Serum Tau Protein Research Articles

Serum and cerebrospinal fluid tau protein level as biomarkers for evaluating acute spinal cord injury severity and motor function outcome.

Tau protein, a microtubule-associated protein, has a high specific expression in neurons and axons. Because traumatic spinal cord injury mainly affects neurons and axons, we speculated that tau protein may be a promising biomarker to reflect the degree of spinal cord injury and prognosis of motor function. In this study, 160 female Sprague-Dawley rats were randomly divided into a sham group, and mild, moderate, and severe spinal cord injury groups. A laminectomy was performed at the T8 level to expose the spinal cord in all groups. A contusion lesion was made with the NYU-MASCIS impactor by dropping a 10 g rod from heights of 12.5 mm (mild), 25 mm (moderate) and 50 mm (severe) upon the exposed dorsal surface of the spinal cord. Tau protein levels were measured in serum and cerebrospinal fluid samples at 1, 6, 12, 24 hours, 3, 7, 14 and 28 days after operation. Locomotor function of all rats was assessed using the Basso, Beattie and Bresnahan locomotor rating scale. Tau protein concentration in the three spinal cord injury groups (both in serum and cerebrospinal fluid) rapidly increased and peaked at 12 hours after spinal cord injury. Statistically significant positive linear correlations were found between tau protein level and spinal cord injury severity in the three spinal cord injury groups, and between the tau protein level and Basso, Beattie, and Bresnahan locomotor rating scale scores. The tau protein level at 12 hours in the three spinal cord injury groups was negatively correlated with Basso, Beattie, and Bresnahan locomotor rating scale scores at 28 days (serum: r = -0.94; cerebrospinal fluid: r = -0.95). Our data suggest that tau protein levels in serum and cerebrospinal fluid might be a promising biomarker for predicting the severity and functional outcome of traumatic spinal cord injury.

Melatonin Promotes Brain-Derived Neurotrophic Factor (BDNF) Expression and Anti-Apoptotic Effects in Neonatal Hemolytic Hyperbilirubinemia via a Phospholipase (PLC)-Mediated Mechanism.

BackgroundMelatonin therapy shows positive effects on neuroprotective factor brain-derived neurotrophic factor (BDNF) expression and neuronal apoptosis in neonatal hemolytic hyperbilirubinemia. We hypothesized that melatonin promotes BDNF expression and anti-apoptotic effects in neonatal hemolytic hyperbilirubinemia through a phospholipase (PLC)-mediated mechanism.Material/MethodsA phenylhydrazine hydrochloride (PHZ)-induced neonatal hemolytic hyperbilirubinemia model was constructed in neonatal rats. Four experimental groups – a control group (n=30), a PHZ group (n=30), a PHZ + melatonin group (n=30), and a PHZ + melatonin+U73122 (a PLC inhibitor) group (n=30) – were constructed. Trunk blood was assayed for serum hemoglobin, hematocrit, total and direct bilirubin, BDNF, S100B, and tau protein levels. Brain tissue levels of neuronal apoptosis, BDNF expression, PLC activity, IP3 content, phospho- and total Ca2+/calmodulin-dependent protein kinase type IV (CaMKIV) expression, and phospho- and total cAMP response element binding protein (CREB) expression were also assayed.ResultsPHZ-induced hemolytic hyperbilirubinemia was validated by significantly decreased serum hemoglobin and hematocrit as well as significantly increased total and direct serum bilirubin (p<0.05). Neonatal bilirubin-induced neurotoxicity was validated by significantly decreased serum BDNF, brain BDNF, and serum S100B, along with significantly increased serum tau protein (p<0.05). PHZ-induced hemolytic hyperbilirubinemia significantly decreased serum BDNF, brain BDNF, and PLC/IP3/Ca2+ pathway activation while increasing neuronal apoptosis levels (p<0.05), all of which were partially rescued by melatonin therapy (p<0.05). Pre-treatment with the PLC inhibitor U73122 largely abolished the positive effects of melatonin on PLC/IP3/Ca2+ pathway activation, downstream BDNF levels, and neuronal apoptosis (p<0.05).ConclusionsPromotion of BDNF expression and anti-apoptotic effects in neonatal hemolytic hyperbilirubinemia by melatonin largely operates via a PLC-mediated mechanism.

