Neutrophil and platelet to lymphocyte ratios in people with subjective, mild cognitive impairment and early Alzheimer's disease

The most common cause of dementia in the elderly is Alzheimer’s disease (AD). Studies have suggested that amyloid β leads to neuroinflammation by promoting synthesis of cytokines and pro-inflammatory mediators, and in turn, chemokines and cytokines induce the production of amyloid β. Mild cognitive impairment (MCI) is an intermediate state between normal ageing and dementia. Subjective cognitive decline (SCD) is also considered an early stage of subsequent cognitive impairment, and it carries a risk of developing into dementia. Neutrophil–lymphocyte ratio (NLR) and platelet–lymphocyte ratio (PLR) are useful and cost-effective biomarkers that show peripheral systemic inflammation. In this study we aimed to explore the role of inflammation in subjects with mild AD, MCI, and SCD via the new potential inflammation markers of NLR and PLR. The study was conducted in the geriatrics and geriatric psychiatry outpatient clinics of the Medical School of Cerrahpasa between 1 January and 31 October 2015. All patients provided written informed consent before clinical assessment. The local ethics committee of Cerrahpasa Medical School approved the study. In the screening phase, after an unstructured interview conducted according to the Diagnostic and Statistical Manual of Mental Disorder, 4th edition (text revision), patients were assessed by the Mini-Mental State Examination, Clinical Dementia Rating Scale, Geriatric Depression Scale, and Hachinski Ischemic Scale. Statistical analyses were performed using SPSS version 16 for Windows (IBM SPSS Inc, Chicago, IL, USA). Significance was set at a P-value <0.05. The study sample consisted of 31 patients with mild AD, 30 with MCI, 31 with SCD, and 31 healthy controls. Sociodemographic characteristics of the groups are shown in Table 1. The NLR value was 2.38 0.81 for AD patients, 2.48 1.19 for MCI patients, 2.24 1.11 for SCD patients, and 1.85 0.80 for healthy controls. NLR was significantly higher in the AD and MCI groups when compared with control group (P = 0.006, P = 0.030, respectively). Pairwise comparisons between AD and MCI groups, AD and SCD groups, and MCI and SCD groups showed no significant difference in NLR (P = 0.757, P = 0.245, P = 0.381, respectively). PLR levels were lowest in the healthy controls (110.29 39.28) and had a rising tendency in AD (124.26 45.41), SCD (124.74 39.60), and MCI subjects (139.61 65.01). NLR, PLR, lymphocyte, neutrophil, and platelet levels are shown in Table 2. In our cross-sectional study, NLR was significantly higher in the AD and MCI groups than in the control group. Strikingly, the same significant difference was not observed between the SCD and control groups. Differences in PLR levels were insignificant among the four groups. The role of NLR in AD patients was first investigated by Kuyumcu et al., who found NLR to be significantly higher in AD patients than in controls. This study also proposed that NLR was a strong independent variable for predicting AD. A study by Rembach et al. evaluated the longitudinal status of NLR in AD, MCI, and healthy controls at baseline and at 18, 36, and 54 months; it reported that the increase in NLR is a function of age and weakly correlates with neocortical amyloid accumulation. In this longitudinal study, Rembach et al. observed that NLR did not significantly differ (except for 18 months) between AD patients and healthy controls after adjustment for age, sex and Apolipoprotein E (APOEε4) allele status. Although inflammation markers have been found to be associated with MCI, a recent meta-