Dietary intake of pantothenic acid is associated with cerebral amyloid burden in patients with cognitive impairment

  • Jae-Ho Lee
  • Soo-Yeon Ahn
  • Hyon Ah Lee
  • Kyoung Sook Won
  • Hyuk Won Chang
  • Jungsu S. Oh
  • Hae-Won Kim Department of Nuclear Medicine, Keimyung University Dongsan Medical Center
Keywords: Alzheimer’s disease, mild cognitive impairment, pantothenic acid, subjective cognitive impairment, vitamin, diet

Abstract

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by the deposition of amyloid-β peptide (Aβ) in diffuse and neuritic plaques. Previous research has suggested that certain vitamins may prevent this process. In the present study, we evaluated the relationship between vitamin intake and cerebral Aβ burden in patients with cognitive impairment. This study included 19 patients with subjective cognitive impairment and 30 patients with mild cognitive impairment. All patients underwent brain MRI and 18F-florbetaben positron emission tomography. The Food Frequency Questionnaire was used to evaluate dietary intake of the 15 vitamins. Intake of vitamin B6 (p = 0.027), vitamin K (p = 0.042), vitamin A (p = 0.063), riboflavin (p = 0.063), β-carotene (p = 0.081), pantothenic acid (p = 0.092), and niacin (p = 0.097) was higher in the Aβ-positive group than in the Aβ-negative group. Multivariate linear regression analysis revealed that pantothenic acid intake was an independent determinant of cerebral Aβ burden (β = 0.287, p = 0.029). No significant correlations were observed between cerebral Aβ burden and the intake of other vitamins. Our findings demonstrated that pantothenic acid intake may be associated with increased cerebral Aβ burden in patients with cognitive impairment. These results may offer insight into potential strategies for AD prevention.

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References


  1. Hebert LE, Weuve J, Scherr PA, Evans DA. Alzheimer disease in the United States (2010–2050) estimated using the 2010 census. Neurology 2013; 80: 1778–83. doi: 10.1212/WNL.0b013e31828726f5.

  2. McKhann GM, Knopman DS, Chertkow H, Hyman BT, Jack CR Jr, Kawas CH, et al. The diagnosis of dementia due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement 2011; 7: 263–9. doi: 10.1016/j.jalz.2011.03.005.

  3. Brickman AM, Provenzano FA, Muraskin J, Manly JJ, Blum S, Apa Z, et al. Regional white matter hyperintensity volume, not hippocampal atrophy, predicts incident Alzheimer disease in the community. Arch Neurol 2012; 69: 1621–7. doi: 10.1001/archneurol.2012.1527.

  4. Ryan NS, Keihaninejad S, Shakespeare TJ, Lehmann M, Crutch SJ, Malone IB, et al. Magnetic resonance imaging evidence for presymptomatic change in thalamus and caudate in familial Alzheimer's disease. Brain 2013; 136: 1399–1414. doi: 10.1093/brain/awt065.

  5. Mikolajczyk K, Szabatin M, Rudnicki P, Grodzki M, Burger C. A JAVA environment for medical image data analysis: initial application for brain PET quantitation. Med Inform (Lond) 1998; 23: 207–14.

  6. Barthel H, Gertz HJ, Dresel S, Peters O, Bartenstein P, Buerger K, et al. Cerebral amyloid-beta PET with florbetaben (18F) in patients with Alzheimer's disease and healthy controls: a multicentre phase 2 diagnostic study. Lancet Neurol 2011; 10: 424–35. doi: 10.1016/S1474-4422(11)70077-1.

  7. Hardy JA, Higgins GA. Alzheimer's disease: the amyloid cascade hypothesis. Science 1992; 256: 184–5.

  8. Yaffe K, Kanaya A, Lindquist K, Simonsick EM, Harris T, Shorr RI, et al. The metabolic syndrome, inflammation, and risk of cognitive decline. JAMA 2004; 292: 2237–42.

  9. Rosengren A, Skoog I, Gustafson D, Wilhelmsen L. Body mass index, other cardiovascular risk factors, and hospitalization for dementia. Arch Intern Med 2005; 165: 321–6.

  10. Jack CR Jr, Lowe VJ, Weigand SD, Wiste HJ, Senjem ML, Knopman DS, et al. Serial PiB and MRI in normal, mild cognitive impairment and Alzheimer’s disease: implications for sequence of pathological events in Alzheimer’s disease. Brain 2009; 132: 1355–65. doi: 10.1093/brain/awp062.

  11. van Norden AG, van Dijk EJ, de Laat KF, Scheltens P, Olderikkert MG, de Leeuw FE. Dementia: Alzheimer pathology and vascular factors: from mutually exclusive to interaction. Biochem Biophys Acta 2012; 1822: 340–9. doi: 10.1016/j.bbadis.2011.07.003.

  12. Latta CH, Brothers HM, Wilcock DM. Neuroinflammation in Alzheimer’s disease; A source of heterogeneity and target for personalized therapy. Neuroscience 2015; 302: 103–111. doi: 10.1016/j.neuroscience.2014.09.061.

  13. Morris MC, Evans DA, Bienias JL, Tangney CC, Bennett DA, Aggarwal N, et al. Dietary intake of antioxidant nutrients and the risk of incident Alzheimer disease in a biracial community study. JAMA 2002; 287: 3230–7.

