. Am J Psychiatry 1985;142:638–40.
83.
Minoshima S, Giordani B, Berent S, Frey KA, Foster NL, Kuhl DE. Metabolic reduction in the posterior cingulate cortex in very early Alzheimer’s disease. Ann Neurol 1997;42:85–94.PubMed
84.
Ouchi Y, Nobezawa S, Okada H, Yoshikawa E, Futatsubashi M, Kaneko M. Altered glucose metabolism in the hippocampal head in memory impairment. Neurology 1998;51:136–42.
85.
de Leon MJ, McRae T, Rusinek H, Convit A, De Santi S, Tarshish C, et al. Cortisol reduces hippocampal glucose metabolism in normal elderly but not in Alzheimer’s disease. J Clin Endocrinol Metab 1997;82:3251–9.
86.
de Leon MJ, Convit A, Wolf OT, Tarshish CY, De Santi S, Rusinek H, et al. Prediction of cognitive decline in normal elderly subjects with 2-[18F]fluoro-2-deoxy-D-glucose/positron-emission tomography (FDG/PET). Proc Natl Acad Sci U S A 2001;98:10966–71.CrossRef
87.
De Santi S, de Leon MJ, Rusinek H, Convit A, Tarshish CY, Boppana M, et al. Hippocampal formation glucose metabolism and volume losses in MCI and AD. Neurobiol Aging 2001;22:529–39.
88.
Nestor PJ, Fryer TD, Smielewski P, Hodges JR. Limbic hypometabolism in Alzheimer’s disease and mild cognitive impairment. Ann Neurol 2003;54:343–51.
89.
Jagust WJ, Eberling JL, Richardson BC, Reed BR, Baker MG, Nordahl TE, et al. The cortical topography of temporal lobe hypometabolism in early Alzheimer’s disease. Brain Res 1993;629:189–98.
90.
McKelvey R, Bergman H, Stern J, Rush C, Zahirney G, Chertkow H. Lack of prognostic significance of SPECT abnormalities in non-demented elderly subjects with memory loss. Can J Neurol Sci 1999;26:23–8.
91.
Ishii K, Sasaki M, Yamaji S, Sakamoto S, Kitagaki H, Mori E. Relatively preserved hippocampal glucose metabolism in mild Alzheimer’s disease. Dement Geriatr Cogn Dis 1998;9:317–22.
92.
Friston KJ, Frith CD, Liddle PF, Frackowiak RSJ. Comparing functional (PET) images: the assessment of significant change. J Cereb Blood Flow Metab 1991;11:690–9.
93.
Friston K, Ashburner J, Frith C, Poline J-B, Heather J, Frackowiak R. Spatial registration and normalization of images. Hum Brain Mapp 1995;3:165–89.
94.
Minoshima S, Frey KA, Koeppe RA, Foster NL, Kuhl DE. A diagnostic approach in Alzheimer’s disease using three-dimensional stereotactic surface projections of fluorine-18-FDG PET. J Nucl Med 1995;36:1238–48.PubMed
95.
Herholz K. PET studies in dementia. Ann Nucl Med 2003;17:79–89.PubMed
96.
Mielke R, Kessler J, Szelies B, Herholz K, Wienhard K, Heiss WD. Normal and pathological aging—findings of positron-emission-tomography. J Neural Transm 1998;105:821–37.
97.
Magistretti PJ, Pellerin L. The contribution of astrocytes to the 18F-2-deoxyglucose signal in PET activation studies. Mol Psychiatry 1996;1:445–52.
98.
Rocher AB, Chapon F, Blaizot X, Baron J-C, Chavoix C. Resting-state brain glucose utilization as measured by PET is directly related to regional synaptophysin levels: a study in baboons. Neuroimage 2004;20:1894–8.
99.
Terry RD, Masliah E, Salmon DP, Butters N, DeTeresa R, Hill R, et al. Physical basis of cognitive alterations in Alzheimer’s disease: synapse loss is the major correlate of cognitive impairment. Ann Neurol 1991;30:572–80.
100.
Messa C, Perani D, Lucignani G, Zenorini A, Zito F, Rizzo G, et al. High-resolution technetium-99m-HMPAO SPECT in patients with probable Alzheimer’s disease: comparison with fluorine-18-FDG PET. J Nucl Med 1994;35:210–6.PubMed
101.
