EXAMINATION OF NEUTROPHIL/LYMPHOCYTE (NLR), MONOCYTE/LYMPHOCYTE (MLR), AND PLATELET/LYMPHOCYTE (PLR) RATIOS BETWEEN ALZHEIMER'S DISEASE AND VASCULAR DEMENTIA

Abstract

Background: The present study aims to investigate whether proinflammatory marker ratios in whole blood differ in these two dementia diseases. Materials and Methods: This study will involve Alzheimer's disease (AD) and vascular dementia (VaD) patients who were treated as outpatients in the outpatient clinic and inpatients in the ward of the Neurology Department of Adnan Menderes University Hospital. The patients’ diagnoses will be scanned in the hospital information system. The admission blood results of patients who presented between January 2018 and September 2020 will be included, and the patients’ hemogram results will be scanned retrospectively. Neutrophil/lymphocyte, monocyte/lymphocyte, and platelet/lymphocyte ratios in the hemogram results will be calculated and recorded. Results: In the AD-VaD comparison of the patients participating in the study, a significant difference was identified between the variability of platelet/lymphocyte (PLR) and NLRs (NLR) (p<0.001). Moreover, a significant difference was found between the mean ages of patients with vascular dementia and those with Alzheimer's dementia (p<0.0001). Conclusion: While proinflammatory markers obtained secondary to inflammation are significant in AD since it is a chronic and progressive process, the use of these markers is limited due to the gradual course after an acute event in vascular dementia. Furthermore, there is a need for additional studies on peripheral blood cells to identify the potential prodromal biomarkers of AD.

Keywords

• Alzheimer
• NLR
• proinflammatory markers
• vascular dementia

References

1. 1.Braak ve Braak, 1991; de Toledo-Morrell, Goncharova, Dickerson, Wilson ve Bennett, 2000
2. 2.Askarova S, Yang X, Lee J. Impacts of MembraneBiophysics in Alzheimer’sDisease: FromAmyloidPrecursor Protein Processingto Aβ Peptide-InducedMembraneChanges. International Journal of Alzheimer’sDisease, 2011;10 (4061):1-12
3. 3. Scheff SW, PriceDA, Schmitt FA, Mufson EJ. Hippocampalsynapticloss in earlyAlzheimer'sdiseaseandmildcognitiveimpairment. NeurobiolAging, 2006;27 (10):1372-1384.
4. 4. Hebert LE, Weuve J, Scherr PA, Evans DA. Alzheimer disease in the United States (2010-2050) estimatedusingthe 2010 census. Neurology. 2013;80(19):1778-83
5. 5. . Frances A, Pincus HA, First MB. Diagnosticand Statistical Manual of MentalDisordersFourth Edition (DSM IV). Washington: AmericanPsychiatricAssociation, 1994; p: 133– 56
6. 6. O ’brien JT, Thomas A. Non-Alzheimer’sdementia 3 Vasculardementia. Lancet. 2015;386:1698–706
7. 7. Kokmen E, Whisnant JP, O’Fallon WM, Chu CP, Beard CM. Dementiaafterischemicstroke: A population-basedstudy in Rochester, Minnesota (1960-1984). Neurology. 1996;46(1):154–9
8. 8. AragaS, Kagimoto H, Funamoto K, Takahashi K. Reducednatural killer cellactivity in patientswithdementia of Alzheimer type. ActaNeurolScand (1991) 844:259–63. doi:10.1111/j.1600-0404.1991.tb04948

9. 9. Le Page A, Bourgade K, Lamoureux J, Frost E, Pawelec G, Larbi A, et al. NK cellsareactivated in amnesticmildcognitiveimpairment but not in MildAlzheimer’sdiseasepatients. J AlzheimersDis (2015) 46(1):93–107.doi:10.3233/JAD-143054
10. 10. Richartz-Salzburger E, Batra A, Stransky E, Laske C, Köhler N, Bartels M, et al. Alteredlymphocytedistribution in Alzheimer’sdisease. J PsychiatrRes (2007)41(1–2):174–8. doi:10.1016/j.jpsychires.2006.01.010
11. 11. De la Fuente M, Miquel J. An update of theoxidation-Inflammationtheory of aging: theinvolvement of theimmunesystem in oxi-inflamm-aging. CurrPharmDes (2009) 15:3003–26. doi:10.2174/138161209789058110
12. 12. Martínez de Toda I, Maté I, Vida C, Cruces J, De la Fuente M. Immunefunctionparameters as markers of biologicalageandpredictors of longevity. Aging (Albany NY) (2017) 28(11):3110–9. doi:10.18632/aging.101116
13. 13. Lattanzi, Simona, et al. "Neutrophil-to-lymphocyteratio in acutecerebralhemorrhage: a systemreview." Translationalstrokeresearch 10.2 (2019): 137-145
14. 14. .Shigemizu, Daichi, et al. "Identification of potentialbloodbiomarkersforearlydiagnosis of Alzheimer’sdiseasethrough RNA sequencinganalysis." Alzheimer'sresearch&therapy 12.1 (2020): 1-12
15. 15. Thompson, Claire, et al. "Behavioralandpsychologicalsymptomsassociatedwithdementiasubtypeandseverity." International Psychogeriatrics 22.2 (2010): 300-305.
16. 16.Groves WC, Brandt J, Steinberg M, Warren A, Rosenblatt A, Baker A, et al. VasculardementiaandAlzheimer’sdisease: Is there a difference? A comparison of symptomsbydiseaseduration. J NeuropsychiatryClinNeurosci. 2000;12(3):305–15
17. 17. Brayne C. Incidence of dementia in EnglandandWales: The MRC cognitivefunctionandageingstudy. Alzheimer DiseaseandAssociatedDisorders. 2006
18. 18. Vida, Carmen, et al. "Impairment of severalimmunefunctionsandredoxstate in bloodcells of Alzheimer’sdiseasepatients. Relevant role of neutrophils in oxidativestress." Frontiers in immunology 8 (2018): 1974.)
19. 19.Long J, Pan G, Ifeachor E, Belshaw R, Li X. Discovery of novelbiomarkersforAlzheimer’sdiseasefromblood. DisMarkers. 2016;2016:4250480 )
20. 20.Rai N, Kumar R, Desai GR, Venugopalan G, Shekhar S, Chatterjee P, Tripathi M, Upadhyay AD, Dwivedi S, Dey AB, Dey S. Relativealterations in bloodbasedlevels of sestrininAlzheimer’sdiseaseandmildcognitiveimpairmentpatients. J AlzheimersDis. 2016;54:1147–55.
21. 21.San Segundo-Acosta P, Montero-Calle A, Fuentes M, Rabano A, Villalba M, Barderas R. Identification of Alzheimer’sdiseaseautoantibodiesandtheirtargetbiomarkersbyphagemicroarrays. J ProteomeRes. 2019;18:2940–53.
22. 22. Dong, Yuan, et al. "NeutrophilhyperactivationcorrelateswithAlzheimer'sdiseaseprogression." Annals of neurology 83.2 (2018): 387-405
23. 23. Kuyumcu, Mehmet Emin, et al. "Theevaluation of neutrophil-lymphocyteratio in Alzheimer’sdisease." Dementiaandgeriatriccognitivedisorders 34.2 (2012): 69-74.