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Table 1 Demographic, clinical, and neuropathological characteristics by diagnosis

From: Pathogenic tau modifications occur in axons before the somatodendritic compartment in mossy fiber and Schaffer collateral pathways

 

Clinical diagnosis

 

Comparison by diagnosis group

 

ND

MCI

Total

(P value)

(N = 31)

(N = 13)

(N = 44)

 

Age at death (years)

 Mean ± SD

83.1 ± 6.1

86.2 ± 5.4

84.0 ± 6.0

0.13#

 (Range)

(69–97)

(74–95)

(69–97)

 

Sex

19 M/12F

(61.3% Male)

8 M/5F

(61.5% Male)

27 M/17F (61.4% Male)

> 0.99‡

Postmortem Interval (hours)

 Mean ± SD

2.7 ± 0.6

2.7 ± 0.5

2.7 ± 0.6

0.84#

 (Range)

(1.5–4.8)

(1.8–3.5)

(1.5–4.8)

 

MMSE

 Mean ± SD

28.5 ± 1.3

27.4 ± 2.4

28.2 ± 1.7

0.34#

 (Range)

(26–30)

(23–30)

(23–30)

 

 No Score (N)

8

4

12

 

Braak Stage

 I

5

3

8

0.85§

 II

7

3

10

 III

19

7

26

NIA-Reagan AD Probability Level

 Not AD (0)

9

4

13

0.87§

 Low (1)

7

2

9

 Intermediate (2)

15

7

22

 High (3)

0

0

0

Global CERAD Plaque Density

 None (0)

9

4

13^

0.96§

 Sparse (1)

7

3

10$

 Moderate (2)

8

4

12$

 Frequent (3)

7

2

9$

  1. ND non-demented, MCI mild cognitive impairment, MMSE Mini-Mental State Examination, NIA-Reagan National Institute on Aging-Reagan Institute AD probability level, CERAD Consortium to Establish a Registry for Alzheimer’s disease, AD Alzheimer’s disease. ^primary age-related tauopathy (PART) cases; $non-PART cases; #Mann-Whitney test; ‡Fisher’s exact test; §Chi-square test