Cerebrospinal fluid VILIP-1 and YKL-40, candidate biomarkers to diagnose, predict and monitor Alzheimer’s disease in a memory clinic cohort

Springer Science and Business Media LLC - Tập 7 - Trang 1-9 - 2015
Maartje I. Kester1, Charlotte E. Teunissen2, Courtney Sutphen3,4,5, Elizabeth M. Herries6, Jack H. Ladenson6, Chengjie Xiong3,7, Philip Scheltens1, Wiesje M. van der Flier1,8, John C. Morris3,4,5, David M. Holtzman3,4,5, Anne M. Fagan3,4,5
1Alzheimer Center and Department of Neurology, VU University Medical Center, Amsterdam, The Netherlands
2Department of Clinical Chemistry, VU University Medical Center, Amsterdam, The Netherlands
3The Knight Alzheimer’s Disease Research Center, Washington University School of Medicine, St Louis, USA
4Department of Neurology, Washington University School of Medicine, St. Louis, USA
5Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, USA
6Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, USA
7Division of Biostatistics, Washington University School of Medicine, St. Louis, USA
8department of Epidemiology and Biostatistics, VU University Medical Center, Amsterdam, The Netherlands

Tóm tắt

We examined the utility of cerebrospinal fluid (CSF) proteins, Chitinase-3-like protein 1 (CHI3L1 or YKL-40), a putative marker of inflammation, and Visinin-like protein-1 (VILIP-1), a marker for neuronal injury, for diagnostic classification and monitoring of disease progression in a memory clinic cohort. CSF levels of YKL-40 and VILIP-1 were measured in 37 cognitively normal, 61 Mild Cognitive Impairment (MCI) and 65 Alzheimer’s disease (AD) patients from the memory clinic-based Amsterdam Dementia Cohort who underwent two lumbar punctures, with minimum interval of 6 months and a mean(SE) interval of 2.0(0.1) years. Mean(SE) cognitive follow-up was 3.8 (0.2) years. ANOVA was used to compare baseline differences of log-transformed CSF measures. Cox proportional hazard models were used to evaluate disease progression as a function of CSF tertiles. Linear mixed models were used to evaluate longitudinal change over time. All analyses were sex and age adjusted. Baseline levels of YKL-40, but not VILIP-1, were higher in MCI and AD patients compared to cognitively normal individuals (mean (SE) pg/mL, 304 (16) and 288 (12) vs. 231 (16), p = 0.03 and p = 0.006). Baseline levels of both YKL-40 and VILIP-1 in MCI predicted progression to AD (HR 95 % CI = 3.0 (1.1–7.9) and 4.4 (1.5–13.0), respectively, for highest vs. lowest tertile). YKL-40 increased longitudinally in patients with MCI and AD (mean (SE) pg/mL per year, 8.9 (3.0) and 7.1 (3.1), respectively), but not in cognitively normal individuals, whereas levels of VILIP-1 increased only in MCI (mean (SE), 10.7 (2.6) pg/mL per year). CSF levels of YKL-40 may have utility for discriminating between cognitively normal individuals and patients with MCI or AD. Increased levels of both YKL-40 and VILIP-1 may be associated with disease progression. These CSF biomarkers should be considered for future evaluation in the characterization of the natural history of AD.

