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. Author manuscript; available in PMC: 2015 Jan 30.

Published in final edited form as: J Neurochem. 2009 May 11;110(2):653–661. doi: 10.1111/j.1471-4159.2009.06158.x

Table 3.

Dkk-3, tau, phospho-tau-181, and β-amyloid (1–42) levels in CSF of controls, MCI, and AD patients

	Control (n = 26)			MCI (n = 25)			AD (n = 23)
	Mean ± SEM	Median	Range	Mean ± SEM	Median	Range	Mean ± SEM	Median	Range
Age [years]	58.9 ± 2.3	62	32–82	68.5 ± 2.1	68	46–86	73.3 ± 1.9	74	53–89
Dkk-3 [nmol/L]	28.2 ± 1.3	27.4	18.6–42.1	30.6 ± 2.8	28.2	4.7–55.1	33.6 ± 2.2^*	30.9	20.3–65.6
Total-tau [pg/mL]	235 ± 18	232	46–441	433 ± 62^**	340	45–1200	797 ± 49^***	794	509–1358
Phospho-tau-181 [pg/mL]	34 ± 3	32	16–69	54 ± 6^**	49	10–109	96 ± 7^***	99	36–156
β-Amyloid (1–42) [pg/mL]	1045 ± 55	1038	523–1728	655 ± 66^***	585	215–1434	357 ± 32^***	324	144–757
Ratio^a	37.8 ± 2.0	36.8	24.4–63.3	22.8 ± 1.7^***	21.4	10.9–46.0	11.2 ± 1.0^***	10.0	4.4–21.6

AD, Alzheimer’s disease; MCI, mild cognitive impairment; Dkk, Dickkopf homolog

^a

β-amyloid (1–42)/Dkk-3. Statistical significance versus controls was determined by unpaired two-sided Student’s t-test

^*

p < 0.05

^**

p < 0.01

^***

p < 0.001.

NODES