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Association of Plasma Aβ40 Peptides, But Not Aβ42, with Coronary Artery Disease and Diabetes Mellitus

Roeben, Benjamin, the TREND study team, Maetzler, Walter, Vanmechelen, Eugeen, Schulte, Claudia, Heinzel, Sebastian, Stellos, Konstantinos, Godau, Jana, Huber, Heiko, Brockmann, Kathrin, Wurster, Isabel, Gaenslen, Alexandra, Grüner, Eva, Niebler, Raphael, Eschweiler, Gerhard W., Berg, Daniela·2016·Journal of Alzheimer's Disease
DOI 10.3233/jad-150575
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Abstract

Background/objective Plasma levels of amyloid-beta (Aβ) 1-40 peptide have been proposed to be associated with cardiovascular mortality in patients with coronary artery disease (CAD). Therefore, we aimed to investigate the association of plasma Aβ levels with CAD, cardiovascular risk factors (CVRF), and APOE genotype in non-demented elderly individuals. Methods Plasma Aβ1 - 40 and Aβ1 - 42 levels of 526 individuals (mean age of 63.0±7.3 years) were quantified with the INNO-BIA plasma Aβ forms assay based on multiplextrademark technique. APOE genotype was determined with an established protocol. Presence of CAD and CVRFs were ascertained using a questionnaire and/or medical records. Results Plasma Aβ1 - 40 levels were significantly higher in individuals with CAD (p = 0.043) and, independently, in individuals with diabetes mellitus (DM) type 2 (p = 0.001) while accounting for age- and gender-effects. Plasma Aβ1 - 42 levels were higher in APOEɛ4 carriers (p = 0.004), but were neither relevantly associated with CAD nor with any CVRF. Plasma Aβ1 - 40 showed no association with APOE genotype. Discussion Our findings argue for an association of circulating plasma Aβ1 - 40 peptides with incident CAD and DM. Further investigations are needed to entangle the role of Aβ1 - 40 role in the pathophysiology of cardiovascular disease independent of its known role in Alzheimer's disease.

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  • Aβ levels are elevated in patients with cardiometabolic diseases including obesity, T2D, and heart failure.

    “However, Aβ levels are elevated in patients with cardiometabolic diseases including obesity, T2D, and heart failure.”

    From BACE1: More than just a β‐secretase (2022) · cites this paper as [195]

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Research works printed but not linked: 41