Herholz K, Schopphoff H, Schmidt M, Mielke R, Scheidhauer K, Schicha H, et al. Direct comparison of spatially normalized PET and SPECT scans in Alzheimer’s disease. J Nucl Med 2002;43:21–6.PubMed
102.
Silverman DHS. Brain 18F-FDG PET in the diagnosis of neurodegenerative dementias: comparison with perfusion SPECT and with clinical evaluations lacking nuclear imaging. J Nucl Med 2004;45:594–607.
103.
Videen TO, Perlmutter JS, Mintun MA, Raichle ME. Regional correction of positron emission tomography data for the effects of cerebral atrophy. J Cereb Blood Flow Metab 1988;8:662–70.
104.
Meltzer CC, Bryan NR, Holcomb HH, Kimball AW, Mayberg HS, Sadzot B, et al. Anatomical localization for PET using MRI imaging. J Comput Assist Tomogr 1990;14:418–26.
105.
Ibanez V, Pietrini P, Alexander GE, Furey ML, Teichberg D, Rajapakse JC, et al. Regional glucose metabolic abnormalities are not the result of atrophy in Alzheimer’s disease. Neurology 1999;50:1585–93.
106.
Small GW, Ercoli LM, Silverman DHS, Huang SC, Komo S, Bookheimer S, et al. Cerebral metabolic and cognitive decline in persons at genetic risk for Alzheimer’s disease. Proc Natl Acad Sci U S A 2000;97:6037–42.CrossRef
107.
Hoffman EJ, Phelps ME. Positron emission tomography: principles and quantitation. In: Phelps ME, Mazziotta J, Schelbert H, editors. Positron emission tomography and autoradiography: principles and applications for the brain and heart. New York: Raven Press; 1986. p 237–86.
108.
Silverman DHS, Small GW, Chang CY, Lu CS, Kung de Aburto MA, Chen W, et al. Positron emission tomography in evaluation of dementia: regional brain metabolism and long-term outcome. JAMA 2001;286:2120–7.CrossRefPubMed
109.
Silverman DHS, Truong CT, Kim SK, Chang CY, Chen W, Kowell AP, et al. Prognostic value of regional cerebral metabolism in patients undergoing dementia evaluation: comparison to a quantifying parameter of subsequent cognitive performance and to prognostic assessment without PET. Mol Genet Metab 2003;80:350–5.
110.
Ashburner J, Csernansky JG, Davatzikos C, Fox NC, Frisoni GB, Thompson PM. Computer-assisted imaging to assess brain structure in healthy and diseased brains. Lancet Neurol 2003;2:79–88.
111.
Herholz K, Salmon E, Perani D, Baron JC, Holthoff V, Frolich L, et al. Discrimination between Alzheimer dementia and controls by automated analysis of multicenter FDG PET. Neuroimage 2002;17:302–16.CrossRef
112.
Alexander GE, Chen K, Pietrini P, Rapoport SI, Reiman EM. Longitudinal PET evaluation of cerebral metabolic decline in dementia: a potential outcome measure in Alzheimer’s disease treatment studies. Am J Psychiatry 2002;159:738–45.CrossRefPubMed
113.
Herholz K, Perani D, Salmon E, Franck G, Fazio F, Heiss WD, et al. Comparability of FDG PET studies in probable Alzheimer’s disease. J Nucl Med 1993;34:1460–6.
114.
Patwardhan MB, McCrory DC, Matchar DB, Samsa GP, Rutschmann OT. Alzheimer disease: operating characteristics of PET—a meta-analysis. Radiology 2004;231:73–80.
115.
Desgranges B, Baron J-C, De La Sayette V, Petit-Taboue MC, Benali K, Landeau B, et al. The neural substrates of memory systems impairment in Alzheimer’s disease: a PET study of resting brain glucose utilization. Brain 1998;121:611–31.
116.
Katzman R. Education and the prevalence of dementia and Alzheimer’s disease. Neurology 1993;43:13–20.
117.
Stern Y, Alexander GE, Prohovnik I, Stricks L, Link B, Lennon MC, et al. Relationship between lifetime occupation and parietal flow: implications for reserve against Alzheimer’s disease pathology. Neurology 1995;45:55–60.
