Does posterior cingulate hypometabolism result from disconnection or local pathology across preclinical and clinical stages of Alzheimer’s disease?

• Published in: European journal of nuclear medicine and molecular imaging 2016-03, Vol.43 (3), p.526-536
• Main Authors: Teipel, Stefan, Grothe, Michel J.
• Format: Article
• Language: English
• Subjects: Aged; Aging; Alzheimer Disease - diagnostic imaging; Alzheimer Disease - metabolism; Alzheimer Disease - physiopathology; Alzheimer's disease; Atrophy; Cardiology; Cognition; Cognitive Dysfunction - diagnostic imaging; Cognitive Dysfunction - metabolism; Cognitive Dysfunction - physiopathology; Female; Fluorodeoxyglucose F18 - chemistry; Gray Matter - diagnostic imaging; Gray Matter - pathology; Gyrus Cinguli - metabolism; Gyrus Cinguli - physiopathology; Hippocampus - diagnostic imaging; Hippocampus - pathology; Humans; Image Processing, Computer-Assisted; Imaging; Magnetic Resonance Imaging; Male; Medical diagnosis; Medicine; Medicine & Public Health; Metabolism; Middle Aged; Nuclear Medicine; Oncology; Original Article; Orthopedics; Pathology; Positron-Emission Tomography; Radiology
• ISSN: 1619-7070; 1619-7089
• DOI: 10.1007/s00259-015-3222-3

Purpose Posterior cingulate cortex (PCC) hypometabolism as measured by FDG PET is an indicator of Alzheimer’s disease (AD) in prodromal stages, such as in mild cognitive impairment (MCI), and has been found to be closely associated with hippocampus atrophy in AD dementia. We studied the effects of local and remote atrophy and of local amyloid load on the PCC metabolic signal in patients with different preclinical and clinical stages of AD. Methods We determined the volume of the hippocampus and PCC grey matter based on volumetric MRI scans, PCC amyloid load based on AV45 PET, and PCC metabolism based on FDG PET in 667 subjects participating in the Alzheimer’s Disease Neuroimaging Initiative spanning the range from cognitively normal ageing through prodromal AD to AD dementia. Results In cognitively normal individuals and those with early MCI, PCC hypometabolism was exclusively associated with hippocampus atrophy, whereas in subjects with late MCI it was associated with both local and remote effects of atrophy as well as local amyloid load. In subjects with AD dementia, PCC hypometabolism was exclusively related to local atrophy. Conclusion Our findings suggest that the effects of remote pathology on PCC hypometabolism decrease and the effects of local pathology increase from preclinical to clinical stages of AD, consistent with a progressive disconnection of the PCC from downstream cortical and subcortical brain regions.