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|Title:||An increased neutrophil-lymphocyte ratio in Alzheimer's disease is a function of age and is weakly correlated with neocortical amyloid accumulation.|
|Authors:||Rembach, Alan;Watt, Andrew D;Wilson, William J;Rainey-Smith, Stephanie R;Ellis, Kathryn A;Rowe, Christopher C;Villemagne, Victor L;Macaulay, S Lance;Bush, Ashley I;Martins, Ralph N;Ames, David;Masters, Colin L;Doecke, James D|
|Institutional Author:||AIBL Research Group|
|Affiliation:||The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Victoria 3052, Australia.|
The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Victoria 3052, Australia; Department of Psychiatry, St George's Hospital, University of Melbourne, Victoria 3101, Australia; National Ageing Research Institute, Parkville, Victoria 3050, Australia.
Department of Nuclear Medicine and Centre for PET, Austin Health, Heidelberg, Victoria 3084, Australia.
CSIRO Preventative Health Flagship, Parkville, Victoria 3010, Australia.
Sir James McCusker Alzheimer's Disease Research Unit, Health Department of WA, Perth, WA 6009, Australia.
National Ageing Research Institute, Parkville, Victoria 3050, Australia.
CSIRO Computational Informatics/Australian e-Health Research Centre, Royal Brisbane and Women's Hospital, Brisbane, QLD 4029, Australia.
|Citation:||Journal of Neuroimmunology 2014; 273(1-2): 65-71|
|Abstract:||Inflammation is a hallmark of Alzheimer's disease (AD). Whether directly involved in the pathogenesis, or a downstream consequence of neuronal death, the blood neutrophil-lymphocyte ratio (NLR) is reported to be a putative, non-invasive peripheral biomarker for AD. The aim of this study was to re-evaluate the diagnostic utility of longitudinal measures of the NLR. The NLR was stable across all time-points and weakly correlated with neocortical amyloid burden (R=0.21 at baseline, 0.27 at 18 months, 0.20 at 36 months and 0.10 at 54 months). Cross-sectionally, the NLR was significantly elevated in AD participants as compared to HC participants at baseline (p<0.0001), 18 months (p<0.0001), 36 months (p=0.002) and at 54 months (p=0.007), however only prior to adjustment for age, sex and APOEε4 allele status (p>0.05 at all time-points except for 18 months; p<0.0001). Longitudinally, the NLR was not significantly different between HC and AD participants (p>0.05) adjusted for age, sex and APOEε4 allele status. Comparing the NLR between cognitive transition groups over time (transition towards an AD type dementia), there was no significant difference in the NLR levels between those participants, who did not transition and those participants who did transition, or those in the stable AD group after adjusting for age, sex and APOEε4 allele status (p>0.05). Despite inflammation being a hallmark in AD and previous reports showing that the NLR can discriminate HC from AD patients, our results suggest that the sensitivity of the NLR itself is not robust enough for diagnostic utility. We identified significant relationships cross sectionally (p<0.05 at baseline, 18 months and 36 months) between the NLR and neocortical amyloid burden, but this relationship was lost after longitudinal analyses (p>0.5). The NLR also had limited association with cognitive decline, although in our cohort, the number of participants transitioning was relatively small. In conclusion, the NLR may reflect AD-related inflammatory processes in the periphery, but age and sex are dominant covariates which need to be controlled for in population-based screening.|
|Internal ID Number:||24907904|
Neocortical amyloid burden
Aged, 80 and over
Alzheimer Disease.complications.genetics.pathology.radionuclide imaging
Aniline Compounds.diagnostic use
Cognition Disorders.etiology.radionuclide imaging
Psychiatric Status Rating Scales
|Appears in Collections:||Journal articles|
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