118.
Stern Y, Gurland B, Tatemichi TK, Tang MX, Wilder D, Mayeux R. Influence of education and occupation on the incidence of Alzheimer’s disease. JAMA 1994;271:1004–10.
119.
Stern Y. What is cognitive reserve? Theory and research application of the reserve concept. J Int Neuropsychol Soc 2002;8:448–60.
120.
Verghese J, Lipton RB, Katz MJ, Hall CB, Derby CA, Kuslansky G, et al. Leisure activities and the risk of dementia in the elderly. N Engl J Med 2003;348:2508–16.
121.
Kidron D, Black SE, Stanchev P, Buck B, Szalai JP, Parker J, et al. Quantitative MR volumetry in Alzheimer’s disease. Topographic markers and the effects of sex and education. Neurol 1997;49:1504–12.
122.
Coffey CE, Saxton JA, Ratcliff G, Bryan RN, Lucke JF. Relation of education to brain size in normal aging: implications for the reserve hypothesis. Neurology 1999;53:189–96.
123.
Stern Y, Alexander GE, Prohovnik I, Mayeux R. Inverse relationship between education and parietotemporal perfusion deficit in Alzheimer’s disease. Ann Neurol 1992;32:371–5.
124.
Alexander GE, Furey ML, Grady CL, Pietrini P, Brady DR, Mentis MJ, et al. Association of premorbid intellectual function with cerebral metabolism in Alzheimer’s disease: implications for the cognitive reserve hypothesis. Am J Psychiatry 1997;154:165–72.
125.
Lawlor BA, Ryan TM, Schmeidler J, Mohs RC, Davis KL. Clinical symptoms associated with age at onset in Alzheimer’s disease. Am J Psychiatry 1994;151:1646–9.
126.
Berg L, McKeel DW, Miller PJ, Storandt M, Rubin EH, Morris JC, et al. Clinicopathologic studies in cognitively healthy aging and Alzheimer disease: relation of histologic markers to dementia severity, age, sex and apolipoprotein E genotype. Arch Neurol 1998;55:326–35.
127.
Bigio EH, Hynan LS, Sontag E, Satumitra S, White CL. Synapse loss is greater in presenile than senile onset Alzheimer disease: implications for the cognitive reserve hypothesis. Neuropathol Appl Neurobiol 2002;28:218–27.
128.
Sullivan EV, Paula SK, Mathalon DH, Kelvin LO, Yesavage JA, Tinklenberg JR, et al. Greater abnormalities of brain cerebrospinal fluid volumes in younger than in older patients with Alzheimer’s disease. Arch Neurol 1993;50:359–73.
129.
Grady CL, Haxby JV, Horwitz B, Sundaram M, Berg G, Schapiro M, et al. Longitudinal study of the early neuropsychological and cerebral metabolic changes in dementia of the Alzheimer type. J Clin Exp Neuropsychol 1987;10:576–96.
130.
Mielke R, Herholz K, Grond M, Kessler J, Heiss W-D. Differences of regional cerebral glucose metabolism between presenile and senile dementia of Alzheimer type. Neurobiol Aging 1992;13:93–8.
131.
Ichimiya A, Herholz K, Mielke R, Kessler J, Slansky I, Heiss WD. Difference of region cerebral metabolic patterns between presenile and senile dementia of Alzheimer type. J Neurol Sci 1994;123:11–7.
132.
Kemp PM, Holmes C, Hoffmann SM, Bolt L, Holmes R, Rowden J, et al. Alzheimer’s disease: differences in technetium-99m HMPAO SPECT scan findings between early onset and late onset dementia. J Neurol Neurosurg Psychiatry 2003;74:715–9.CrossRef
133.
Mosconi L, Herholz K, Prohovnik I, Nacmias B, De Cristofaro MT, Fayyaz M, et al. Metabolic interaction between ApoE genotype and onset age in Alzheimer’s disease: implications for brain reserve. J Neurol Neurosurg Psychiatry 2005;76:15–23.
134.
Tanzi R, Bertram L. New frontiers in Alzheimer’s disease genetics. Neuron 2001;32:181–4.
135.
