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Table 1 Characteristics of Cohort #1 (Religious Order Study) and Cohort #2 (US other sources)

From: Higher angiotensin-converting enzyme 2 (ACE2) levels in the brain of individuals with Alzheimer’s disease

Religious Order Study (Cohort #1)

Characteristics

Control

AD

Statistical Analysis

N

22

38

–

Men, %

41

29

C; Pearson test, x2 = 0.897; p = 0.3436

Mean age at death

86.7 (4.3)

87.5 (5.7)

Mann Whitney test, p = 0.5548

Post-mortem delay, hours

7.9 (5.1)

7.5 (5.1)

Mann Whitney test, p = 0.6648

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 (0.8)

− 0.94 (0.9)#

Mann Whitney test, p = 0.0044

apoE s4 allele carriage (%)

9

45 $

C; Pearson test, x2 = 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

C; Pearson test, x2 = 3.830; p = 0.4295

Presence of chronic cortical macroinfarcts 0/1 (n)

20/2

33/5

C; Pearson test, x2 = 0.224; p = 0.6363

Presence of chronic cortical microinfarcts 0/1 (n)

17/5

34/4

C; Pearson test, x2 = 1.627; p = 0.2021

Usage of antihypertensive medications 0/1 (n)

2/20

5/33

C; Pearson test, x2 = 0.224; p = 0.6363

Usage of diabetes medications 0/1 (n)

15/7

33/5

C; Pearson test, x2 = 3.032; p = 0.0816

Cerebellar pH

6.4 (0.37)

6.3 (0.36)

Mann Whitney test, p = 0.2933

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 concentrations, pmol/L

125.4 (245.9)

363.2 (695.2)1

Mann Whitney test, p = 0.0009

Soluble Aβ42 concentrations, 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)

Claudin5 levels in microvessel extracts (normalized ROD)

CD31 levels in microvessel extracts (normalized ROD)

2.74 (0.77) 1.17 (0.50)

0.45 (0.40)

2.66 (0.79)

1.16 (0.41)

0.41 (0.36)

Mann Whitney test, p = 0.7309 Mann Whitney test, p = 0.6613 Mann Whitney test, p = 0.7366

Other US sources (Cohort #2)

Characteristics

Control

AD

Statistical Analysis

N

30

52

 

Men, %

70

52

C; Pearson test, x2 = 2.561; p = 0.1095

Mean age at death

74.9 (9.7)

78.9 (14.0)

Unpaired t test, p = 0.0784

Post-mortem delay (h)

16.3 (4.9)

17.6 (4.8)

Unpaired t test, p = 0.2185

Braak stages 0–2/3–6 (n)

30/0

0/52

 

Atherosclerosis (%)

n.d

61,5

 
  1. Cohort #1 characteristics (Religious Order Study): Participants were assigned to the “Control” or “AD” group based on the level of AD neuropathological changes associated with their ABC scores [61]. 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 [61]. 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 [61]. 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. Claudin5 and CD31 data in microvessel extracts were normalized with cyclophilin B as a loading control. Cohort #2 characteristics (Other US Sources): Brain samples of this cohort were provided by Harvard Brain Tissue Resource Center (Boston), Miller School of Medicine (Miami) and Human Brain and Spinal Fluid Resource Center (Los Angeles). Participants were assigned to the “Control” or “AD” group based on the Braak score. Values are expressed as means (SD). Statistical analysis (compared to controls): Unpaired t test, Pearson test. AD Alzheimer’s disease, C Contingency, CAA Cerebral amyloid angiopathy, CERAD Consortium to Establish a Registry for Alzheimer’s Disease, MCI Mild cognitive impairment, MMSE Mini-Mental State Examination, NCI Healthy controls with no cognitive impairment ROD Relative optical density
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Acta Neuropathologica Communications

ISSN: 2051-5960

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