Abstract
INTRODUCTION: We examined associations between nutritional biomarkers and clinical progression in individuals with subjective cognitive decline (SCD), mild cognitive impairment (MCI), and Alzheimer's disease (AD)-type dementia. METHODS: We included 528 individuals (64 ± 8 years, 46% F, follow-up 2.1 ± 0.87 years) with SCD (n = 204), MCI (n = 130), and AD (n = 194). Baseline levels of cholesterol, triglycerides, glucose, homocysteine, folate, vitamin A, B12, E and uridine were measured in blood and S-adenosylmethionine and S-adenosylhomocysteine in cerebrospinal fluid. We determined associations between nutritional biomarkers and clinical progression using Cox proportional hazard models. RESULTS: Twenty-two (11%) patients with SCD, 45 (35%) patients with MCI, and 100 (52%) patients with AD showed clinical progression. In SCD, higher levels of low-density lipoprotein (LDL) cholesterol were associated with progression (hazard ratio [HR] [95% confidence interval (CI)] 1.88 [1.04 to 3.41]). In AD, lower uridine levels were associated with progression (0.79 [0.63 to 0.99]). DISCUSSION: Our findings suggest that LDL cholesterol and uridine play a—stage-dependent—role in the clinical progression of AD.
| Original language | English |
|---|---|
| Article number | e12120 |
| Journal | Alzheimer's and Dementia: Diagnosis, Assessment and Disease Monitoring |
| Volume | 12 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 2020 |
Keywords
- Alzheimer's disease
- cholesterol
- clinical progression
- memory clinic
- nutritional biomarkers
- uridine
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In: Alzheimer's and Dementia: Diagnosis, Assessment and Disease Monitoring, Vol. 12, No. 1, e12120, 2020.
Research output: Contribution to journal › Article › Academic › peer-review
TY - JOUR
T1 - LDL cholesterol and uridine levels in blood are potential nutritional biomarkers for clinical progression in Alzheimer's disease
T2 - The NUDAD project
AU - de Leeuw, Francisca A.
AU - Tijms, Betty M.
AU - Doorduijn, Astrid S.
AU - Hendriksen, Heleen M.A.
AU - van de Rest, Ondine
AU - de van der Schueren, Marian A.E.
AU - Visser, Marjolein
AU - van den Heuvel, Ellen G.H.M.
AU - van Wijk, Nick
AU - Bierau, Jörgen
AU - van Berckel, Bart N.
AU - Scheltens, Philip
AU - Kester, Maartje I.
AU - van der Flier, Wiesje M.
AU - Teunissen, Charlotte E.
N1 - Funding Information: Francisca A. de Leeuw, Betty M. Tijms, Astrid S. Doorduijn, Heleen M. A. Hendriksen, Ondine van de Rest, Marian A. E. de van der Schueren, Marjolein Visser, Jorgen Bierau, and Maartje I. Kester report no disclosures. Ellen G. H. M. Heuvel is an employee of FrieslandCampina. Nick van Wijk is an employee of Danone Nutricia Research. Bart N. van Berckel received research support from ZonMW, AVID radiopharmaceuticals, CTMM,. and Janssen Pharmaceuticals. He is a trainer for Piramal and GE. He receives no personal honoraria. Philip Scheltens has received consultancy/speaker fees (paid to the institution) from Novartis, Vivoryon, Genentech, and EIP Pharma. C. E. Teunissen has a collaboration contract with ADx Neurosciences, performed contract research or received grants from Probiodrug, Biogen, Esai, Toyama, Janssen prevention center, Boehringer, AxonNeurosciences, Fujirebio, EIP farma, PeopleBio, and Roche. Research programs of Wiesje M. van der Flier have been funded by ZonMW, NWO, EU‐FP7, EU‐JPND, Alzheimer Nederland, CardioVascular Onderzoek Nederland, Health∼Holland, Topsector Life Sciences and Health, stichting Dioraphte, Gieskes‐Strijbis fonds, stichting Equilibrio, Pasman stichting, Biogen MA Inc, Boehringer Ingelheim, Life‐MI, AVID, Roche BV, Janssen Stellar, Combinostics. Wiesje M. van der Flier has performed contract research for Biogen MA Inc and Boehringer Ingelheim. Wiesje M. van der Flier has been an invited speaker at Boehringer Ingelheim and Biogen MA Inc. All funding is paid to her institution. Funding Information: The NUDAD project is funded by NWO‐FCB (project number 057‐14‐004) and Francisca A. de Leeuw, Astrid S. Doorduijn, Maartje I. Kester, Heleen M A. Hendriksen are appointed on this project. Funding Information: The Alzheimer Center Amsterdam is supported by Stichting Alzheimer Nederland and Stichting VUmc fonds. The clinical database structure was developed with funding from Stichting Dioraphte. Research by the Alzheimer Center Amsterdam is part of the neurodegeneration research program of Amsterdam Neuroscience. W.F. is recipient of a donation by stichting Equilibrio, and of a ZonMW Memorabel grant (#733050814). F.L., A.D., M.K., H.H. are appointed on the NUDAD project, which is funded by NWO‐FCB (project number 057‐14‐004). W.F. holds the Pasman chair. We acknowledge members of the NUDAD project team: Amsterdam University Medical Center location VUmc: Wiesje van der Flier, Maartje Kester, Philip Scheltens, Charlotte