Table 1.
Descriptive table of demographic and biomarker data
| AD | Non-AD | p | |
| N | 106 | 57 | |
| Gender (f/m) | 47/59 | 18/39 | 0.156 |
| Age at CSF sampling (y) | 77 (72–85)a,c | 70 (60–76)a,b | <0.001* |
| TLPD (y) | 0.2 (0.1–1.5)c | 0.7 (0.1–2.1)b | 0.083 |
| AD suggestive IWG-2 algorithm | 84 | 22 | <0.001* |
| ES | *0.001* | ||
| 0 | 2 | 8 | |
| 1 | 1 | 4 | |
| 2-3 | 34 | 32 | |
| 4 | 69 | 13 | |
| Aβ1-42 (pg/ml) | 389 (290–493)a,c | 585 (407–774)a,b | <0.001* |
| T-tau (pg/ml) | 570 (361–927)a,c | 336 (214–547)a,b | <0.001* |
| P-tau181 (pg/ml) | 65.0 (44.6–94.3)a,c | 39.0 (27.2–55.2)b | <0.001* |
| APOE ɛ4 (carrier/non-carrier) | 37/37 | 12/24 | *0.148* |
All data are presented as median values and corresponding interquartile ranges between brackets. Significant differences between groups are marked as asignificant difference with control group, bsignificant difference with AD group, csignificant difference with Non-AD group. The level of significance was set at a p-value below 0.05 (*). Only a fraction (67%) of cases had APOE genotyping by cause of blood sample availability. AD, Alzheimer’s disease; APOE, apolipoprotein E; ES, Erlangen Score; TLPD, time between LP and death.