Dynamics of changes in the content of thyroid hormones and some neurotransmitters in brain of rats with experimental Alzheimer’s disease

Objective: Alzheimer's disease is one of the most common neurodegenerative diseases, and mechanisms of its development have been studied for many years. The aim of the research was to study the content of thyroid-stimulating hormone (TSH), thyroid hormones and tau protein in the blood serum, as well as the content of thyroid hormones and some neurotransmitters in the cerebral cortex in the dynamics of experimental Alzheimer’s disease in rats. Materials and methods. The experiment was performed on 45 WAG rats, which were divided into 3 groups. The first group was the control one. Animals from the second and third groups were intraperitoneally administered with scopolamine for 14 and 27 days, which led to the development of Alzheimer's disease. Brain homogenate was prepared. Concentrations of T3, T4 in blood serum and homogenates of the cerebral cortex, as well as TSH and tau protein in serum, were determined by ELISA. Determination of the content of neurotransmitter amino acids (aspartate and glutamate) was carried out by thin-layer chromatography. The content of dopamine and norepinephrine in the cerebral cortex homogenate was determined by column chromatography, and acetylcholine levels were measured by spectrophotometry. Morphological examination included staining of brain tissue with congo-rot + hematoxylin. Results. It was established that in cerebral cortex homogenates of rats with experimental Alzheimer’s disease the T3 content was reduced, and T4 levels were similar to rats of the control group, which in combination with the normal concentration of thyroid hormones in blood serum indicates the development of local hypothyroidism in the cerebral cortex. In rats with Alzheimer's disease, glutamic and aspartic acid levels were increased against the background of GABA reduction. There was also a decrease in the levels of noradrenaline and dopamine in the cerebral cortex homogenates, which contributes to the abnormal energy metabolism and impaired cognitive functions. Morphological study demonstrated the presence of congophilic masses in the brain tissue and in the walls of small arteries with the development of brain atrophy. Conclusions. Alzheimer's disease caused by the administration of scopalamine is characterized by the development of local hypothyroidism in the cerebral cortex, an increase in the level of glutamic and aspartic acids with a decrease in GABA, a decrease in the level of dopamine and norepinephrine in the cerebral cortex.

Tau protein (MAPT) as a possible biochemical marker of traumatic brain injury in postmortem examination

MAPT is a neuronal protein that plays an important role in axonal stabilization, neuronal development, and neuronal polarity. MAPT release into the CSF and blood has been interpreted as indicative of axonal injury as its elevated levels were observed in olympic boxers even after a mild head trauma suggesting minor CNS injuries. In our study we wanted to check the potential relevance of MAPT examination for forensic purposes. The study was carried out using cases of head injury group and cases of sudden death (cardiopulmonary failure, no injuries of the head — control group) provided by forensic pathologists at the Department of Forensic Medicine, Medical University of Warsaw. CSF and blood were collected within 24h after death using suboccipital puncture and femoral vein puncture. Serum and cerebrospinal fluid Tau protein concentrations were compared using an enzyme-linked immunosorbent assay (elisa). Brain specimens (frontal cortex) were collected during forensic autopsies. Sections were stained histologically (hematoxylin-eosin) and immunohistochemically with anti human Tau antibody, anti glial fibrillary acid protein (GFAP), anti human macrosialin (CD68) or anti human endothelial cells (CD34). In our study we documented that elevated levels of serum and CSF MAPT may also be considered a marker for mild traumatic brain injury and traumatic brain injury (mTBI and TBI). An increase in CSF and serum levels of MAPT in the absence of visible macroscopic traumatic CNS changes indicates that even minor head injuries may result in changes at the neuronal level that could remain undiagnosed during regular forensic autopsy and routine histopathological examination.

Tau protein as a possible marker of cerebrospinal fluid leakage in cerebrospinal fluid rhinorrhoea: A pilot study.

