Table 5.
APOE genotype unaccounted for | APOE genotype accounted for | |||||
---|---|---|---|---|---|---|
Group | Markers | Samples (n) | Correlation | p-value | Partial correlation | p-value |
Whole cohort | MMSE scores | 125 | ρ = 0.263 | 0.003 | r(122) = 0.168 | 0.062 |
CSF Aβ42 (pg/mL) | 119 | ρ = 0.340 | < 0.001 | r(116) = 0.220 | 0.017 | |
CSF Aβ42/Aβ40 | 109 | ρ = 0.349 | < 0.001 | r(106) = 0.242 | 0.012 | |
CSF t-tau (pg/mL) | 120 | ρ = − 0.322 | < 0.001 | r(117) = − 0.212 | 0.021 | |
CSF p-tau (pg/mL) | 120 | ρ = − 0.221 | 0.016 | r(117) = − 0.121 | 0.190 | |
CSF NfL (pg/mL) | 94 | ρ = − 0.227 | 0.028 | r(91) = − 0.203 | 0.051 | |
Controls | Plasma NfL (pg/μL) | 39 | ρ = − 0.335 | 0.037 | r(36) = − 0.328 | 0.044 |
MCI-MCI | CSF Aβ42 (pg/mL) | 30 | r = 0.467 | 0.009 | r(27) = 0.398 | 0.033 |
MCI-ADD | CSF t-tau (pg/mL) | 28 | r = − 0.515 | 0.005 | r(25) = − 0.403 | 0.037 |
CSF p-tau (pg/mL) | 28 | r = − 0.436 | 0.020 | r(25) = − 0.293 | 0.139 | |
CSF α-synuclein (pg/mL) | 27 | r = − 0.414 | 0.032 | r(24) = − 0.333 | 0.096 | |
CSF KLK6 (ng/mL) | 28 | r = − 0.495 | 0.007 | r(25) = − 0.382 | 0.049 |
MCI-MCI amnestic mild cognitive impairment patients that did not progress to an ADD diagnosis after 2 years, MCI-ADD patients with mild cognitive impairment that after two years fulfilled the criteria for an ADD diagnosis, MMSE mini mental state examination, Aβ42 Amyloid-β42 peptide, t-tau Total tau, p-tau: tau phosphorylated at Threonine 181 residue, NfL Neurofilament light chain, KLK6 kallikrein 6. Correlation analysis was performed using Pearson’s (r), or Spearman’s (ρ) tests. Partial correlations were shown as (r(degrees of freedom)) and obtained after controlling for APOE genotype