Tài liệu tham khảo

Akiyama H, Barger S, Barnum S, Bradt B, Bauer J, Cole GM, et al. Inflammation and Alzheimer’s disease. Neurobiol Aging. 2000;21:383–421. Albert MS, DeKosky ST, Dickson D, Dubois B, Feldman HH, Fox NC, et al. The diagnosis of mild cognitive impairment 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;7:270–9. Alcolea D, Carmona-Iragui M, Suarez-Calvet M, Sanchez-Saudinos MB, Sala I, Anton-Aguirre S, et al. Relationship between beta-secretase, inflammation and core cerebrospinal fluid biomarkers for Alzheimer’s disease. J Alzheimers Dis. 2014;42:157–67. Antonell A, Mansilla A, Rami L, Llado A, Iranzo A, Olives J, et al. Cerebrospinal fluid level of YKL-40 protein in preclinical and prodromal Alzheimer’s disease. J Alzheimers Dis. 2014;42:901–8. Blennow K, Hampel H. CSF markers for incipient Alzheimer’s disease. Lancet Neurol. 2003;2:605–13. Blennow K, Zetterberg H, Minthon L, Lannfelt L, Strid S, Annas P, et al. Longitudinal stability of CSF biomarkers in Alzheimer’s disease. Neurosci Lett. 2007;419:18–22. Bonneh-Barkay D, Bissel SJ, Wang G, Fish KN, Nicholl GC, Darko SW, et al. YKL-40, a marker of simian immunodeficiency virus encephalitis, modulates the biological activity of basic fibroblast growth factor. Am J Pathol. 2008;173:130–43. Bonneh-Barkay D, Wang G, Starkey A, Hamilton RL, Wiley CA. In vivo CHI3L1 (YKL-40) expression in astrocytes in acute and chronic neurological diseases. J Neuroinflammation. 2010;7:34. Bouwman FH, Schoonenboom NS, Verwey NA, van Elk EJ, Kok A, Blankenstein MA, et al. CSF biomarker levels in early and late onset Alzheimer’s disease. Neurobiol Aging. 2009;30:1895–901. Bouwman FH, van der Flier WM, Schoonenboom NS, van Elk EJ, Kok A, Rijmen F, et al. Longitudinal changes of CSF biomarkers in memory clinic patients. Neurology. 2007;69:1006–11. Bouwman FH, van der Flier WM, Schoonenboom NS, van Elk EJ, Kok A, Scheltens P, et al. Usefulness of longitudinal measurements of beta-amyloid1-42 in cerebrospinal fluid of patients with various cognitive and neurologic disorders. Clin Chem. 2006;52:1604–6. Braunewell K, Riederer P, Spilker C, Gundelfinger ED, Bogerts B, Bernstein HG. Abnormal localization of two neuronal calcium sensor proteins, visinin-like proteins (vilips)-1 and −3, in neocortical brain areas of Alzheimer disease patients. Dement Geriatr Cogn Disord. 2001;12:110–6. Braunewell KH. The visinin-like proteins VILIP-1 and VILIP-3 in Alzheimer’s disease-old wine in new bottles. Front Mol Neurosci. 2012;5:20. Buchhave P, Blennow K, Zetterberg H, Stomrud E, Londos E, Andreasen N, et al. Longitudinal study of CSF biomarkers in patients with Alzheimer’s disease. PLoS One. 2009;4:e6294. Craig-Schapiro R, Perrin RJ, Roe CM, Xiong C, Carter D, Cairns NJ, et al. YKL-40: a novel prognostic fluid biomarker for preclinical Alzheimer’s disease. Biol Psychiatry. 2010;68:903–12. Fagan AM, Roe CM, Xiong C, Mintun MA, Morris JC, Holtzman DM. Cerebrospinal fluid tau/beta-amyloid(42) ratio as a prediction of cognitive decline in nondemented older adults. Arch Neurol. 2007;64:343–9. Fagan AM, Xiong C, Jasielec MS, Bateman RJ, Goate AM, Benzinger TL, et al. Longitudinal change in CSF biomarkers in autosomal-dominant Alzheimer’s disease. Sci Transl Med. 2014;6:226ra30. Hansson O, Zetterberg H, Buchhave P, Londos E, Blennow K, Minthon L. Association between CSF biomarkers and incipient Alzheimer’s disease in patients with mild cognitive impairment: a follow-up study. Lancet Neurol. 2006;5:228–34. Hjalmarsson C, Bjerke M, Andersson B, Blennow K, Zetterberg H, Aberg ND, et al. Neuronal and glia-related biomarkers in cerebrospinal fluid of patients with acute ischemic stroke. J Cent Nerv Syst Dis. 2014;6:51–8. Jack Jr CR, Knopman DS, Jagust WJ, Shaw LM, Aisen PS, Weiner MW, et al. Hypothetical model of dynamic biomarkers of the Alzheimer’s pathological cascade. Lancet Neurol. 2010;9:119–28. Jack Jr CR, Knopman DS, Jagust WJ, Petersen RC, Weiner MW, Aisen PS, et al. Tracking pathophysiological processes in Alzheimer’s disease: an updated hypothetical model of dynamic biomarkers. Lancet Neurol. 2013;12:207–16. Kester MI, Scheffer PG, Koel-Simmelink MJ, Twaalfhoven H, Verwey NA, Veerhuis R, et al. Serial CSF sampling in Alzheimer’s disease: specific versus non-specific markers. Neurobiol Aging. 2012;33:1591–8. Kester MI, Verwey NA, van Elk EJ, Blankenstein MA, Scheltens P, van der Flier WM. Progression from MCI to AD: predictive value of CSF Abeta42 is modified by APOE genotype. Neurobiol Aging. 