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  • Open Access

Correction to: Cerebrovascular and amyloid pathology in predementia stages: the relationship with neurodegeneration and cognitive decline

  • 1Email author,
  • 1,
  • 1,
  • 1,
  • 2, 3,
  • 4,
  • 5, 6,
  • 7,
  • 8,
  • 9,
  • 10,
  • 11,
  • 12,
  • 13,
  • 13,
  • 1,
  • 1, 13 and
  • 1
Alzheimer's Research & Therapy201810:56

https://doi.org/10.1186/s13195-018-0391-x

  • Received: 20 February 2018
  • Accepted: 30 May 2018
  • Published:

The original article was published in Alzheimer's Research & Therapy 2017 9:101

Correction

Upon publication of this article [1], it was noticed that there were some inconsistencies in Tables 1, 2 and 3. Some of the superscript letters were incorrectly assigned. Please see below the correct tables:
Table 1

Comparisons of baseline and follow-up characteristics by Aβ and WMH status

 

Aβ- WMH-

Aβ- WMH+

Aβ + WMH-

Aβ + WMH+

n = 140

n = 39

n = 63

n = 29

Baseline characteristics

 Age

61.7 (8.3)B,C,D

71.3 (7.7)A,C

66.7 (7.8)A,B,D

74.1 (5.0)A,C

 Female, n

94 (67)C

23 (59)

32 (51)A

16 (55)

 Education in years

10.9 (3.1)

11.9 (3.3)

11.1 (3.1)

10.3 (2.9)

 Hypertension, n*

43 (34)

9 (25)

15 (25)

9 (32)

 Obesity, n*

15 (14)

3 (11)

4 (8)

4 (21)

 Diabetes, n*

16 (21)

3 (15)

3 (7)

5 (28)

 APOE-ε4 carrier, n*

33 (51)B

5 (24)A,C,D

29 (62)B

10 (56)B

 Diagnosis MCI, n

70 (50)D

21 (54)D

40 (64)

22 (76)A,B

  amnestic MCI (% within MCI group)

40 (57)

15 (71)

27 (68)

17 (77)

  non-amnestic MCI (% within MCI group)

30 (43)

6 (29)

13 (33)

5 (23)

 CSF Aβ 1–42, pg/ml

973.6 (312.0)C,D

885.0 (242.0)C,D

404.3 (102.6)A,B

419.3 (97.2)A,B

 White matter hyperintensities

0.7 (0.5)B,D

2.3 (0.4)A,C

0.8 (0.4)B,D

2.4 (0.5)A,C

Follow-up characteristics

 Follow-up time

2.1 (1.5)

2.2 (1.3)

2.1 (1.2)

2.4 (1.2)

 Time to progression to dementia

1.3 (0.5)B

2.0 (0.7)A

1.7 (0.7)

2.1 (1.2)

 Progression to dementia, n

8 (6)B,C,D

9 (23)A

18 (29)A

11 (38)A

- AD-type dementia, n

2 (1)B,C,D

7 (18)A

18 (29)A

10 (35)A

- Vascular dementia, n

0 (0)

2 (5)

0 (0)

1 (3)

- Frontotemporal dementia, n

4 (3)

0 (0)

0 (0)

0 (0)

- Lewy Body dementia, n

1 (1)

0 (0)

0 (0)

0 (0)

- Dementia with unknown etiology, n

1 (1)

0 (0)

0 (0)

0 (0)

Results are mean (SD) for continuous variables or frequency (%). Hypertension, obesity, diabetes and APOE ε4 genotype were only available in a subgroup of the sample

Abbreviations: amyloid-beta, AD Alzheimer’s disease, APOE Apolipoprotein E, MCI mild cognitive impairment

WMH measured by the Fazekas scale, range 0–3

Ap < 0.05 compared to Aβ- WMH-

Bp < 0.05 compared to Aβ- WMH+

Cp < 0.05 compared to Aβ + WMH-

Dp < 0.05 compared to Aβ + WMH+

Table 2

Values of neurodegenerative markers by Aβ/WMH groups

 

Aβ- WMH-

Aβ- WMH+

Aβ + WMH-

Aβ + WMH+

Neurodegeneration markers

n = 140

n = 39

n = 63

n = 29

MTA score

1.2 (1.2)B,C,D

2.6 (1.6)A,D

2.1 (1.6)A,D

3.4 (1.8)A,B,C

 MTA abnormal, n

62 (45)B,C,D

32 (82)A

41 (67)A,D

26 (93)A,C

P-tau, pg/ml

54.5 (27.7)C

63.2 (29.3)

77.0 (56.3)A

65.2 (38.2)

 P-tau abnormal, n

53 (38)C

22 (58)

45 (71)A

15 (52)

T-tau, pg/ml

314.7 (202.0)B,C,D

438.4 (248.0)A

499.3 (413.8)A

426.2 (275.2)A

 T-tau abnormal, n

36 (26)B,C,D

20 (53)A

36 (57)A

14 (48)A

Results are mean (SD) and number (%). All analyses were adjusted for study, baseline diagnosis and demographics

Abbreviations: amyloid-beta, MTA medial temporal lobe atrophy, P-tau phosphorylated tau, T-tau Total tau, WMH white matter hyperintensities

Ap < 0.05 compared to Aβ- WMH-

Bp < 0.05 compared to Aβ- WMH+.

