nach oben

European Journal of Nuclear Medicine and Molecular Imaging

Erschienen in:

01.05.2009 | Original Article

FDG-PET changes in brain glucose metabolism from normal cognition to pathologically verified Alzheimer’s disease

verfasst von: Lisa Mosconi, Rachel Mistur, Remigiusz Switalski, Wai Hon Tsui, Lidia Glodzik, Yi Li, Elizabeth Pirraglia, Susan De Santi, Barry Reisberg, Thomas Wisniewski, Mony J. de Leon

Erschienen in: European Journal of Nuclear Medicine and Molecular Imaging | Ausgabe 5/2009

Einloggen, um Zugang zu erhalten

Abstract

Purpose

We report the first clinicopathological series of longitudinal FDG-PET scans in post-mortem (PM) verified cognitively normal elderly (NL) followed to the onset of Alzheimer’s-type dementia (DAT), and in patients with mild DAT with progressive cognitive deterioration.

Methods

Four NL subjects and three patients with mild DAT received longitudinal clinical, neuropsychological and dynamic FDG-PET examinations with arterial input functions. NL subjects were followed for 13 ± 5 years, received FDG-PET examinations over 7 ± 2 years, and autopsy 6 ± 3 years after the last FDG-PET. Two NL declined to mild cognitive impairment (MCI), and two developed probable DAT before death. DAT patients were followed for 9 ± 3 years, received FDG-PET examinations over 3 ± 2 years, and autopsy 7 ± 1 years after the last FDG-PET. Two DAT patients progressed to moderate-to-severe dementia and one developed vascular dementia.

Results

The two NL subjects who declined to DAT received a PM diagnosis of definite AD. Their FDG-PET scans indicated a progression of deficits in the cerebral metabolic rate for glucose (CMRglc) from the hippocampus to the parietotemporal and posterior cingulate cortices. One DAT patient showed AD with diffuse Lewy body disease (LBD) at PM, and her last in vivo PET was indicative of possible LBD for the presence of occipital as well as parietotemporal hypometabolism.

Conclusion

Progressive CMRglc reductions on FDG-PET occur years in advance of clinical DAT symptoms in patients with pathologically verified disease. The FDG-PET profiles in life were consistent with the PM diagnosis.

Nur mit Berechtigung zugänglich

Mirra SS, Heyman A, McKeel D, et al. The Consortium to Establish a Registry for Alzheimer’s Disease (CERAD). Part II. Standardization of the neuropathologic assessment of Alzheimer’s disease. Neurol 1991;41:479–86.

Price JL, Morris JC. Tangles and plaques in nondemented aging and “preclinical” Alzheimer’s disease. Ann Neurol 1999;45:358–68.PubMedCrossRef

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 and Human Services Task Force on Alzheimer’s Disease. Neurology 1984;34:939–44.PubMed

Mosconi L. Brain glucose metabolism in the early and specific diagnosis of Alzheimer’s disease. Eur J Nucl Med 2005;32:486–510.CrossRef

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.PubMed

Drzezga A, Lautenschlager N, Siebner H, 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.PubMedCrossRef

Mosconi L, Perani D, Sorbi S, et al. MCI conversion to dementia and the APOE genotype: a prediction study with FDG-PET. Neurology 2004;63:2332–40.PubMed

Ball MJ, Hachinski V, Fox A, et al. A new definition of Alzheimer’s disease: a hippocampal dementia. Lancet 1985;1:14–6.PubMedCrossRef

de Leon MJ, Convit A, Wolf OT, 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.PubMedCrossRef

10.

Mosconi L, De Santi S, Li J, et al. Hippocampal hypometabolism predicts cognitive decline from normal aging. Neurobiol Aging 2007;29:676–92.PubMedCrossRef

11.

De Santi S, de Leon MJ, Rusinek H, et al. Hippocampal formation glucose metabolism and volume losses in MCI and AD. Neurobiol Aging 2001;22:529–39.PubMedCrossRef

12.

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.PubMed

13.

Hachinski VC, Lassen NA, Marshall J. Multi-infarct dementia, a cause of mental deterioration in the elderly. Lancet 1974;2:207–10.PubMedCrossRef

14.

American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, D.C.: American Psychiatric Association; 1994.

15.

De Santi S, Pirraglia E, Barr W, Babb J, Williams S, Rogers K, et al. Robust and conventional neuropsychological norms: diagnosis and prediction of age-related cognitive decline. Neuropsychology 2008;22:469–84.PubMedCrossRef

16.

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.PubMedCrossRef

17.

Wegiel J, Kuchna I, Nowicki K, et al. Intraneuronal Abeta immunoreactivity is not a predictor of brain amyloidosis-beta or neurofibrillary degeneration. Acta Neuropathol 2007;113:389–402.PubMedCrossRef

18.

Braak H, Braak E. Neuropathological stageing of Alzheimer-related changes. Acta Neuropathol 1991;82:239–59.PubMedCrossRef

19.