IntroductionThe management of posttraumatic cerebrospinal fluid (CSF) rhinorrhoea remains a clinical challenge. Cerebrospinal fistula is a dural defect responsible for possible CSF leakage into the contiguous air-filled cavities located at the skull base. The risk of central nervous system infection in these conditions is severe and can be life threatening. Consequently, a specific CSF biomarker might be used in case of difficult diagnosis of CSF rhinorrhoea. CSF Tau protein is a neuronal protein, commonly assessed for diagnosis of Alzheimer Disease (AD). The aim of this study was to determine whether the Tau protein could be a relevant marker of CSF leakage.Materials and methodsTau protein measurement was performed by enzyme-linked immunosorbent assay in 13 patients with CSF leakage (CSF rhinorrhoea group), and 8 patients with spontaneous aqueous rhinorrhoea (non-CSF leakage group). The serum concentration of Tau protein was measured by ELISA in both CSF rhinorrhoea group and non-CSF leakage group.ResultsIn patients with CSF leakage, CSF Tau protein median concentration was 479 ng/L (197 - 2325 ng/L). On the other hand, the Tau protein concentration was below the lower limit of quantification (LLoQ) (< 87 ng/L) in non-CSF leakage group. Serum Tau protein concentration by ELISA was also below LLoQ (< 87 ng/L) for all subjects.ConclusionELISA measurement of Tau protein in rhinorrhoea fluid may be a reliable and relevant marker for detecting the presence of CSF in the nasal discharge and sign the existence of a CSF leakage.

Predictive Value of Neurodevelopmental Outcome and Serum Tau Protein Level in Neonates with Hypoxic Ischemic Encephalopathy.

Tau protein is s specific protein expressed by neurons in the central nervous system. Elevated serum Tau protein is associated with many diseases of the central nervous system. The serum Tau protein level in neonates with hypoxic ischemic encephalopathy (HIE) is still poorly understood. Forty-one human neonates with HIE and thirty-five healthy neonates (control group) within 24 hours after birth were studied. Tau protein in serum was detected by enzyme-linked immunosorbent assay. Neurological outcome was assessed at 9 months of age according to the Gesell developmental scale. Tau protein in serum was significantly higher in the HIE group than in the control group (p < 0.01), in neonates with severe HIE than neonates with moderate HIE (p < 0.01), and in infants with neurodevelopmental retardation compared with those with normal neurodevelopment (p < 0.01). The result of this study showed an obvious negative correlation between the serum Tau protein level and development quotients of neonates with HIE (rs = -0.6172, p < 0.01). Receiver operator characteristic curve analysis showed that Tau protein (cutoff value 933.04 pg/mL) was a predictor of neurodevelopmental retardation outcome (AUC value = 0.860 (95% CI: 0.736 - 0.983, p < 0.01), sensitivity 100%, specificity 70.8%). Serum Tau protein level within 24 hours after birth can be used as a marker for the early diagnosis of neonatal HIE and predicting neurodevelopmental outcomes.

Effect of erythropoietin combined with hypothermia on serum tau protein levels and neurodevelopmental outcome in neonates with hypoxic-ischemic encephalopathy.

Although hypothermia therapy is effective to treat neonatal hypoxic-ischemic encephalopathy, many neonatal patients die or suffer from severe neurological dysfunction. Erythropoietin is considered one of the most promising neuroprotective agents. We hypothesized that erythropoietin combined with hypothermia will improve efficacy of neonatal hypoxic-ischemic encephalopathy treatment. In this study, 41 neonates with moderate/severe hypoxic-ischemic encephalopathy were randomly divided into a control group (hypothermia alone for 72 hours, n = 20) and erythropoietin group (hypothermia + erythropoietin 200 IU/kg for 10 days, n = 21). Our results show that compared with the control group, serum tau protein levels were lower and neonatal behavioral neurological assessment scores higher in the erythropoietin group at 8 and 12 days. However, neurodevelopmental outcome was similar between the two groups at 9 months of age. These findings suggest that erythropoietin combined with hypothermia reduces serum tau protein levels and improves neonatal behavioral neurology outcome but does not affect long-term neurodevelopmental outcome.

Neurofilaments in blood and CSF for diagnosis and prediction of onset in Creutzfeldt-Jakob disease.