Kennedy AM, Frackowiak RSJ, Newman SK, Bloomfield PM, Seaward J, Roques P, et al. Deficits in cerebral glucose metabolism demonstrated by positron emission tomography in individuals at risk of familial Alzheimer’s disease. Neurosci Lett 1995;186:17–20.CrossRefPubMed
136.
Perani D, Grassi F, Sorbi S, Nacmias B, Piacentini S, Piersanti P, et al. PET study in subjects from two Italian FAD families with APP717 Val to llue mutation. Eur J Neurol 1997;4:214–20.
137.
Mosconi L, Sorbi S, Nacmias B, De Cristofaro MTR, Fayazz M, Cellini E, et al. Brain metabolic differences between sporadic and familial Alzheimer’s disease. Neurol 2003;61:1138–40.
138.
Strittmatter WJ, Saunders AM, Schmechel D, Pericak-Vance M, Enghild J, Salvesen GS, et al. Apolipoprotein E: high-avidity binding to β-amyloid and increased frequency of type 4 allele in late-onset familial Alzheimer disease. Proc Natl Acad Sci U S A 1993;90:1977–81.
139.
Laws SM, Hone E, Gandy S, Martins RN. Expanding the association between the APOE gene and the risk of Alzheimer’s disease: possible roles for APOE promoter polymorphisms and alterations in APOE transcription. J Neurochem 2003;84:1215–36.CrossRef
140.
Blesa R, Adroer R, Santacruz P, Ascaso C, Tolosa E, Oliva R. High apolipoprotein E ɛ4 Allele frequency in age-related memory decline. Ann Neurol 1996;39:548–51.
141.
Marquis S, Moore MM, Howieson DB, Sexton G, Payami H, Kaye JA, et al. Independent predictors of cognitive decline in healthy elderly persons. Arch Neurol 2002;59:601–6.
142.
Petersen RC, Smith GE, Ivnik RJ, Tangalos EG, Schaid DJ, Thibodeau SN, et al. Apolipoprotein E status as a predictor of the development of Alzheimer’s disease in memory-impaired individuals. JAMA 1995;273:1274–8.
143.
Reiman EM, Uecker A, Caselli RJ, Lewis S, Bandy D, de Leon MJ, et al. Hippocampal volumes in cognitively normal persons at genetic risk for Alzheimer’s disease. Ann Neurol 1998;44:288–91.
144.
Geroldi C, Pihlajamaki M, Laakso MP, DeCarli C, Beltramello A, Bianchetti A, et al. APOE-epsilon4 is associated with less frontal and more medial temporal lobe atrophy in AD. Neurology 1999;53:1825–32.
145.
Reiman EM, Caselli RJ, Chen K, Alexander GE, Bandy D, Frost J. Declining brain activity in cognitively normal apolipoprotein E epsilon 4 heterozygotes: a foundation for using positron emission tomography to efficiently test treatments to prevent Alzheimer’s disease. Proc Natl Acad Sci U S A 2001;98:3334–9.CrossRef
146.
Reiman EM, Chen K, Alexander GE, Caselli RJ, Bandy D, Osborne D, et al. Functional brain abnormalities in young adults at genetic risk for late-onset Alzheimer’s dementia. Proc Natl Acad Sci U S A 2004;101:284–9.CrossRefPubMed
147.
Small GW, Mazziotta JC, Collins MT, Baxter LR, Phelps ME, Mandelkern MA, et al. Apolipoprotein E type 4 allele and cerebral glucose metabolism in relatives at risk for familial Alzheimer disease. JAMA 1995;273:942–7.
148.
Reiman EM, Caselli RJ, Yun LS, Chen K, Bandy D, Minoshima S, et al. Preclinical evidence of Alzheimer’s disease in persons homozygous for the E4 allele for apolipoprotein E. N Engl J Med 1996;334:752–8.CrossRefPubMed
149.
Mosconi L, Perani D, Sorbi S, Herholz K, Nacmias B, Holthoff V, et al. MCI conversion to dementia and the APOE genotype: a prediction study with FDG-PET. Neurology 2004;63:2332–40.
150.
Herholz K, Nordberg A, Salmon E, Perani D, Kessler J, Mielke R, et al. Impairment of neocortical metabolism predicts progression in Alzheimer’s disease. Dement Geriatr Cogn Dis 1999;10:494–504.CrossRef
