Mild Cognitive Impairment (MCI): Predicting Conversion to Clinically Probable Alzheimer’s Disease with Fluoro-Deoxy-Glucose PET
Optimal implementation of disease-modifying treatment for sporadic Alzheimer’ s disease (AD) will require detection of patients at the pre-dementia stage. Resting-state mapping of brain glucose utilization with PET and 18F-fluorodeoxy-glucose (FDG) is sensitive to early changes in synaptic activity/density in neurodegenerative diseases such as AD. In this study, we assessed memory-impaired patients with mild cognitive impairment (MCI) and used voxel-based analysis to search for an FDG-PET profile associated with rapid conversion to AD.
We prospectively recruited 17 patients with neuropsychologically proven significant and isolated memory impairment fulfilling current criteria for amnestic MCI. We obtained resting-state 18FDG PET and followed each patient up for a fixed period of 18 months to assess conversion to AD based on NINDS-ADRDA criteria.
At the end of follow-up, seven patients had converted to AD (“converters”) and the remaining ten still fulfilled criteria for MCI (“non-converters”). Using SPM99, FDG uptake in the right temporo-parietal association cortex was significantly lower in converters relative to non-converters and discriminated the two groups without overlap. FDG uptake was also lower in the converters in the posterior cingulate cortex, but discrimination was less complete and high statistical significance was not maintained after controlling for MMSE score.
This study, using an objective and comprehensive voxel-based data analysis, suggests that FDG-PET may accurately identify rapid converters.
KeywordsCatheter Depression Dementia Neurol
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- Arnaiz E, Jelic V, Almkvist O, Wahlund LO, Winblad B, Valind S, Nordberg A (2001) Impaired cerebral glucose metabolism and cognitive functioning predict deterioration in mild cognitive impairment. Neuro Report 12: 851–855Google Scholar
- Baron JC (1998) Démences et troubles de la mémoire d’origine dégénérative: Apport de l’imagerie fonctionnelle. Rev Neurol (Paris) 154: 122–130Google Scholar
- Braak H, Braak E (1996) Evolution of the neuropathology of Alzheimer’s disease. Acta Neurol Scand 165: 3–12Google Scholar
- Johnson KA, Lopera F, Jones K, Becker A, Sperling R, Hilson J, Londono J, Siegert I, Arcos M, Moreno S, Madrigal L, Ossa J, Pineda N, Ardila A, Roselli M, Albert MS, Kosik KS, Rios A (2001) Presenilin-l-associated abnormalities in regional cerebral perfusion. Neurology 56: 1545–1551PubMedGoogle Scholar
- Kennedy AM, Newman SK, Frackowiak RS, Cunningham VJ, Rogues P, Stevens J, Neary D, Bruton CJ, Warrington EK, Rossor MN (1995) Deficits in cerebral glucose metabolism demonstrated by positron emission tomography in individuals at risk of familial Alzheimer’s disease. Neurosci Lett 186: 17–20PubMedCrossRefGoogle Scholar
- Small GW, Ercoli LM, Silverman DH, Huang SC, Komo S, Bookheimer SY, Lavretsky H, Miller K, Siddarth P, Rasgon NL, Mazziotta JC, Saxena S, Wu HM, Mega MS, Cummings JL, Saunders AM, Pericak-Vance MA, Roses AD, Barrio JR, Phelps ME (2000) Cerebral metabolic and cognitive decline in persons at genetic risk for Alzheimer’s disease. Proc Natl Acad Sci USA 97: 6037–6042PubMedCrossRefGoogle Scholar