While cerebrospinal fluid (CSF) biomarkers for Creutzfeldt-Jakob disease (CJD) are established and partly included in the diagnostic criteria, no blood biomarkers are available. Here, we assessed the utility of serum neurofilament light chain (NF-L) and tau protein in comparison to CSF markers (NF-L and phosphorylated NF heavy chain (pNF-H), tau, S100B, 14-3-3) and prion conversion assay (real-time quaking induced conversion (RT-QuIC)) for sporadic and genetic CJD. Importantly, a Gerstmann-Sträussler-Scheinker mutation carrier in the asymptomatic phase and at disease onset was included as well. Both NF-L and tau were markedly increased in CJD serum, reaching similar or even better performance as in CSF (sensitivity and specificity for serum NF-L 100% and 85.5%, and for serum tau 84.6% and 96.2%, respectively). Serum S100B showed high sensitivity as well (84.2%), but lower specificity (63%). CSF neurofilaments were increased before symptom onset, while prion seeding assay was negative. Just before a clinical diagnosis could be made, all CSF markers and NF-L in the serum were increased and CSF prion conversion assay was positive. The data suggest that neurofilaments are sensitive and specific blood markers for the diagnosis of genetic and sporadic CJD and might represent promising tools to predict disease onset.

Detection of the tau protein in human serum by a sensitive four-electrode electrochemical biosensor

This study presents a novel approach based on a four-electrode electrochemical biosensor for the detection of tau protein – one of the possible markers for the prediction of Alzheimer's disease (AD). The biosensor is based on the formation of stable antibody–antigen complexes on gold microband electrodes covered with a layer of a self-assembled monolayer and protein G. Antibodies were immobilized on the gold electrode surface in an optimal orientation by protein G interaction. Electrochemical impedance spectroscopy was used to analyze impedance change, which revealed a linear response with increasing tau concentrations. The assay is fast (<1h for incubation and measurement) and very sensitive. The limit of quantification for the full-length 2N4R tau protein is 0.03pM, a value unaltered when the assay was processed in bovine serum albumin or human serum. This technology could be adapted for the detection of other biomarkers to provide a multiple assay to identify AD progression in a point of care setting.

A Preliminary Study on Investigation of Serum α-Synuclein and Tau Protein Levels in Children with Attention Deficit Hyperactivity Disorder

Neurodegenerative molecules play an important role in maintaining a supply for synaptic vesicles; and they are also likely to help regulate the dopamine release which is the primary mechanism of action in pharmacological treatments for attention deficit hyperactivity disorder (ADHD). It is suggested that there could be interactions between α-synuclein and tau in cytoskeletal disorganization and synaptic dystrophy. Therefore, we aim to determine the serum levels of neurodegenerative molecules such as α-synuclein and tau in children with ADHD. The study group consisted of 25 children, aged 6-10, diagnosed with ADHD according to DSM-IV criteria and who appeared at Dicle University, Faculty of Medicine, and Department of Child Psychiatry in Diyarbakır, Turkey. 25 children, having no psychiatric disorders and medical illnesses, were selected as healthy control group. Serum α-synuclein and tau concentrations were determined by Enzyme-Linked Immuno Sorbent Assay. The α-synuclein levels of ADHD were not significantly different than those of controls. The tau levels of ADHD were found to be statistically significantly higher than those of controls. Moreover, α-synuclein levels showed a statistically significantly positive correlation with tau levels in children with ADHD. The results of our preliminary study can suggest that ADHD might possibly share a common disease mechanism with other diseases in terms of tau pathology. Increased serum tau level may be an indication of disturbance of microtubule transportation in the brains of children with ADHD.

Wpływ omdlenia u młodocianych na stężenie białka tau w surowicy krwi

Wpływ omdlenia u młodocianych na stężenie białka tau w surowicy krwi

PT560. A comparative study of serum Tau protein and Aß levels on intestinal endotoxemia among Alzheimer’s disease rats and in Chinese sample of Alzheimer’s disease patients and healthy controls

PT560. A comparative study of serum Tau protein and Aß levels on intestinal endotoxemia among Alzheimer’s disease rats and in Chinese sample of Alzheimer’s disease patients and healthy controls

Changes of serum Tau, GFAP, TNF-α and malonaldehyde after blast-related traumatic brain injury