Cp < 0.05 compared to Aβ + WMH-.

Dp < 0.05 compared to Aβ + WMH+.

Table 3

Cognitive performance and decline by Aβ/WMH groups

  

Aβ- WMH-

Aβ- WMH+

Aβ + WMH-

Aβ + WMH+

MMSE*

n

140

39

62

27

Baseline

27.79 (27.39, 28.19)

27.52 (26.83, 28.21)

27.20 (26.62, 27.78)

27.40 (26.54, 28.25)

Slope

−0.01 (− 0.15, 0.12)

− 0.29 (− 0.55, − 0.02)

−0.22 (− 0.44, − 0.01)

− 0.31 (− 0.62, 0.00)

Memory delayed recall z-score

n

133

37

58

27

Baseline

−0.48 (− 0.72, − 0.24)B,C,D

−1.04 (− 1.48, − 0.61)A

−1.04 (− 1.41, − 0.68)A

−1.33 (− 1.86, − 0.80)A

Slope

0.05 (− 0.03, 0.13)

0.02 (− 0.12, 0.17)

0.02 (− 0.11, 0.14)

−0.07 (− 0.24, 0.09)

Executive functioning z-score

n

130

37

60

24

Baseline

−0.48 (− 0.76, − 0.21)

−0.41 (− 0.92, 0.09)

−0.78 (− 1.18, − 0.37)

−1.12 (− 1.73, − 0.50)

Slope

0.06 (− 0.02, 0.13)

−0.00 (− 0.15, 0.15)

−0.03 (− 0.16, 0.10)

−0.04 (− 0.23, 0.15)

Results are mean (95% confidence interval). Bold slope estimates = p < 0.05. All analyses were adjusted for study. The analyses on MMSE scores were also corrected for demographics and baseline diagnosis

Abbreviations: amyloid-beta, MMSE mini mental state examination, WMH white matter Hyperintensities

Ap < 0.05 compared to Aβ- WMH-

Bp < 0.05 compared to Aβ- WMH+.

Cp < 0.05 compared to Aβ + WMH-.

Dp < 0.05 compared to Aβ + WMH+.

Notes

Declarations

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Authors’ Affiliations

(1)
Department of Psychiatry and Neuropsychology, School of Mental Health and Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands
(2)
Institute of Clinical Medicine, Neurology, University of Eastern Finland, Kuopio, Finland
(3)
Neurocenter and Department of Neurology, Kuopio University Hospital, Kuopio, Finland
(4)
Department of Neurobiology, Caring Sciences and Society (NVS), Karolinska University Hospital Huddinge, Stockholm, Sweden
(5)
AXA Research Fund and UPMC Chair Sorbonne Universités, Université Pierre et Marie Curie (UPMC), Paris, France
(6)
Institut du cerveau et de la moelle (ICM), Hôpital Pitié-Salpêtrière, Paris, France
(7)
Memory and Dementia Center, 3rd Department of Neurology, Aristotle University of Thessaloniki, G Papanicolau” General Hospital, Thessaloniki, Greece
(8)
Department of Clinical Sciences Malmö, Clinical Memory Research Unit, Lund University, Lund, Sweden
(9)
Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands
(10)
Department of Gerontology and Geriatrics, Leiden University Medical Center, Leiden, The Netherlands
(11)
Departments of Neurology and Laboratory Medicine, Donders Institute for Brain, Cognition and Behaviour, Radboud Alzheimer Center, Radboud University Medical Center, Nijmegen, The Netherlands
(12)
Radboudumc Alzheimer Centre, Department of Geriatric Medicine, Radboud University Medical Center, Nijmegen, The Netherlands
(13)
Department of Neurology, Alzheimer Centre, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, Netherlands

Reference

  1. Bos I, Verhey FR, Ramakers IHGB, Jacobs HIL, Soininen H, Freund-Levi Y, Hampel H, Tsolaki M, Wallin ÅK, van Buchem MA, Oleksik A, Verbeek MM, Olde Rikkert M, van der Flier WM, Scheltens P, Aalten P, Visser PJ, Vos SJB. Cerebrovascular and amyloid pathology in predementia stages: the relationship with neurodegeneration and cognitive decline. Alzheimers Res Ther. 2017;9:101. https://doi.org/10.1186/s13195-017-0328-9.View ArticlePubMedPubMed CentralGoogle Scholar

Copyright

© The Author(s). 2018

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