Hippocampal hypometabolism predicts cognitive decline from normal aging.

TitleHippocampal hypometabolism predicts cognitive decline from normal aging.
Publication TypeJournal Article
Year of Publication2008
AuthorsMosconi L, de Santi S, Li J, Tsui WHon, Li Y, Boppana M, Laska E, Rusinek H, de Leon MJ
JournalNeurobiol Aging
Volume29
Issue5
Pagination676-92
Date Published2008 May
ISSN1558-1497
KeywordsAged, 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.

DOI10.1016/j.neurobiolaging.2006.12.008
Alternate JournalNeurobiol Aging
PubMed ID17222480
PubMed Central IDPMC2430185
Grant ListR01 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)

Weill Cornell Medicine
Department of Radiology
525 East 68th Street New York, NY 10065