151.
Arnaiz E, Jelic V, Almkvist O, Wahlund L-O, Winblad B, Valind S, et al. Impaired cerebral glucose metabolism and cognitive functioning predict deterioration in mild cognitive impairment. Neuroreport 2001;12:851–5.
152.
Chetelat G, Desgranges B, De La Sayette V, Viader F, Eustache F, Baron JC. Mild cognitive impairment: can FDG-PET predict who is to rapidly convert to Alzheimer’s disease? Neurology 2003;60:1374–7.
153.
Jagust WJ. Functional imaging in dementia: an overview. J Clin Psychiatry 1994;55(Suppl):5–11.
154.
Small GW, Okonek A, Mandelkern MA, LaRue A, Chang L, Khonsary A, et al. Age-associated memory loss: initial neuropsychological and cerebral metabolic findings of a longitudinal study. Int Psychogeriatr 1994;6:23–44.
155.
Berent S, Giordani B, Foster N, Minoshima S, Lajiness-O’Neill R, Koeppe R, et al. Neuropsychological function and cerebral glucose utilization in isolated memory impairment and Alzheimer’s disease. J Psychiatr Res 1999;33:7–16.
156.
Drzezga A, Lautenschlager N, Siebner H, Riemenschneider M, Willoch F, Minoshima S, et al. Cerebral metabolic changes accompanying conversion of mild cognitive impairment into Alzheimer’s disease: a PET follow-up study. Eur J Nucl Med Mol Imaging 2003;30:1104–13.CrossRef
157.
Salmon E, Sadzot B, Maquet P, Degueldre C, Lemaire C, Rigo P, et al. Differential diagnosis of Alzheimer’s disease with PET. J Nucl Med 1994;35:391–8.
158.
Mielke R, Schroder R, Fink GR, Kessler J, Herholz K, Heiss WD. Regional cerebral glucose metabolism and postmortem pathology in Alzheimer’s disease. Acta Neuropathol 1996;91:174–9.
159.
Hoffman JM, Welsh-Bohmer KA, Hanson M, Crain B, Hulette C, Earl N, et al. FDG PET imaging in patients with pathologically verified dementia. J Nucl Med 2000;41:1920–8.PubMed
160.
Tedeschi E, Hasselbalch SG, Waldemar G, Juhler M, Hogh P, Holm S, et al. Heterogeneous cerebral glucose metabolism in normal pressure hydrocephalus. J Neurol Neurosurg Psychiatry 1995;59:608–15.
161.
Minoshima S, Foster NL, Sima AA, Frey KA, Albin RL, Kuhl DE. Alzheimer’s disease versus dementia with Lewy bodies: cerebral metabolic distinction with autopsy confirmation. Ann Neurol 2001;50:358–65.CrossRefPubMed
162.
Albin RL, Minoshima S, DAmato CJ, Frey KA, Kuhl DE, Sima AAF. Fluoro-deoxyglucose positron emission tomography in diffuse Lewy body disease. Neurology 1996;47:462–6.
163.
Barber R, Snowden JS, Craufurd D. Frontotemporal dementia and Alzheimer’s disease: retrospective differentiation using information from informants. J Neurol Neurosurg Psychiatry 1995;59:61–70.
164.
Ishii K, Imamura T, Sasaki M, Yamaji S, Sakamoto S, Kitagaki H, et al. Regional cerebral glucose metabolism in dementia with Lewy bodies and Alzheimer’s disease. Neurology 1998;51:125–30.
165.
Santens P, De Bleecker J, Goethals P, Strijckmans K, Lemahieu I, Slegers G, et al. Differential regional cerebral uptake of 18F-fluoro-2-deoxy-D-glucose in Alzheimer’s disease and frontotemporal dementia at initial diagnosis. Eur Neurol 2001;45:19–27.
166.
Perry RJ, Hodges JR. Differentiating frontal and temporal variant frontotemporal dementia from Alzheimer’s disease. Neurology 2000;54:2277–84.
167.
Chan D, Fox NC, Scahill RI, Crum WR, Whitwell JL, Leschziner G, et al. Patterns of temporal lobe atrophy in semantic dementia and Alzheimer’s disease. Ann Neurol 2001;49:433–42.
168.