The National Institute on Aging, the Reagan Institute Working Group on Diagnostic Criteria for the Neuropathological Assessment of Alzheimer’s disease. Consensus recommendations for the postmortem diagnosis of Alzheimer’s disease. Neurobiol Aging 1997;18:S1–2.CrossRef

20.

Sokoloff L, Reivich M, Kennedy C, et al. The [14C]deoxyglucose method for the measurement of local cerebral glucose utilization: theory, procedure, and normal values in the conscious and anesthetized albino rat. J Neurochem 1977;28:897–916.PubMedCrossRef

21.

Reivich M, Alavi A, Wolf A, et al. Glucose metabolic rate kinetic model parameter determination in humans: the lumped constants and rate constants for [18F]fluorodeoxyglucose and [11C]deoxyglucose. J Cereb Blood Flow Metab 1985;5:179–92.PubMed

22.

George AE, de Leon MJ, Kalnin A, Rosner L, Goodgold A, Chase N. Leukoencephalopathy in normal and pathologic aging: 2. MRI and brain lucencies. AJNR Am J Neuroradiol 1986;7:567–70.PubMed

23.

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.PubMedCrossRef

24.

Talairach J, Tournoux P. Co-planar stereotaxic atlas of the human brain. Stuttgart: Thieme; 1988.

25.

Mosconi L, Tsui WH, Pupi A, et al. (18)F-FDG PET database of longitudinally confirmed healthy elderly individuals improves detection of mild cognitive impairment and Alzheimer’s disease. J Nucl Med 2007;48:1129–34.PubMedCrossRef

26.

Mosconi L, Tsui WH, De Santi S, et al. Reduced hippocampal metabolism in mild cognitive impairment and Alzheimer’s disease: automated FDG-PET image analysis. Neurology 2005;64:1860–7.PubMedCrossRef

27.

Li Y, Rinne JO, Mosconi L, Pirraglia E, Rusinek H, Desanti S, et al. Regional analysis of FDG and PIB-PET images in normal aging, mild cognitive impairment and Alzheimer’s disease. Eur J Nucl Med Mol Imaging 2008;35:2169–81.PubMedCrossRef

28.

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.PubMedCrossRef

29.

Braak H, Braak E. Development of Alzheimer-related neurofibrillary changes in the neocortex inversely recapitulates cortical myelogenesis. Acta Neuropathol 1996;92:197–201.PubMedCrossRef

30.

Delacourte A, David JP, Sergeant N, et al. The biochemical pathway of neurofibrillary degeneration in aging and Alzheimer’s disease. Neurol 1999;52:1158–65.

31.

DeCarli C, Atack JR, Ball MJ, et al. Post-mortem regional neurofibrillary tangle densities but not senile plaque densities are related to regional cerebral metabolic rates for glucose life in Alzheimer’s disease patients. Neurodegeneration 1992;1:113–21.

32.

Bradley KM, O’Sullivan VT, Soper ND, et al. Cerebral perfusion SPET correlated with Braak pathological stage in Alzheimer’s disease. Brain 2002;125:1772–81.PubMedCrossRef

33.

Silverman DHS, Small GW, Chang CY, et al. Positron emission tomography in evaluation of dementia: regional brain metabolism and long-term outcome. JAMA 2001;286:2120–7.PubMedCrossRef

Titel: FDG-PET changes in brain glucose metabolism from normal cognition to pathologically verified Alzheimer’s disease
verfasst von: Lisa Mosconi
Rachel Mistur
Remigiusz Switalski
Wai Hon Tsui
Lidia Glodzik
Yi Li
Elizabeth Pirraglia
Susan De Santi
Barry Reisberg
Thomas Wisniewski
Mony J. de Leon
Publikationsdatum: 01.05.2009
Verlag: Springer-Verlag
Erschienen in: European Journal of Nuclear Medicine and Molecular Imaging / Ausgabe 5/2009
Print ISSN: 1619-7070
Elektronische ISSN: 1619-7089
DOI: https://doi.org/10.1007/s00259-008-1039-z

Springer Medizin

Abstract

Purpose

Methods

Results

Conclusion

Bitte loggen Sie sich ein, um Zugang zu diesem Inhalt zu erhalten

Weitere Artikel der Ausgabe 5/2009

Computer-assisted diagnostic system for neurodegenerative dementia using brain SPECT and 3D-SSP

Diagnostics of “non-acute” vascular prosthesis infection using 18F-FDG PET/CT: our experience with 96 prostheses

Disseminated tuberculosis infection: a ‘super’ 18F-FDG PET/CT appearance

Cerebral perfusion (HMPAO-SPECT) in patients with depression with cognitive impairment versus those with mild cognitive impairment and dementia of Alzheimer’s type: a semiquantitative and automated evaluation

[18F]FDG PET/CT in the diagnosis of malignant peripheral nerve sheath tumours in neurofibromatosis type-1

Mean and maximum standardized uptake values in [18F]FDG-PET for assessment of histopathological response in oesophageal squamous cell carcinoma or adenocarcinoma after radiochemotherapy