ObjectiveTo determine the changes of serum Tau protein, glial fibrillary acidic protein (GFAP), tumor necrosis factor alpha (TNF-α), and malonaldehyde (MDA) in rats after blast-related traumatic brain injury (BTBI) and to provide relative information for further studies on BTBI mechanism and seek specific biomarkers for BTBI. MethodsNinety male Sprague-Dawley rats were randomly assigned into three groups: control group, moderate blast injury group, and severe blast injury group (n=30 for each). Rats in the moderate and severe blast injury groups were respectively exposed to corresponding levels of BTBI. After explosion, serum levels of Tau, GFAP, TNF-α, and MDA in each group were determined by Elisa assay at different time points after injury (8h, 24h, 3 d, and 6 d). The extent of brain damage was detected by Nissl staining and TUNEL assay. ResultsSerum levels of Tau and GFAP rapidly increased and reached the peak at 24h after either moderate or severe blast injury. All the values were significantly higher than control group at all time points (P<0.05). Serum TNF-α level of both injury groups peaked at 8h after BTBI and stayed significantly higher than control group at all time points (P<0.05). Serum MDA of two injury groups began to significantly increase at 3 d and the level stayed significantly higher than control group until 6 d (P<0.05). Moreover, unlike the other biomarkers, serum MDA of severe blast injury group was significantly higher than moderate blast injury group at 6 d (P<0.05). ConclusionThe changes of serum Tau, GFAP, and TNF-α showed a good sensitivity at the acute phase after BTBI (within 24h). However, their specificity and correlation with the extent of injury were limited in this experiment. Moreover, although the change of serum MDA showed a poor sensitivity and specificity to the diagnosis of BTBI during the first few days, it can reflect the injury degree at 6 d after injury. Therefore, further studies are needed to improve the methods of detecting more serum markers and investigate the significance of multiple markers in diagnosing BTBI.

Low Serum Level α-Synuclein and Tau Protein in Autism Spectrum Disorder Compared to Controls.

α-Synuclein (α-syn) and tau proteins are thought to be related with the synaptic loss and cell death underlying several important neurodegenerative diseases. The aim of our study was to investigate serum α-syn and tau levels in autism. Serum levels of α-syn and tau were measured, and autism spectrum disorder (ASD) severity was assessed at admission using the Childhood Autism Rating Scale (CARS) total score. The mean CARS score of the autism group on admission was 47.91 points (SD: 5.97). The results indicated that the mean serum α-syn and serum tau levels were significantly (p < 0.001) lower in children with ASD as compared with normal cases (33.01 ± 20.78 and 55.19 ± 15.34 ng/mL and 241.23 ± 290.5 and 509.78 ± 269.25 ng/mL, respectively). There was a significant positive correlation between serum α-syn levels and serum levels of tau identified by Pearson correlation analysis (r = 0.922, n = 28, p < 0.001). Synaptic abnormality in autism may result from microglial activity. Furthermore, α-syn and tau aggregation may lead to synaptic dysfunction, and this may contribute to either neuronal or synaptic dysfunction or neurodegeneration. Our preliminary study suggests that low levels of serum α-syn and tau may be implicated in the relationship between synaptic activity and autism.

Serum tau protein as a marker of disease activity in enterohemorrhagic Escherichia coli O111-induced hemolytic uremic syndrome

Tau protein levels in cerebrospinal fluid (CSF) and serum are elevated in patients with various central nervous system diseases. We investigated whether serum tau protein levels are useful for predicting and assessing disease activity of acute encephalopathy (AE) in enterohemorrhagic Escherichia coli (EHEC) O111-induced hemolytic uremic syndrome (HUS; EHEC encephalopathy). Serum samples were obtained from 14 patients with EHEC O111/HUS, 20 patients with non-EHEC-related AE, and 20 age- and sex-matched healthy controls. CSF samples were obtained from 2 patients with EHEC encephalopathy and 20 patients with non-EHEC-related AE. Tau protein levels and levels of several proinflammatory cytokines were quantified by enzyme-linked immunosorbent assays. Results were compared with the clinical features of EHEC encephalopathy, including magnetic resonance image (MRI) findings. Serum tau levels in patients with EHEC encephalopathy were significantly elevated compared with those in patients with EHEC O111/HUS without encephalopathy, patients with non-EHEC-related AE, and healthy controls. The ratio of CSF tau levels to serum tau levels was >1.0 in all patients with non-EHEC-related AE but <1.0 in 2 patients with EHEC encephalopathy. Serum tau protein levels increased rapidly and markedly in patients with severe EHEC 0111/HUS and encephalopathy when HUS occurred, but were not elevated in mild patients, even in the HUS phase. Furthermore, changes in serum tau protein levels in patients with EHEC encephalopathy were consistent with abnormalities on brain MRI and were positively correlated with proinflammatory cytokine levels. Our results indicate that serum tau protein might be useful to predict and assess disease activity of EHEC encephalopathy.

