TABLE 1.
Cohort characteristics
| BACS/UCSF | ADNI | |||||||
|---|---|---|---|---|---|---|---|---|
| YC | OC | MCI | ADdem | non‐AD a | OC | MCI | ADdem | |
| N | 11 | 51 | 8 | 36 | 31 | 60 | 47 | 30 |
| Age | 39.2 ± 16.0 | 76.8 ± 6.1 | 71.0 ± 6.0 | 62.6 ± 8.0 | 66.6 ± 7.6 | 75.5 ± 7.0 | 76.8 ± 7.6 | 78.5 ± 9.7 |
| Age (range) | 21–59 | 60–93 | 63–80 | 48–82 | 46–79 | 59–94 | 60–92 | 56‐94 |
| Females (%) | 10 (91%) | 24 (46%) | 3 (38%) | 23 (64%) | 15 (48%) | 29 (48%) | 31 (66%) | 14 (47%) |
| Years of education | 16.8 ± 2.0 | 16.7 ± 1.9 | 18.3 ± 3.2 | 16.9 ± 3.0 | 16.4 ± 3.1 | 16.5 ± 2.3 | 16.6 ± 2.9 | 15.1 ± 2.6 |
| MMSE | 29.0 ± 1.5 | 28.8 ± 1.2 | 27.9 ± 2.2 | 21.3 ± 5.0 | 24.1 ± 5.7 | 29.1 ± 1.1 | 28.0 ± 2.0 | 21.7 ± 4.9 |
| Aβ‐positive (%) b | 0 (0%) b | 23 (45%) | 8 (100%) | 36 (100%) | 7 (23%) b | 16 (27%) | 20 (43%) | 27 (90%) |
| APOE ε4 carriers (%) c | 4 (44%) b | 15 (29%) | 5 (63%) | 21 (58%) | 8 (26%) | 19 (32%) | 14 (30%) | 13 (43%) |
Abbreviations: Aβ, amyloid beta; ADdem, patients with a clinical diagnosis of Alzheimer's disease dementia; ADNI, Alzheimer's Disease Neuroimaging Initiative; APOE, apolipoprotein E; BACS, Berkeley Aging Cohort Study; MCI, patients with a clinical diagnosis of mild cognitive impairment; MMSE, Mini‐Mental State Examination; non‐AD, patients with a clinical diagnosis of non‐AD neurodegenerative syndrome; OC, older controls; PET, positron emission tomography; PiB, Pittsburgh compound B; UCSF, University of California San Francisco; YC, young controls.
Notes: Clinical diagnoses were independent from Aβ status. For continuous variables, mean ± SD is indicated unless specified otherwise.
Non AD cases: eight with behavioral variant frontotemporal dementia, seven with non‐fluent primary progressive aphasia, six with corticobasal syndrome, four with Parkinson's disease, three with progressive supranuclear palsy, two with semantic variant primary progressive aphasia.
Missing data in the BACS/UCSF data: Aβ status for 7 YC and 1 non‐AD (patient with behavioral variant frontotemporal dementia who carried a V337M MAPT mutation known to cause Alzheimer's like 3R/4R paired helical filaments tau), and APOE genotype for 2 YC. The Aβ tracer used in BACS/UCSF was PiB, while in ADNI florbetapir was used for 128 subjects and florbetaben for 9. PiB‐PET was missing for a UCSF patient with clinical AD dementia who died 36 months after FTP‐PET and showed high Aβ burden at autopsy (Thal 5 and CERAD frequent); this patient was considered Aβ‐positive in all tables, figures, and analyses.
APOE ε4 indicates the percentage of patients with APOE ε4/ε2, APOE ε4/ε3 or APOE ε4/ε4.