TY - JOUR
T1 - Heterogeneity of brain glucose metabolism in mild cognitive impairment and clinical progression to alzheimer disease
AU - Anchisi, Davide
AU - Borroni, Barbara
AU - Franceschi, Massimo
AU - Kerrouche, Nasser
AU - Kalbe, Elke
AU - Beuthien-Beumann, Bettina
AU - Cappa, Stephano
AU - Lenz, Olaf
AU - Ludecke, Stephan
AU - Marcone, Alessandra
AU - Mielke, Rüdiger
AU - Ortelli, Paola
AU - Padovani, Alessandro
AU - Pelati, Oriana
AU - Pupi, Alberto
AU - Scarpini, Elio
AU - Weisenbach, Simon
AU - Herholz, Karl
AU - Salmon, Erik
AU - Holthoff, Vjera
AU - Sorbi, Sandro
AU - Fazio, Ferruccio
AU - Perani, Daniela
PY - 2005/11
Y1 - 2005/11
N2 - Background: Subjects with amnesic mild cognitive impairment (aMCI) may include patients at high risk for progression to Alzheimer disease (AD) and a population with different underlying pathologic conditions. Objective: To evaluate the potential roles of positron emission tomography with fluodeoxyglucose F 18 (18FDG-PET) and memory scores in identifying subjects with aMCI and in predicting progression to dementia. Design, Setting, and Patients: Sixty-seven patients at European centers for neurologic and AD care who were diagnosed as having aMCI each underwent an extensive clinical and neuropsychological examination and an 18FDG-PET study. Forty-eight subjects were followed up periodically for at least 1 year, and progression to dementia was evaluated. Main Outcome Measures: Brain glucose metabolism and memory scores. Results: Fourteen subjects with aMCI who converted to AD within 1 year showed bilateral hypometabolism in the inferior parietal, posterior cingulate, and medial temporal cortex. Subjects with "stable" aMCI presented with hypometabolism in the dorsolateral frontal cortex. The severity of memory impairment, as evaluated by the California Verbal Learning Test-Long Delay Free Recall scores, correlated with the following brain metabolic patterns: scores less than 7 were associated with a typical 18FDG-PET AD pattern, and scores of 7 or higher were associated with hypometabolism in the dorsolateral frontal cortex and no progression to AD. Conclusion: These data provide evidence for clinical and functional heterogeneity among subjects with aMCI and suggest that 18FDG-PET findings combined with memory scores may be useful in predicting short-term conversion to AD.
AB - Background: Subjects with amnesic mild cognitive impairment (aMCI) may include patients at high risk for progression to Alzheimer disease (AD) and a population with different underlying pathologic conditions. Objective: To evaluate the potential roles of positron emission tomography with fluodeoxyglucose F 18 (18FDG-PET) and memory scores in identifying subjects with aMCI and in predicting progression to dementia. Design, Setting, and Patients: Sixty-seven patients at European centers for neurologic and AD care who were diagnosed as having aMCI each underwent an extensive clinical and neuropsychological examination and an 18FDG-PET study. Forty-eight subjects were followed up periodically for at least 1 year, and progression to dementia was evaluated. Main Outcome Measures: Brain glucose metabolism and memory scores. Results: Fourteen subjects with aMCI who converted to AD within 1 year showed bilateral hypometabolism in the inferior parietal, posterior cingulate, and medial temporal cortex. Subjects with "stable" aMCI presented with hypometabolism in the dorsolateral frontal cortex. The severity of memory impairment, as evaluated by the California Verbal Learning Test-Long Delay Free Recall scores, correlated with the following brain metabolic patterns: scores less than 7 were associated with a typical 18FDG-PET AD pattern, and scores of 7 or higher were associated with hypometabolism in the dorsolateral frontal cortex and no progression to AD. Conclusion: These data provide evidence for clinical and functional heterogeneity among subjects with aMCI and suggest that 18FDG-PET findings combined with memory scores may be useful in predicting short-term conversion to AD.
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U2 - 10.1001/archneur.62.11.1728
DO - 10.1001/archneur.62.11.1728
M3 - Article
C2 - 16286547
AN - SCOPUS:27744540147
VL - 62
SP - 1728
EP - 1733
JO - Archives of Neurology
JF - Archives of Neurology
SN - 0003-9942
IS - 11
ER -