Skip to main content

Table 1 Information on the donors of the occipital lobe sections that were used in the present study

From: Proteomics-based investigation of cerebrovascular molecular mechanisms in cerebral amyloid angiopathy by the FFPE-LMD-PCT-SWATH method

Donor number

Gender

Age

Aβ expression level normalized by average in ADNC −/CAA − capillary

COL6A2 expression level normalized by average in ADNC −/CAA − capillary

PMI (hours)

Thal phase for amyloid plaques by IHC

Braak stage for neurofibrillary degeneration

Neuritic plaque CERAD

NIA-AA Alzheimer’s disease neuropathologic change

NIA-Reagan criteria for Alzheimer's disease

CAA

Old macroinfarct

Old microinfarct (lacunar infarct)

Intracerebral hemorrhage

ADNC +/CAA +

 1 (H)

Male

90

239

1.76

5

5

4

3

2

4

3

–

+ 

+ , due to CAA

 2 (H)

Female

93

57.9

2.41

5

3

4

2

2

2

3

–

–

Old subcortical hemorrhage frontal lobe due to CAA

 3 (H)

Female

94

12.7

3.10

2

5

5

3

3

3

2

–

–

–

 4 (L)

Male

69

8.12

1.13

41.5

4

5

3

3

3

3

–

–

–

 5 (L)

Female

94

4.23

1.72

1

4

4

3

2

4

2

–

–

–

 6 (L)

Male

84

2.07

1.31

1.5

3

3

2

2

2

2

–

–

Old subdural hematoma due to trauma

ADNC +/CAA −

 1

Female

93

4.04

1.40

8.5

3

4

3

2

4

0

–

–

Old subdural hematoma due to trauma

 2

Female

111

1.97

2.31

11

3

3

2

2

2

0

–

+ , cerebral cortex and basal ganglia

–

 3

Male

80

1.51

0.690

4

4

3

2

2

2

1

–

–

Thalamic hemorrhage

 4

Female

90

0.807

1.00

3

4

3

2

2

2

0

Right, opposite side of the studied section

–

–

 5

Female

96

0.655

1.71

7.5

4

3

2

2

2

0

–

–

–

ADNC −/CAA −

 1

Male

69

1.71

0.876

1.5

0

1

0

0

4

0

–

Lacunar infarct

–

 2

Male

89

1.64

1.26

9

0

3

0

0

4

0

–

Lacunar infarct

–

 3

Female

74

0.705

1.23

2.5

0

0

0

0

0

0

–

–

Cerebellar hemorrhage

 4

Female

71

0.488

0.607

3.5

0

1

0

0

4

0

Cardiac embolism

–

–

 5

Female

61

0.457

1.02

2.5

0

2

0

0

4

0

–

–

–

  1. FFPE sections of occipital lobes were provided by Mihara Memorial Hospital brain bank. Neuropathological evaluation is based on “The NIA Alzheimer’s disease research centers program (v11)” in National Alzheimer’s Coordinating Center (https://naccdata.org/data-collection/forms-documentation/np-11). National Institute on Aging-Alzheimer’s Association (NIA-AA) guidelines (2012) were applied to determine the level of AD pathological change on the basis of neuropathological analysis. Thal phase for amyloid plaques by immunohistochemistry (IHC) (Thal’s phase), Phase 0–5; Braak stage for neurofibrillary degeneration (Phospho-Tau IHC by AT8 antibody), Stage I–VI; Neuritic plaque
  2. CERAD, 0 = No neuritic plaques, 1 = Sparse neuritic plaques, 2 = Moderate neuritic plaques, 3 = Frequent neuritic plaques; NIA-AA Alzheimer’s disease neuropathologic change (ADNC), 0 = Not AD, 1 = Low ADNC, 2 = Intermediate ADNC, 3 = High ADNC; NIA-Reagan criteria for Alzheimer's disease, 0 = not AD, 1 = low likelihood, 2 = intermediate likelihood, 3 = high likelihood, 4 = unclassified. Whether the AD brain includes the pathology of CAA is determined by immunohistochemical analysis for Aβ vascular deposition. CAA, 0 = none, 1 = mild, 2 = moderate, 3 = severe. When the level of AD pathological changes was “intermediate to high” with moderate to severe CAA, the cases were assigned to ADNC +/CAA + group. The Aβ depositions for this group were observed in all the cortical vessels in FFPE sections. The cases having “intermediate” pathologic changes without CAA were assigned to ADNC +/CAA − group. The cases having no immunoreactive deposits of Aβ were assigned to ADNC −/CAA − group. CAA scores were statistically significantly larger in ADNC +/CAA + group than those in the other two groups (p < 0.001). The expression levels of Aβ and COL6A2 described in this table are the experimental results obtained by the SWATH analysis of the isolated capillary samples in the present study (not by ELISA), and were not used for the purpose to distinguish the ADNC +/CAA +, ADNC +/CAA − and ADNC −/CAA − groups. The expression levels of Aβ and COL6A2 in the capillary were normalized by those in the ADNC −/CAA − capillary as described in "Materials and methods" section. For the ADNC +/CAA + group, the three donors with highly abundant Aβ in capillaries (donors 1, 2 and 3) were classified as “ADNC +/CAA +/H”, and the other three donors (donors 4, 5 and 6) were classified as “ADNC +/CAA +/L”. The total levels of Aβ40 and Aβ42 (not separately) were quantified by the peak area of the tryptic peptide “LVFFAEDVGSNK” which is shared in Aβ40 and Aβ42. The expression levels of Aβ and COL6A2 were not statistically significantly different among three groups (p > 0.05), except for the comparison of ADNC +/CAA + and ADNC −/CAA − group for COL6A2 (p < 0.05). PMI (hours), post mortem interval
Back to article page

Fluids and Barriers of the CNS

ISSN: 2045-8118