Boccardi M, Pennanen C, Laakso MP, Testa C, Geroldi C, Soininen H, et al. Amygdaloid atrophy in frontotemporal dementia and Alzheimer’s disease. Neurosci Lett 2002;335:139–43.
169.
Boxer AL, Rankin KP, Miller BL, Schuff N, Weiner M, Gorno-Tempini ML, et al. Cinguloparietal atrophy distinguishes Alzheimer disease from semantic dementia. Arch Neurol 2003;60:949–96.
170.
Higuchi M, Tashiro M, Arai H, Okamura N, Hara S, Higuchi S, et al. Glucose hypometabolism and neuropathological correlates in brains of dementia with Lewy bodies. Exp Neurol 2000;162:247–56.
171.
Gerlach M, Stadler K, Aichner F, Ransmayr G. Dementia with Lewy bodies and AD are not associated with occipital lobe atrophy on MRI. Neurology 2002;59:1476.
172.
Barber R, Ballard C, McKeith IG, Gholkar A, O’Brien JT. MRI volumetric study of dementia with Lewy bodies: a comparison with AD and vascular dementia. Neurology 2000;54:1304–9.PubMed
173.
Cousins DA, Burton EJ, burn D, Gholkar A, McKeith IG, O’Brien JT. Atrophy of the putamen in dementia with Lewy bodies but not Alzheimer’s disease: an MRI study. Neurology 2003;61:1191–5.
174.
Barber R, McKeith I, Ballard C, O’Brien J. Volumetric MRI study of the caudate nucleus in patients with dementia with Lewy bodies, Alzheimer’s disease, and vascular dementia. J Neurol Neurosurg Psychiatry 2002;72:406–7.
175.
O’Brien JT, Paling S, Barber R, Williams ED, Ballard C, McKeith IG, et al. Progressive brain atrophy on serial MRI in dementia with Lewy bodies, AD, and vascular dementia. Neurol 2001;56:1386–8.
176.
Szelies B, Mielke R, Herholz K, Heiss W-D. Quantitative topographical EEG compared to FDG PET for classification of vascular and degenerative dementia. Electroencephalogr Clin Neurophysiol 1994;91:131–9.
177.
Guze BH, Baxter LR, Schwartz JM, Szuba MP, Mazziotta JC, Phelps ME. Changes in glucose metabolism in dementia of the Alzheimer type compared with depression: a preliminary report. Psychiatry Res 1991;40:195–202.
178.
Ebmeier KP, Prentice N, Ryman A, Halloran E, Rimmington JE, Best JK, et al. Temporal lobe abnormalities in dementia and depression: a study using high resolution single photon emission tomography and magnetic resonance imaging. J Neurol Neurosurg Psychiatry 1997;63:597–604.
179.
Ebmeier KP, Glabus M, Prentice N, Ryman A, Goodwin GM. A voxel-based analysis of cerebral perfusion in dementia and depression of old age. Neuroimage 1998;7:199–208.
180.
O’Brien J, Desmond P, Ames D, Schweitzer I, Tuckwell V, Tress B. The differentiation of depression from dementia by temporal lobe magnetic resonance imaging. Psychol Med 1994;24:633–40.
181.
O’Brien JT, Desmond P, Ames D, Schweitzer I, Tress B. Magnetic resonance imaging correlates of memory impairment in the healthy elderly: association with medial temporal lobe atrophy but not white matter lesions. Int J Geriatr Psychiatry 1997;12:369–74.
182.
O’Brien JT, Ames D, Schweitzer I, Colman P, Desmond P, Tress B. Clinical and magnetic resonance imaging correlates of hypothalamic-pituitary-adrenal axis function in depression and Alzheimer’s disease. Br J Psychiatry 1996;168:679–87.
183.
Good CD, Scahill RI, Fox NC, Ashburner J, Friston KJ, Chan D, et al. Automatic differentiation of anatomical patterns in the human brain: validation with studies of degenerative dementias. Neuroimage 2002;17:29–46.
184.
Phelps ME, Mazziotta JC. Positron emission tomography: human brain function and biochemistry. Science 1985;228:799–809.
185.
