Title | Hippocampal hypometabolism predicts cognitive decline from normal aging. |
Publication Type | Journal Article |
Year of Publication | 2008 |
Authors | Mosconi L, de Santi S, Li J, Tsui WHon, Li Y, Boppana M, Laska E, Rusinek H, de Leon MJ |
Journal | Neurobiol Aging |
Volume | 29 |
Issue | 5 |
Pagination | 676-92 |
Date Published | 2008 May |
ISSN | 1558-1497 |
Keywords | Aged, Aged, 80 and over, Aging, Cognition Disorders, Dementia, Female, Fluorodeoxyglucose F18, Glucose, Glucose Metabolism Disorders, Hippocampus, Humans, Male, Middle Aged, Radionuclide Imaging, Radiopharmaceuticals, Statistics as Topic |
Abstract | OBJECTIVE: This longitudinal study used FDG-PET imaging to predict and monitor cognitive decline from normal aging. METHODS: Seventy-seven 50-80-year-old normal (NL) elderly received longitudinal clinical examinations over 6-14 years (561 person-years, mean per person 7.2 years). All subjects had a baseline FDG-PET scan and 55 subjects received follow-up PET exams. Glucose metabolic rates (MRglc) in the hippocampus and cortical regions were examined as predictors and correlates of clinical decline. RESULTS: Eleven NL subjects developed dementia, including six with Alzheimer's disease (AD), and 19 declined to mild cognitive impairment (MCI), on average 8 years after the baseline exam. The baseline hippocampal MRglc predicted decline from NL to AD (81% accuracy), including two post-mortem confirmed cases, from NL to other dementias (77% accuracy), and from NL to MCI (71% accuracy). Greater rates of hippocampal and cortical MRglc reductions were found in the declining as compared to the non-declining NL. CONCLUSIONS: Hippocampal MRglc reductions using FDG-PET during normal aging predict cognitive decline years in advance of the clinical diagnosis. Future studies are needed to increase preclinical specificity in differentiating dementing disorders. |
DOI | 10.1016/j.neurobiolaging.2006.12.008 |
Alternate Journal | Neurobiol Aging |
PubMed ID | 17222480 |
PubMed Central ID | PMC2430185 |
Grant List | R01 AG022374 / AG / NIA NIH HHS / United States M01 RR000096 / RR / NCRR NIH HHS / United States MO1RR0096 / RR / NCRR NIH HHS / United States R01 AG013616 / AG / NIA NIH HHS / United States M01 RR000096-46 / RR / NCRR NIH HHS / United States P30 AG008051 / AG / NIA NIH HHS / United States R01 AG012101 / AG / NIA NIH HHS / United States R01 AG013616-17 / AG / NIA NIH HHS / United States AG022374 / AG / NIA NIH HHS / United States P30 AG008051-18 / AG / NIA NIH HHS / United States R01 AG012101-15 / AG / NIA NIH HHS / United States AG13616 / AG / NIA NIH HHS / United States AG08051 / AG / NIA NIH HHS / United States R01 AG022374-04 / AG / NIA NIH HHS / United States AG12101 / AG / NIA NIH HHS / United States |
Related Institute:
Brain Health Imaging Institute (BHII)