Table 1.
Cohort characteristics
| Characteristics | Control | AD | Statistical Analysis |
|---|---|---|---|
| N | 22 | 38 | — |
| Men, % | 41 | 29 | C; Pearson test, χ2 = 0.897; p = 0.3436 |
| Mean age at death | 86.7 (4.3) | 87.5 (5.7) | Mann Whitney test, p = 0.5548 |
| Mean education, years | 18.3 (3.5) | 18.1 (3.1) | Mann Whitney test, p = 0.5236 |
| Mean MMSE | 25.0 (4.5) | 21.6 (7.9) | Mann Whitney test, p = 0.0791 |
| Global cognition score | −0.32 (0.81) | −0.94 (0.93)# | Mann Whitney test, p = 0.0044 |
| apoE ε4 allele carriage (%) | 9 | 45$ | C; Pearson test, χ2 = 8.182; p = 0.0042 |
| Clinical diagnosis NCI/MCI/AD (n) | 11/8/3 | 9/12/17 | — |
| Thal amyloid score 0/1/2/3 (n) | 7/13/2/0 | 0/3/15/20 | — |
| Braak score 0/1/2/3 (n) | 0/7/15/0 | 0/0/27/11 | — |
| CERAD score 0/1/2/3 (n) | 14/4/4/0 | 1/3/16/18 | — |
| Parenchymal CAA stage in parietal cortex 0/1/2/3/4 (n) | 15/4/1/1/0 | 18/7/5/2/3 | — |
| Presence of chronic cortical macroinfarcts 0/1 (n) | 20/2 | 33/5 | — |
| Presence of chronic cortical microinfarcts 0/1 (n) | 17/5 | 34/4 | — |
| Usage of antihypertensive medications 0/1 (n) | 2/20 | 5/33 | — |
| Usage of diabetes medications 0/1 (n) | 15/7 | 33/5 | — |
| Cerebellar pH | 6.39 (0.37) | 6.29 (0.36) | Mann Whitney test, p = 0.2933 |
| Postmortem delay, hours | 7.93 (5.11) | 7.53 (5.15) | Mann Whitney test, p = 0.6652 |
| Diffuse Plaque Counts in parietal cortex | 3.8 (8.0) | 20.3 (16.8)& | Mann Whitney test, p < 0.0001 |
| Neuritic Plaque Counts in parietal cortex | 1.3 (3.2) | 15.7 (12.5)& | Mann Whitney test, p < 0.0001 |
| Neurofibrillary Tangle Counts | 0.09 (0.43) | 2.92 (8.35)# | Mann Whitney test, p = 0.0096 |
| Soluble Aβ40 concentration, pmol/L | 125.4 (245.9) | 363.2 (695.2)¶ | Mann Whitney test, p = 0.0009 |
| Soluble Aβ42 concentration, pmol/L | 299.6 (475.0) | 1173.6 (503.9)& | Mann Whitney test, p < 0.0001 |
| Soluble Aβ40/Aβ42 ratio | 0.99 (1.09) | 0.34 (0.59) | Mann Whitney test, p < 0.0001 |
| Cyclophilin B in microvessel extracts (loading control) | 2.74 (0.77) | 2.66 (0.79) | Mann Whitney test, p = 0.7309 |
| Claudin5 levels in microvessel extracts (normalized ROD) | 1.17 (0.50) | 1.16 (0.41) | Mann Whitney test, p = 0.6613 |
| CD31 levels in microvessel extracts (normalized ROD) | 0.45 (0.40) | 0.41 (0.36) | Mann Whitney test; p = 0.7366 |
Participants were assigned to the “Control” or “AD” group based on the level of AD neuropathological changes associated with their ABC scores [70]. ABC scores were converted into one of the four levels of AD neuropathological changes (not, low, intermediate or high) using the chart described in the revised NIA-AA guidelines [70]. Intermediate or high levels of AD neuropathological changes were assigned to the “AD” group, while those with no or a low level of AD neuropathological changes were rather assigned to the “Control” group [70]. Parenchymal CAA stages in parietal cortex were determined in the angular gyrus. Brain pH was measured in cerebellum extracts. Soluble Aβ peptide concentrations were determined by ELISA in whole homogenates of inferior parietal cortex. Values are expressed as means (SD) unless specified otherwise. Statistical analysis (compared to controls): Mann Whitney test,
p < 0.01;
p < 0.001;
p < 0.0001; Pearson test,
p < 0.01. Claudin-5 and CD31 data in microvessel extracts were normalized with cyclophilin B as loading control. Abbreviations: AD, Alzheimer’s disease; C, contingency; CAA, cerebral amyloid angiopathy; CERAD, Consortium to Establish a Registry for Alzheimer’s Disease; MCI, mild cognitive impairment; NCI, healthy controls with no cognitive impairment; ROD, relative optical density.