  14. Ousset PJ, Nourhashemi F, Reynish E, Vellas B. Nutritional status is associated with disease progression in very mild Alzheimer disease. Alzheimer Dis Assoc Disord 2008; 22: 66–71. doi: 10.1097/WAD.0b013e31815a9dbb.

  15. Kamphuis PJ, Scheltens P. Can nutrients prevent or delay onset of Alzheimer’s disease? J Alzheimers Dis 2010; 20: 765–75. doi: 10.3233/JAD-2010-091558.

  16. Gu Y, Scarmeas N. Dietary patterns in Alzheimer’s disease and cognitive aging. Curr Alzheimer Res 2011; 8: 510–19.

  17. Paleologos M, Cumming RG, Lazarus R. Cohort study of vitamin C intake and cognitive impairment. Am J Epidemiol 1998; 148: 45–50.

  18. Masaki KH, Losonczy KG, Izmirlian G, Foley DJ, Ross GW, Petrovitch H et al. Association of vitamin E and C supplement use with cognitive function and dementia in elderly men. Neurology 2000; 54: 1265–72.

  19. Luchsinger JA, Tang MX, Shea S, Mayeux R. Antioxidant vitamin intake and risk of Alzheimer disease. Arch Neurol 2003; 6: 203–8.

  20. Zandi PP, Anthony JC, Khachaturian AS, Stone SV, Gustafson D, Tschanz JT, et al. Cache County Study Group. Reduced risk of Alzheimer disease in users of antioxidant vitamin supplements: the Cache County Study. Arch Neurol 2004; 61: 82–8. doi: 10.1001/archneur.61.1.82

  21. Kim WY, Yang EJ. A study on development and validation of food frequency questionnaire for Koreans. Korean J Nutr 1998; 31: 220–30.

  22. Ahn Y, Kwon E, Shim JE, Park MK, Joo Y, Kimm K et al. Validation and reproducibility of food frequency questionnaire for Korean genome epidemiologic study. Eur J Clin Nutr 2007; 61: 1435–41. doi: 10.1038/sj.ejcn.1602657

  23. Jack CR Jr, Bennett DA, Blennow K, Carrillo MC, Dunn B, Haeberlein SB et al. NIA-AA research framework: toward a biological definition of Alzheimer's disease. Alzheimers Dement 2018; 14: 535–62. doi: 10.1016/j.jalz.2018.02.018.

  24. Folstein MF, Folstein SE, McHugh PR. ‘Mini-mental state’. A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res 1975; 12: 189–98.

  25. Morris JC, Roe CM, Xiong C, Fagan AM, Goate AM, Holtzman DM et al. APOE predicts amyloid-beta but not tau Alzheimer pathology in cognitively normal aging. Ann Neurol 2010; 67: 122–31. doi: 10.1002/ana.21843.

  26. Vidoni ED, Townley RA, Honea RA, Burns JM. Alzheimer disease biomarkers are associated with body mass index. Neurology 2011; 77: 1913–20. doi: 10.1212/WNL.0b013e318238eec1.

  27. Jung S, Kim MK, Choi BY. The long-term relationship between dietary pantothenic acid (vitamin B5) intake and C-reactive protein concentration in adults aged 40 years and older. Nutr Metab Cardiovasc Dis 2017; 27: 806–16. doi: 10.1016/j.numecd.2017.05.008.

  28. Slyshenkov VS, Dymkowska D, Wojtczak L. Pantothenic acid and pantothenol increase biosynthesis of glutathione by boosting cell energetics. FEBS Lett 2004; 569(1e3): 169e72. doi: 10.1016/j.febslet.2004.05.044

  29. Zempleni J, Rucker RB, McCormick DB, Suttie JW. Handbook of vitamins, 4th ed. Boca Raton, FL: CRC Press; 2007, p. 240.

  30. Friedland RP, Tedesco JM, Wilson AC, Atwood CS, Smith MA, Perry G, et al. Antibodies to potato virus Y bind the amyloid beta peptide: immunohistochemical and NMR studies. J Biol Chem 2008; 283: 22550–6. doi: 10.1074/jbc.M802088200.

  31. Park SK, Ha JS, Kim JM, Kang JY, Lee du S, Guo TJ et al. Antiamnesic effect of broccoli (Brassica oleracea var. italica) leaves on amyloid beta (aβ)1-42- induced learning and memory impairment. J Agric Food Chem 2016; 64: 3353–61. doi: 10.1021/acs.jafc.6b00559.

  32. Leonardi R, Zhang YM, Rock CO, Jackowski S. Coenzyme A. Back in action. Prog Lipid Res 2005; 44(2e3): 125e53. doi: 10.1016/j.plipres.2005.04.001

Published
2018-12-10
How to Cite
1.
Lee J-H, Ahn S-Y, Lee HA, Won KS, Chang HW, Oh JS, Kim H-W. Dietary intake of pantothenic acid is associated with cerebral amyloid burden in patients with cognitive impairment. fnr [Internet]. 2018Dec.10 [cited 2019Mar.21];620. Available from: https://foodandnutritionresearch.net/index.php/fnr/article/view/1415
Section
Original Articles