Table 2.
ADC | ADNI | DCN | UCSF | Pooled sample | ||||||
---|---|---|---|---|---|---|---|---|---|---|
|
|
|
|
|
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Characteristics | Memory (n = 352) (71%) |
Nonmemory (n = 144) (29%) |
Memory (n = 182) (48%) |
Nonmemory (n = 194) (52%) |
Memory (n = 335) (64%) |
Nonmemory (n = 186) (36%) |
Memory (n = 326) (55%) |
Nonmemory (n = 263) (45%) |
Memory (n = 1195) (60%) |
Nonmemory (n = 787) (40%) |
Demographics | ||||||||||
Age (years) | 67.7 ± 7.8 | 64.7 ± 8.4* | 76.2 ± 7.2 | 74.1 ± 8.3 | 72.3 ± 7.8 | 71.1 ± 9.0 | 72.1 ± 9.7 | 70.3 ± 11.0 | 71.5 ± 8.7 | 70.4 ± 9.9‡ |
Female | 180 (51%) | 78 (54%) | 78 (43%) | 87 (45%) | 201 (60%) | 112 (60%) | 171 (52%) | 157 (60%) | 630 (53%) | 434 (55%) |
Education | 0.03 ± 1.00 | −0.06 ± 1.01 | 0.01 ± 0.97 | −0.01 ± 1.03 | 0.03 ± 1.00 | −0.05 ± 1.00 | 0.1 ± 1.00 | −0.13 ± 0.99 | 0.04 ± 0.99 | −0.07 ± 1.01‡ |
Duration complaints | 3.1 ± 2.2 | 2.7 ± 1.7 | — | — | 2.7 ± 2.3 | 2.4 ± 1.8 | — | — | 2.9 ± 2.3 | 2.5 ± 1.8‡ |
Global cognition | ||||||||||
MMSE | 22.6 ± 3.0 | 21.5 ± 3.2† | 23.5 ± 1.9 | 23.0 ± 2.3 | 23.4 ± 2.6 | 22.9 ± 3.0 | 24.4 ± 3.1 | 22.7 ± 3.8* | 23.5 ± 2.8 | 22.6 ± 3.2* |
APOE ε4 genotype | ||||||||||
APOE ε4 positive | 225 (70%) | 74 (59%) | 72 (67%) | 56 (63%) | 175 (67%) | 80 (58%) | 61 (66%) | 39 (48%)‡ | 533 (68%) | 249 (58%)* |
AD biomarkers | ||||||||||
AD biomarker available | 275 (78%) | 114 (79%) | 52 (29%) | 50 (26%) | 123 (38%) | 70 (38%) | 25 (8%) | 28 (11%) | 475 (40%) | 262 (33%) |
AD biomarker positive | 253 (92%) | 105 (92%) | 45 (87%) | 44 (88%) | 106 (86%) | 58 (83%) | 24 (96%) | 28 (100%) | 423 (89%) | 231 (88%) |
MRI | ||||||||||
Hippocampus | −0.07 ± 1.00 | 0.18 ± 0.97 | −0.05 ± 1.01 | 0.05 ± 1.00 | −0.09 ± 0.95 | 0.17 ± 1.07 | — | — | −0.07 ± 1.00 | 0.12 ± 1.00† |
Posterior cortex | 0.11 ± 0.94 | −0.29 ± 1.10† | — | — | 0.08 ± 0.98 | −0.15 ± 1.03‡ | — | — | 0.09 ± 0.96 | −0.21 ± 1.06* |
WMH | 0.10 ± 0.01 | −0.07 ± 0.01 | 0.01 ± 0.32 | −0.01 ± 0.95 | −0.04 ± 0.96 | 0.07 ± 1.07 | — | — | 0.03 ± 0.01 | 0.00 ± 1.05 |
Abbreviations: AD, Alzheimer’s disease; ADC, Amsterdam Dementia Cohort; ADNI, Alzheimer’s Disease Neuroimaging Initiative; APOE, apolipoprotein E; CSF, cerebrospinal fluid; DCN, German Dementia Competence Network; MMSE, Mini–Mental State Examination; MRI, magnetic resonance imaging; UCSF, University of California, San Francisco; WMH, white matter hyperintensity.
NOTE. Data are presented in number (%) or mean ± standard deviation, also when not normally distributed enabling clearer comparison between clusters. P values are based on t tests, χ2, or Kruskal-Wallis analyses, where appropriate. Normalized values are given for education and MRI characteristics. AD biomarkers are available as CSF total tau/amyloid β1–42 (abnormal when >0.52 according to Duits et al. [38] in the ADC and DCN cohorts, and abnormal when >0.39 according to Shaw et al. [39] in the ADNI cohort), or as Pittsburgh compound B positron emission tomography positivity (in the UCSF cohort). When MRI atrophy characteristics were measured using a visual rating scale in which a higher score reflects more severe atrophy, results were inverted so that higher scores reflect less atrophy. Differences between memory and nonmemory clusters are shown in bold and are indicated as follows:
P ≤ .001,
P ≤ .01,
P ≤ .05.
Interpretation: the nonmemory clusters were younger (pooled sample, ADC), less educated (pooled sample), had shorter duration of complaints (pooled sample), lower MMSE scores (ADC, UCSF, pooled sample), were more often APOE ε4 negative (UCSF, pooled sample), had less hippocampal atrophy (pooled sample), but more severe atrophy of the posterior cortex (ADC, DCN, pooled sample) than the memory clusters.