  1. Roher, 2009, Amyloid beta peptides in human plasma and tissues and their significance for Alzheimer’s disease, Alzheimers Dement, 5, 18, 10.1016/j.jalz.2008.10.004 · DOI
  2. Stamatelopoulos, 2015, Amyloid-beta (1-40) and the risk of death from cardiovascular causes in patients with coronary heart disease, J Am Coll Cardiol, 65, 904, 10.1016/j.jacc.2014.12.035 · DOI
  3. Vassar, 1999, Beta-secretase cleavage of Alzheimer’s amyloid precursor protein by the transmembrane aspartic protease BACE, Science, 286, 735, 10.1126/science.286.5440.735 · DOI · Paper page
  4. Thal, 2002, Phases of A beta-deposition in the human brain and its relevance for the development of AD, Neurology, 58, 1791, 10.1212/WNL.58.12.1791 · DOI · Paper page
  5. Dickson, 1997, The pathogenesis of senile plaques, J Neuropathol Exp Neurol, 56, 321, 10.1097/00005072-199704000-00001 · DOI · Paper page
  6. Thal, 2008, Cerebral amyloid angiopathy and its relationship to Alzheimer’s disease, Acta Neuropathol, 115, 599, 10.1007/s00401-008-0366-2 · DOI · Paper page
  7. Thal, 2008, Parenchymal and vascular Abeta-deposition and its effects on the degeneration of neurons and cognition in Alzheimer’s disease, J Cell Mol Med, 12, 1848, 10.1111/j.1582-4934.2008.00411.x · DOI · Paper page
  8. Yaffe, 2011, Association of plasma beta-amyloid level and cognitive reserve with subsequent cognitive decline, JAMA, 305, 261, 10.1001/jama.2010.1995 · DOI
  9. Graff-Radford, 2007, Association of low plasma Abeta42/Abeta40 ratios with increased imminent risk for mild cognitive impairment and Alzheimer disease, Arch Neurol, 64, 354, 10.1001/archneur.64.3.354 · DOI
  10. Hansson, 2012, Evaluation of plasma Abeta as predictor of Alzheimer’s disease in older individuals without dementia: A population-based study, J Alzheimers Dis, 28, 231, 10.3233/JAD-2011-111418 · DOI
  11. Vukic, 2009, Expression of inflammatory genes induced by beta-amyloid peptides in human brain endothelial cells and in Alzheimer’s brain is mediated by the JNK-AP1 signaling pathway, Neurobiol Dis, 34, 95, 10.1016/j.nbd.2008.12.007 · DOI · Paper page
  12. Giri, 2000, beta-amyloid-induced migration of monocytes across human brain endothelial cells involves RAGE and PECAM-1, Am J Physiol Cell Physiol, 279, C1772, 10.1152/ajpcell.2000.279.6.C1772 · DOI · Paper page
  13. De Meyer, 2002, Platelet phagocytosis and processing of beta-amyloid precursor protein as a mechanism of macrophage activation in atherosclerosis, Circ Res, 90, 1197, 10.1161/01.RES.0000020017.84398.61 · DOI
  14. Puglielli, 2005, Alzheimer disease beta-amyloid activity mimics cholesterol oxidase, J Clin Invest, 115, 2556, 10.1172/JCI23610 · DOI
  15. Hansson, 2007, Prediction of Alzheimer’s disease using the CSF Abeta42/Abeta40 ratio in patients with mild cognitive impairment, Dement Geriatr Cogn Disord, 23, 316, 10.1159/000100926 · DOI
  16. Song, 2011, Meta-analysis of plasma amyloid-beta levels in Alzheimer’s disease, J Alzheimers Dis, 26, 365, 10.3233/JAD-2011-101977 · DOI
  17. van Oijen, 2006, Plasma Abeta(1-40) and Abeta(1-42) and the risk of dementia: A prospective case-cohort study, Lancet Neurol, 5, 655, 10.1016/S1474-4422(06)70501-4 · DOI · Paper page
  18. Rembach, 2014, Changes in plasma amyloid beta in a longitudinal study of aging and Alzheimer’s disease, Alzheimers Dement, 10, 53, 10.1016/j.jalz.2012.12.006 · DOI
  19. Verbeek, 2009, Cerebrospinal fluid amyloid beta(40) is decreased in cerebral amyloid angiopathy, Ann Neurol, 66, 245, 10.1002/ana.21694 · DOI · Paper page
  20. Hyman, 1996, Epidemiological, clinical, and neuropathological study of apolipoprotein E genotype in Alzheimer’s disease, Ann N Y Acad Sci, 802, 1, 10.1111/j.1749-6632.1996.tb32592.x · DOI
  21. Maetzler, 2012, Lowered serum amyloid-beta1-42 autoantibodies in individuals with lifetime depression, J Alzheimers Dis, 32, 95, 10.3233/JAD-2012-120625 · DOI
  22. Hansson, 2010, Evaluation of plasma Abeta(40) and Abeta(42) as predictors of conversion to Alzheimer’s disease in patients with mild cognitive impairment, Neurobiol Aging, 31, 357, 10.1016/j.neurobiolaging.2008.03.027 · DOI
  23. Berg, 2012, Is pre-motor diagnosis possible? The European experience, Parkinsonism Relat Disord, 18, S195, 10.1016/S1353-8020(11)70061-X · DOI
