Table 1 Demographic, clinical, and biomarker characteristics of donor subjects.

From: Age-linked suppression of lipoxin A4 associates with cognitive deficits in mice and humans

 

Healthy controls (HC)

Mild cognitive impairment (MCI)

Alzheimer’s disease (AD)

Dementia with Lewy bodies (DLB)

F, χ2 (p-value)

Sex, male/female

10/15

8/5

4/10

2/7

4.5 (0.21)

Age (years)

67.8 ± 4.8

71.5 ± 6.1

74.2 ± 7.1*

73.7 ± 6.7

4.4 (0.01)

(61–79)

(61–83)

(60–85)

(65–81)

Antidepressant use, yes/no

6/19

6/7

6/8

6/3

5.6 (0.13)

Anti-inflammatory use, yes/no

5/20

1/12

4/10

1/8

2.3 (0.50)

BMI

26.6 ± 5.0

27.1 ± 3.1

26.3 ± 4.4

27.7 ± 6.0

0.2 (0.90)

(20–40.8)

(23.7–33.1)

(20.6–35.8)

(20–40.3)

MMSE

27.6 ± 1.2

26.1 ± 1.5

20.9 ± 4.1****

21.7 ± 3.2****

39.9 (<0.0001)

(25–29)

(23–28)

(14–26)

(18–26)

ApoE4, positive/ negative

7/18

6/7

6/8

5/4

2.7 (0.44)

CSF Aβ42 (pg/mL)

507 ± 242

364 ± 185

260 ± 68.7**

347 ± 145

12.44 (0.002)

(156–1296)

(122–695)

(169–403)

(152–597)

CSF t-tau (pg/mL)

374 ± 207

457 ± 184

583 ± 227***

452 ± 229

10.5 (0.01)

(162–999)

(244–844)

(230–1,181)

(250–947)

  1. Values are presented as means ± SD (range). Statistical significances presented as F (p-value) based on two-tailed one-way ANOVA followed by Holm–Sidak adjustment for multiple comparisons, except for sex, APOE4, antidepressant use, and anti-inflammatory use (Chi-Square Test, χ2 (p-value); Aβ 42 and tau (Kruskal–Wallis test followed by Dunn’s adjustment for multiple comparisons). Asterisks indicate statistically significant differences from HC (*p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001).
  2. Aβ 42 amyloid-β1–42, AD Alzheimer’s disease, APOE4 apolipoprotein E4, CSF cerebrospinal fluid, DLB Dementia with Lewy bodies, HC healthy controls, MCI mild cognitive impairment, MMSE Mini-Mental State Exam, t-tau total tau.
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