Comparing brain amyloid deposition, glucose metabolism, and atrophy in mild cognitive impairment with and without a family history of dementia.
| Publication Type | Academic Article |
| Authors | Mosconi L, Andrews R, Matthews D |
| Journal | J Alzheimers Dis |
| Volume | 35 |
| Issue | 3 |
| Pagination | 509-24 |
| Date Published | 01/01/2013 |
| ISSN | 1875-8908 |
| Keywords | Alzheimer Disease, Amyloidosis, Familial, Blood Glucose, Brain, Cognitive Dysfunction, Image Interpretation, Computer-Assisted, Magnetic Resonance Imaging, Positron-Emission Tomography |
| Abstract | This study compares the degree of brain amyloid-β (Aβ) deposition, glucose metabolism, and grey matter volume (GMV) reductions in mild cognitive impairment (MCI) patients overall and as a function of their parental history of dementia. Ten MCI with maternal history (MH), 8 with paternal history (PH), and 24 with negative family history (NH) received 11C-PiB and 18F-FDG PET and T1-MRI as part of the Alzheimer's Disease Neuroimaging Initiative. Statistical parametric mapping, voxel based morphometry, and Z-score mapping were used to compare biomarkers across MCI groups, and relative to 12 normal controls. MCI had higher PiB retention, hypometabolism, and GMV reductions in Alzheimer-vulnerable regions compared to controls. Biomarker abnormalities were more pronounced in MCI with MH than those with PH and NH. After partial volume correction of PET, Aβ load exceeded hypometabolism and atrophy with regard to the number of regions affected and magnitude of impairment in those regions. Hypometabolism exceeded atrophy in all MCI groups and exceeded Aβ load in medial temporal and posterior cingulate regions of MCI MH. While all three biomarkers were abnormal in MCI compared to controls, Aβ deposition was the most prominent abnormality, with MCI MH having the greatest degree of co-occurring hypometabolism. |
| DOI | 10.3233/JAD-121867 |
| PubMed ID | 23478305 |