2011;32:1372–8. Laterza OF, Modur VR, Crimmins DL, Olander JV, Landt Y, Lee JM, et al. Identification of novel brain biomarkers. Clin Chem. 2006;52:1713–21. Lee JM, Blennow K, Andreasen N, Laterza O, Modur V, Olander J, et al. The brain injury biomarker VLP-1 is increased in the cerebrospinal fluid of Alzheimer disease patients. Clin Chem. 2008;54:1617–23. da Lopes SS, Vellas B, Elemans S, Luchsinger J, Kamphuis P, Yaffe K, et al. Plasma nutrient status of patients with Alzheimer’s disease: Systematic review and meta-analysis. Alzheimers Dement. 2013;10:485–502. Luo X, Hou L, Shi H, Zhong X, Zhang Y, Zheng D, et al. CSF levels of the neuronal injury biomarker visinin-like protein-1 in Alzheimer’s disease and dementia with Lewy bodies. J Neurochem. 2013;127:681–90. Magdalinou NK, Paterson RW, Schott JM, Fox NC, Mummery C, Blennow K, et al. A panel of nine cerebrospinal fluid biomarkers may identify patients with atypical parkinsonian syndromes. J Neurol Neurosurg Psychiatry. 2015. [Epub ahead of print]. doi:10.1136/jnnp-2014-309562. Martinez MA, Olsson B, Bau L, Matas E, Cobo CA, Andreasson U, et al. Glial and neuronal markers in cerebrospinal fluid predict progression in multiple sclerosis. Mult Scler. 2015;21:550–61. Mattsson N, Tabatabaei S, Johansson P, Hansson O, Andreasson U, Mansson JE, et al. Cerebrospinal fluid microglial markers in Alzheimer’s disease: elevated chitotriosidase activity but lack of diagnostic utility. Neuromol Med. 2011;13:151–9. McKeith IG, Dickson DW, Lowe J, Emre M, O’Brien JT, Feldman H, et al. Diagnosis and management of dementia with Lewy bodies: third report of the DLB Consortium. Neurology. 2005;65:1863–72. McKhann G, Drachman D, Folstein M, Katzman R, Price D, Stadlan EM. Clinical diagnosis of Alzheimer’s disease: report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer’s Disease. Neurology. 1984;34:939–44. Mollenhauer B, Bibl M, Trenkwalder C, Stiens G, Cepek L, Steinacker P, et al. Follow-up investigations in cerebrospinal fluid of patients with dementia with Lewy bodies and Alzheimer’s disease. J Neural Transm. 2005;112:933–48. Neary D, Snowden JS, Gustafson L, Passant U, Stuss D, Black S, et al. Frontotemporal lobar degeneration: a consensus on clinical diagnostic criteria. Neurology. 1998;51:1546–54. Olsson B, Hertze J, Lautner R, Zetterberg H, Nagga K, Hoglund K, et al. Microglial markers are elevated in the prodromal phase of Alzheimer’s disease and vascular dementia. J Alzheimers Dis. 2013;33:45–53. Perrin RJ, Craig-Schapiro R, Malone JP, Shah AR, Gilmore P, Davis AE, et al. Identification and validation of novel cerebrospinal fluid biomarkers for staging early Alzheimer’s disease. PLoS One. 2011;6:e16032. Petersen RC, Smith GE, Waring SC, Ivnik RJ, Tangalos EG, Kokmen E. Mild cognitive impairment: clinical characterization and outcome. Arch Neurol. 1999;56:303–8. Raber J, Huang Y, Ashford JW. ApoE genotype accounts for the vast majority of AD risk and AD pathology. Neurobiol Aging. 2004;25:641–50. Roman GC, Tatemichi TK, Erkinjuntti T, Cummings JL, Masdeu JC, Garcia JH, et al. Vascular dementia: diagnostic criteria for research studies. Report of the NINDS-AIREN International Workshop. Neurology. 1993;43:250–60. Schnurra I, Bernstein HG, Riederer P, Braunewell KH. The neuronal calcium sensor protein VILIP-1 is associated with amyloid plaques and extracellular tangles in Alzheimer’s disease and promotes cell death and tau phosphorylation in vitro: a link between calcium sensors and Alzheimer’s disease? Neurobiol Dis. 2001;8:900–9. Sutphen CL, Fagan AM, Holtzman DM. Progress update: fluid and imaging biomarkers in Alzheimer’s disease. Biol Psychiatry. 2013;75:520–6. Tarawneh R, D’Angelo G, Macy E, Xiong C, Carter D, Cairns NJ, et al. Visinin-like protein-1: diagnostic and prognostic biomarker in Alzheimer disease. Ann Neurol. 2011;70:274–85. Tarawneh R, Lee JM, Ladenson JH, Morris JC, Holtzman DM. CSF VILIP-1 predicts rates of cognitive decline in early Alzheimer disease. Neurology. 2012;78:709–19. Toledo JB, Xie SX, Trojanowski JQ, Shaw LM. Longitudinal change in CSF Tau and Abeta biomarkers for up to 48 months in ADNI. Acta Neuropathol. 2013;126:659–70. Twisk JW. Applied longitudinal data analysis for epidemiology. Cambridge: Cambridge University Press; 2003. Verwey NA, Bouwman FH, van der Flier WM, Veerhuis R, Scheltens P, Blankenstein MA. Variability in longitudinal cerebrospinal fluid tau and phosphorylated tau measurements. Clin Chem Lab Med. 2008;46:1300–4. Vos SJ, Xiong C, Visser PJ, Jasielec MS, Hassenstab J, Grant EA, et al. Preclinical Alzheimer’s disease and its outcome: a longitudinal cohort study. Lancet Neurol. 2013;12:957–65. Zhou B, Teramukai S, Yoshimura K, Fukushima M. Validity of cerebrospinal fluid biomarkers as endpoints in early-phase clinical trials for Alzheimer’s disease. J Alzheimers Dis. 2009;18:89–102.