scholarly journals Proteomics for Cerebrospinal Fluid Biomarker Identification in Parkinsons Disease: Methods and Critical Aspects

2015 ◽  
Vol 2 (1) ◽  
pp. 1-6
Author(s):  
Antonio Conti ◽  
◽  
Massimo Alessio
Keyword(s):  
Cerebrospinal Fluid ◽  
Parkinsons Disease ◽  
Biomarker Identification ◽  
Fluid Biomarker ◽  
Critical Aspects

scholarly journals Toll-like receptor linked cytokine profiles in cerebrospinal fluid discriminate neurological infection from sterile inflammation

2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Simone M Cuff ◽  
Joseph P Merola ◽  
Jason P Twohig ◽  
Matthias Eberl ◽  
William P Gray
Keyword(s):  
Cerebrospinal Fluid ◽  
Clinical Practice ◽  
Inflammatory Response ◽  
Nosocomial Infection ◽  
Pathway Analysis ◽  
Interleukin 6 ◽  
Sterile Inflammation ◽  
Interleukin 17 ◽  
Toll Like Receptor ◽  
Fluid Biomarker

Abstract Rapid determination of an infective aetiology causing neurological inflammation in the cerebrospinal fluid can be challenging in clinical practice. Post-surgical nosocomial infection is difficult to diagnose accurately, as it occurs on a background of altered cerebrospinal fluid composition due to the underlying pathologies and surgical procedures involved. There is additional diagnostic difficulty after external ventricular drain or ventriculoperitoneal shunt surgery, as infection is often caused by pathogens growing as biofilms, which may fail to elicit a significant inflammatory response and are challenging to identify by microbiological culture. Despite much research effort, a single sensitive and specific cerebrospinal fluid biomarker has yet to be defined which reliably distinguishes infective from non-infective inflammation. As a result, many patients with suspected infection are treated empirically with broad-spectrum antibiotics in the absence of definitive diagnostic criteria. To begin to address these issues, we examined cerebrospinal fluid taken at the point of clinical equipoise to diagnose cerebrospinal fluid infection in 14 consecutive neurosurgical patients showing signs of inflammatory complications. Using the guidelines of the Infectious Diseases Society of America, six cases were subsequently characterized as infected and eight as sterile inflammation. Twenty-four contemporaneous patients with idiopathic intracranial hypertension or normal pressure hydrocephalus were included as non-inflamed controls. We measured 182 immune and neurological biomarkers in each sample and used pathway analysis to elucidate the biological underpinnings of any biomarker changes. Increased levels of the inflammatory cytokine interleukin-6 and interleukin-6-related mediators such as oncostatin M were excellent indicators of inflammation. However, interleukin-6 levels alone could not distinguish between bacterially infected and uninfected patients. Within the patient cohort with neurological inflammation, a pattern of raised interleukin-17, interleukin-12p40/p70 and interleukin-23 levels delineated nosocomial bacteriological infection from background neuroinflammation. Pathway analysis showed that the observed immune signatures could be explained through a common generic inflammatory response marked by interleukin-6 in both nosocomial and non-infectious inflammation, overlaid with a toll-like receptor-associated and bacterial peptidoglycan-triggered interleukin-17 pathway response that occurred exclusively during infection. This is the first demonstration of a pathway dependent cerebrospinal fluid biomarker differentiation distinguishing nosocomial infection from background neuroinflammation. It is especially relevant to the commonly encountered pathologies in clinical practice, such as subarachnoid haemorrhage and post-cranial neurosurgery. While requiring confirmation in a larger cohort, the current data indicate the potential utility of cerebrospinal fluid biomarker strategies to identify differential initiation of a common downstream interleukin-6 pathway to diagnose nosocomial infection in this challenging clinical cohort.

O2-07-03: Validating predicted biological effects of Alzheimer's disease associated SNPs using cerebrospinal fluid biomarker levels

2010 ◽  
Vol 6 ◽  
pp. S112-S113 ◽  
Author(s):  
John S.K. Kauwe ◽  
Carlos Cruchaga ◽  
Sarah Bertelsen ◽  
Kevin Mayo ◽  
Wayne Latu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Biological Effects ◽  
Fluid Biomarker

Clusterin, a New Cerebrospinal Fluid Biomarker in Severe Subarachnoid Hemorrhage: A Pilot Study

2017 ◽  
Vol 107 ◽  
pp. 424-428 ◽  
Author(s):  
Norbert Wąsik ◽  
Bartosz Sokół ◽  
Marcin Hołysz ◽  
Witold Mańko ◽  
Robert Juszkat ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Pilot Study ◽  
Fluid Biomarker

Kynurenine Is a Cerebrospinal Fluid Biomarker for Bacterial and Viral Central Nervous System Infections

2019 ◽  
Vol 220 (1) ◽  
pp. 127-138 ◽  
Author(s):  
Kurt-Wolfram Sühs ◽  
Natalia Novoselova ◽  
Maike Kuhn ◽  
Lena Seegers ◽  
Volkhard Kaever ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Central Nervous System Infections ◽  
Fluid Biomarker

scholarly journals Age and the association between apolipoprotein E genotype and Alzheimer disease: A cerebrospinal fluid biomarker–based case–control study

PLoS Medicine ◽  
2020 ◽  
Vol 17 (8) ◽  
pp. e1003289 ◽  
Author(s):  
Hana Saddiki ◽  
Aurore Fayosse ◽  
Emmanuel Cognat ◽  
Séverine Sabia ◽  
Sebastiaan Engelborghs ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Alzheimer Disease ◽  
Apolipoprotein E ◽  
Case Control Study ◽  
Case Control ◽  
Fluid Biomarker ◽  
Control Study ◽  
Apolipoprotein E Genotype

Cerebrospinal Fluid Biomarker-Based Diagnosis of Sporadic Creutzfeldt-Jakob Disease: A Validation Study for Previously Established Cutoffs

2017 ◽  
Vol 43 (1-2) ◽  
pp. 71-80 ◽  
Author(s):  
Franc Llorens ◽  
André Karch ◽  
Ewa Golanska ◽  
Matthias Schmitz ◽  
Peter Lange ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Negative Correlation ◽  
Disease Duration ◽  
Population Sample ◽  
Clinical Accuracy ◽  
Jakob Disease ◽  
And Control ◽  
Fluid Biomarker ◽  
Prnp Codon ◽  
Codon 129

Background: Several biomarkers have been proposed to discriminate sporadic Creutzfeldt-Jakob disease (sCJD) from other dementias and control cases. However, their clinical accuracy depends on the PRNP codon 129 genotype, leaving it unclear how well established markers behave in untested conditions. Methods: We analyzed 14-3-3, tau, p-tau levels, and the p-tau/tau ratio in a population sample collected from Polish hospitals including nondementia, dementia, and definite sCJD cases and validated their parameters according to previously established cutoffs. Additionally, the correlation between biomarkers and disease duration as well as the influence of the PRNP129 polymorphism are reported. Results: The tau levels and p-tau/tau ratios differed considerably between sCJD and clinically characterized non-CJD cases (p < 0.001). p-tau was only elevated in sCJD when compared to cases without dementia (p < 0.05). Tau and the p-tau/tau ratio showed a sensitivity of 95 and 100%, respectively, in detecting sCJD cases. A negative correlation between tau levels and disease duration, but not the timing of lumbar puncture was observed. Conclusion: The present findings confirmed the value of the p-tau/tau ratio as a robust sCJD biomarker and suggest a role for tau as prognostic marker.

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