Meguro K, Blaizot X, Kondoh Y, Le Mestric C, Baron JC, Chavoix C. Neocortical and hippocampal glucose hypometabolism following neurotoxic lesions of the entorhinal and perirhinal cortices in the non-human primate as shown by PET. Implications for Alzheimer’s disease. Brain 1999;122:1519–31.
186.
Millien I, Blaizot X, Giffard C, Mezenge F, Insausti R, Baron J-C, et al. Brain glucose hypometabolism after perirhinal lesions in baboons: implications for Alzheimer disease and aging. J Cereb Blood Flow Metab 2002;22:1248–61.
187.
Hayashi T, Fukuyama H, Katsumi Y, Hanakawa T, Nagahama Y, Yamauchi H, et al. Cerebral glucose metabolism in unilateral entorhinal cortex-lesioned rats: an animal PET study. Neuroreport 1999;10:2113–8.
188.
Mosconi L, Pupi A, De Cristofaro MT, Fayyaz M, Sorbi S, Herholz K. Functional interactions of the entorhinal cortex: an 18F-FDG PET study on normal aging and Alzheimer’s disease. J Nucl Med 2004;45:382–92.
189.
Horwitz B, Duara R, Rapoport SI. Intercorrelations of glucose metabolic rates between brain regions: application to healthy males in a state of reduced sensory input. J Cereb Blood Flow Metab 1984;4:484–99.
190.
Horwitz B, McIntosh AR, Haxby JV, Furey M, Salerno JA, Schapiro MB, et al. Network analysis of PET-mapped visual pathways in Alzheimer type dementia. Neuroreport 1995;6:2287–92.
191.
Friston KJ, Frith CD, Liddle PF, Frackowiak RSJ. Functional connectivity, the principal-component analysis of large (PET) data sets. J Cereb Blood Flow Metab 1993;13:5–14.
192.
Buchanan RW, Vladar K, Barta PE, Pearlson GD. Structural evaluation of the prefrontal cortex in schizophrenia. Am J Psychiatry 1998;155:1049–55.PubMed
193.
de Leon MJ, Ferris SH, George AE, Blau I, Kricheff II, Reisberg B, et al. A new method for the CT evaluation of brain atrophy in senile dementia. IRCS Med Sci 1979;7:404–12.
194.
de Leon MJ, Golomb J, Convit A, De Santi S, McRae TD, George AE. Measurement of medial temporal lobe atrophy in diagnosis of Alzheimer’s disease. Lancet 1993;341:125–6.
195.
Tsui WH, Rusinek H, Van Gelder P, Lebedev S. Analyzing multi-modality tomographic images and associated regions of interest with MIDAS. Proc SPIE Med Imaging Image Process 2001;4322:1725–34.
196.
Duara R, Barker WW, Pascal S. Lack of correlation of regional neuropathology to the regional PET metabolic deficits in Alzheimer’s disease. J Cereb Blood Flow Metab 1991;11(Suppl 2):19.
Metadaten
Titel
Brain glucose metabolism in the early and specific diagnosis of Alzheimer’s disease
FDG-PET studies in MCI and AD
verfasst von
Lisa Mosconi
Publikationsdatum
01.04.2005
Erschienen in
European Journal of Nuclear Medicine and Molecular Imaging / Ausgabe 4/2005
Print ISSN: 1619-7070
Elektronische ISSN: 1619-7089
DOI
https://doi.org/10.1007/s00259-005-1762-7

Weitere Artikel der Ausgabe 4/2005

European Journal of Nuclear Medicine and Molecular Imaging 4/2005 Zur Ausgabe

Image of the Month

The detection of aortic valve infection by FDG-PET/CT in a patient with infection following total knee replacement

Editorial Commentary

PET: too much of a good thing? Does the plethora of choices impact on patient management?

Letter to the Editor

Pre-therapeutic dosimetry with radiolabelled somatostatin analogues in patients with advanced neuroendocrine tumours

Original Article

In vivo imaging of adenosine A2A receptors in rat and primate brain using [11C]SCH442416

Letter to the Editor

Heterogeneity of cerebral blood flow in dementia

Blue pages

First EANM learning course on clinical PET in Russian Language