Teunissen, Marian de van der Schueren, Francien de Leeuw, Astrid Doorduijn, Jay Fieldhouse, Heleen Hendriksen, José Overbeek, Els Dekkers; Vrije Universiteit Amsterdam: Marjolein Visser; Wageningen University & Research: Ondine van de Rest, Sanne Boesveldt; DSM: Peter van‐Dael, Manfred Eggersdorfer; Nutricia Research: John Sijben, Nick van Wijk, Amos Attali, Martin Verkuijl; FrieslandCampina: Rolf Bos, Cecile Singh‐Povel, Ellen van den Heuvel, Martijn Veltkamp. Funding Information: The Alzheimer Center Amsterdam is supported by Stichting Alzheimer Nederland and Stichting VUmc fonds. The clinical database structure was developed with funding from Stichting Dioraphte. Research by the Alzheimer Center Amsterdam is part of the neurodegeneration research program of Amsterdam Neuroscience. W.F. is recipient of a donation by stichting Equilibrio, and of a ZonMW Memorabel grant (#733050814). F.L., A.D., M.K., H.H. are appointed on the NUDAD project, which is funded by NWO-FCB (project number 057-14-004). W.F. holds the Pasman chair. We acknowledge members of the NUDAD project team: Amsterdam University Medical Center location VUmc: Wiesje van der Flier, Maartje Kester, Philip Scheltens, Charlotte Teunissen, Marian de van der Schueren, Francien de Leeuw, Astrid Doorduijn, Jay Fieldhouse, Heleen Hendriksen, Jos? Overbeek, Els Dekkers; Vrije Universiteit Amsterdam: Marjolein Visser; Wageningen University & Research: Ondine van de Rest, Sanne Boesveldt; DSM: Peter van-Dael, Manfred Eggersdorfer; Nutricia Research: John Sijben, Nick van Wijk, Amos Attali, Martin Verkuijl; FrieslandCampina: Rolf Bos, Cecile Singh-Povel, Ellen van den Heuvel, Martijn Veltkamp. Publisher Copyright: © 2020 The Authors. Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring published by Wiley Periodicals, LLC on behalf of Alzheimer's Association Copyright: Copyright 2021 Elsevier B.V., All rights reserved.
PY - 2020
Y1 - 2020
N2 - INTRODUCTION: We examined associations between nutritional biomarkers and clinical progression in individuals with subjective cognitive decline (SCD), mild cognitive impairment (MCI), and Alzheimer's disease (AD)-type dementia. METHODS: We included 528 individuals (64 ± 8 years, 46% F, follow-up 2.1 ± 0.87 years) with SCD (n = 204), MCI (n = 130), and AD (n = 194). Baseline levels of cholesterol, triglycerides, glucose, homocysteine, folate, vitamin A, B12, E and uridine were measured in blood and S-adenosylmethionine and S-adenosylhomocysteine in cerebrospinal fluid. We determined associations between nutritional biomarkers and clinical progression using Cox proportional hazard models. RESULTS: Twenty-two (11%) patients with SCD, 45 (35%) patients with MCI, and 100 (52%) patients with AD showed clinical progression. In SCD, higher levels of low-density lipoprotein (LDL) cholesterol were associated with progression (hazard ratio [HR] [95% confidence interval (CI)] 1.88 [1.04 to 3.41]). In AD, lower uridine levels were associated with progression (0.79 [0.63 to 0.99]). DISCUSSION: Our findings suggest that LDL cholesterol and uridine play a—stage-dependent—role in the clinical progression of AD.
AB - INTRODUCTION: We examined associations between nutritional biomarkers and clinical progression in individuals with subjective cognitive decline (SCD), mild cognitive impairment (MCI), and Alzheimer's disease (AD)-type dementia. METHODS: We included 528 individuals (64 ± 8 years, 46% F, follow-up 2.1 ± 0.87 years) with SCD (n = 204), MCI (n = 130), and AD (n = 194). Baseline levels of cholesterol, triglycerides, glucose, homocysteine, folate, vitamin A, B12, E and uridine were measured in blood and S-adenosylmethionine and S-adenosylhomocysteine in cerebrospinal fluid. We determined associations between nutritional biomarkers and clinical progression using Cox proportional hazard models. RESULTS: Twenty-two (11%) patients with SCD, 45 (35%) patients with MCI, and 100 (52%) patients with AD showed clinical progression. In SCD, higher levels of low-density lipoprotein (LDL) cholesterol were associated with progression (hazard ratio [HR] [95% confidence interval (CI)] 1.88 [1.04 to 3.41]). In AD, lower uridine levels were associated with progression (0.79 [0.63 to 0.99]). DISCUSSION: Our findings suggest that LDL cholesterol and uridine play a—stage-dependent—role in the clinical progression of AD.
KW - Alzheimer's disease
KW - cholesterol
KW - clinical progression
KW - memory clinic
KW - nutritional biomarkers
KW - uridine
UR - http://www.scopus.com/inward/record.url?scp=85100497203&partnerID=8YFLogxK
U2 - https://doi.org/10.1002/dad2.12120
DO - https://doi.org/10.1002/dad2.12120
M3 - Article
C2 - 33392381
SN - 2352-8729
VL - 12
JO - Alzheimer's and Dementia: Diagnosis, Assessment and Disease Monitoring
JF - Alzheimer's and Dementia: Diagnosis, Assessment and Disease Monitoring
IS - 1
M1 - e12120
ER -