  24. Miller, 1988, A simple salting out procedure for extracting DNA from human nucleated cells, Nucleic Acids Res, 16, 1215, 10.1093/nar/16.3.1215 · DOI
  25. DeMattos, 2002, Brain to plasma amyloid-beta efflux: A measure of brain amyloid burden in a mouse model of Alzheimer’s disease, Science, 295, 2264, 10.1126/science.1067568 · DOI · Paper page
  26. Iadecola, 2004, Neurovascular regulation in the normal brain and in Alzheimer’s disease, Nat Rev Neurosci, 5, 347, 10.1038/nrn1387 · DOI · Paper page
  27. Zlokovic, 2011, Neurovascular pathways to neurodegeneration in Alzheimer’s disease and other disorders, Nat Rev Neurosci, 12, 723, 10.1038/nrn3114 · DOI · Paper page
  28. Jack, 2014, Age-specific population frequencies of cerebral beta-amyloidosis and neurodegeneration among people with normal cognitive function aged 50-89 years: A cross-sectional study, Lancet Neurol, 13, 997, 10.1016/S1474-4422(14)70194-2 · DOI · Paper page
  29. Bates, 2009, Clearance mechanisms of Alzheimer’s amyloid-beta peptide: Implications for therapeutic design and diagnostic tests, Mol Psychiatry, 14, 469, 10.1038/mp.2008.96 · DOI · Paper page
  30. Yamashiro, 2010, Alterations in nitric oxide and endothelin-1 bioactivity underlie cerebrovascular dysfunction in ApoE-deficient mice, J Cereb Blood Flow Metab, 30, 1494, 10.1038/jcbfm.2010.34 · DOI
  31. Kivipelto, 2001, Midlife vascular risk factors and Alzheimer’s disease in later life: Longitudinal, population based study, BMJ, 322, 1447, 10.1136/bmj.322.7300.1447 · DOI · Paper page
  32. Haase, 2013, Amyloid-beta peptides activate alpha1-adrenergic cardiovascular receptors, Hypertension, 62, 966, 10.1161/HYPERTENSIONAHA.113.01348 · DOI
  33. Crawford, 1998, Alzheimer’s beta-amyloid vasoactivity: Identification of a novel beta-amyloid conformational intermediate, FEBS Lett, 436, 445, 10.1016/S0014-5793(98)01170-3 · DOI
  34. Zhao, 2009, Insulin resistance and amyloidogenesis as common molecular foundation for type 2 diabetes and Alzheimer’s disease, Biochim Biophys Acta, 1792, 482, 10.1016/j.bbadis.2008.10.014 · DOI · Paper page
  35. Bomfim, 2012, An anti-diabetes agent protects the mouse brain from defective insulin signaling caused by Alzheimer’s disease- associated Abeta oligomers, J Clin Invest, 122, 1339, 10.1172/JCI57256 · DOI
  36. Sato, 2011, Role of insulin signaling in the interaction between Alzheimer disease and diabetes mellitus: A missing link to therapeutic potential, Curr Aging Sci, 4, 118, 10.2174/1874609811104020118 · DOI
  37. Zhang, 2013, Amyloid-beta induces hepatic insulin resistance in vivo via JAK2, Diabetes, 62, 1159, 10.2337/db12-0670 · DOI
  38. Bitel, 2012, Amyloid-beta and tau pathology of Alzheimer’s disease induced by diabetes in a rabbit animal model, J Alzheimers Dis, 32, 291, 10.3233/JAD-2012-120571 · DOI
  39. Jimenez-Palomares, 2012, Increased Abeta production prompts the onset of glucose intolerance and insulin resistance, Am J Physiol Endocrinol Metab, 302, E1373, 10.1152/ajpendo.00500.2011 · DOI
  40. Yan, 2012, RAGE is a key cellular target for Abeta-induced perturbation in Alzheimer’s disease, Front Biosci (Schol Ed), 4, 240, 10.2741/s265 · DOI
  41. Han, 2011, RAGE: The beneficial and deleterious effects by diverse mechanisms of actions, Mol Cells, 31, 91, 10.1007/s10059-011-0030-x · DOI

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Metadata

Authors
Roeben, B., the TREND study team, Maetzler, W., Vanmechelen, E., Schulte, C., Heinzel, S., Stellos, K., Godau, J., Huber, H., Brockmann, K., Wurster, I., Gaenslen, A., Grüner, E., Niebler, R., Eschweiler, G. W., & Berg, D.
Affiliations
  • Department of Neurodegeneration, Hertie Institute for Clinical Brain Research (HIH), University of Tübingen, Tübingen, Germany
  • Key4AD, Eke, Belgium
  • Institute of Cardiovascular Regeneration, Centre of Molecular Medicine, J.W. Goethe University Frankfurt, Frankfurt am Main, Germany
  • Department of Psychiatry and Psychotherapy, University of Tübingen, Tübingen, Germany
Venue
Journal of Alzheimer's Disease
Publisher
SAGE Publications
Published
2016-04-26
Volume
52
Issue
1
Pages
161-169
ISSN
  • 1387-2877
  • 1875-8908
DOI
10.3233/jad-150575
Cited by
19
References
10

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