Serum tau protein level serves as a predictive factor for neurological prognosis in neonatal asphyxia

Background: Tau protein is a microtubule-associated protein that is present in axons. Elevated tau protein levels in cerebrospinal fluid or serum are associated with several central nervous system diseases and can indicate neuronal injury. Objective: In the present study, we measured and then compared serum tau protein levels between infants with neonatal asphyxia and control subjects. We examined these data to investigate the correlation between serum tau protein levels and neurological outcomes after neonatal asphyxia. Patients and methods: Serum tau protein levels were determined by an enzyme-linked immunosorbent assay in 19 neonates with neonatal asphyxia. Of these 19 neonates, 3 had severe spastic tetraplegia, and 1 had west syndrome. A group of 19 unaffected neonates was included in the study as a control group. Results: Serum tau protein levels on postnatal day 3 were significantly higher in the poor outcome group than those in the good outcome (p=0.010) and control groups (p=0.006). On postnatal day 7, serum tau protein levels again were significantly higher in the poor outcome group than those in the good outcome (p=0.007) and control groups (p=0.006). Conclusions: The present findings indicate serum tau protein levels measured on postnatal days 3 and 7 can predict neurological prognosis following neonatal asphyxia.

The Clinical Value of Serum Tau Protein in Sepsis-associated Encephalopathy Patients

The Clinical Value of Serum Tau Protein in Sepsis-associated Encephalopathy Patients

Tau proteins in serum predict neurological outcome after hypoxic brain injury from cardiac arrest: Results of a pilot study

ObjectiveTo conduct a pilot study to evaluate the prognostic potential of serum tau protein measurements to predict neurological outcome 6 months following resuscitation from cardiac arrest. MethodsIn this retrospective observational study, we employed a new ultra sensitive digital immunoassay technology to examine serial serum samples from 25 cardiac arrest patients to examine tau release into serum as a result of brain hypoxia, and probe for its significance predicting six-month neurological outcome. Serial blood samples were obtained from resuscitated cardiac arrest survivors during their first five days in an intensive care unit, and serum total tau was measured. Cerebral function assessments were made using Cerebral Performance Categorization (CPC) at discharge from the ICU and six months later. Tau data were analyzed in the context of 6-month CPC scores. ResultsTau elevations ranged from modest (<10pg/mL) to very high (hundreds of pg/mL), and exhibited unexpected bi-modal kinetics in some patients. Early tau elevations appeared within 24h of cardiac arrest, and delayed elevations appeared after 24–48h. In patients with delayed elevations, areas under the curves of tau concentration vs. hours since cardiac arrest were highly predictive of 6-month outcome (P<0.0005). ConclusionHigh-sensitivity serum tau measurements combined with an understanding of tau release kinetics could have utility for hypoxic brain injury assessment and prediction of cerebral function outcome.

Serum tau protein level for neurological injuries in carbon monoxide poisoning

Introduction. Carbon monoxide (CO) poisoning causes hypoxia that results tissue injury, especially in the brain and heart. Delayed neurologic sequela is one of the most serious complications that may occur up to 40% of severe CO poisoning cases. Objective. The aim of the study was to determine an association between the serum tau protein and severe neurologic symptoms/signs upon presentation. Methods. Seventy-eight patients with CO poisoning were evaluated in this cross-sectional study. The patients were divided into two groups, Group 1: those with loss of consciousness (LOC)/syncope, seizure, coma, altered mental status (n = 19), and Group 2; without LOC (n = 59). Serum tau protein levels were studied on admission. Results. Mean age of the patients was 37.3 ± 15.4 and 53.6% were male. Headache was the most common presenting symptom observed among 67 patients (86%). The median serum tau protein level was 76.54 pg/mL (35.56–152.65) within group 1, 64.04 pg/mL (23.85–193.64) in patients within group 2 (p = 0.039), respectively. The median serum tau protein levels were 79.80 pg/mL (35.56–193.64) in patients who received HBO therapy and 65.79 pg/mL (23.85–167.29) in patients who did not receive HBO therapy (p = 0.032). The value of area under the curve was 0.642 for detecting CO poisoning with severe neurological symptoms. Conclusion. Although tau protein levels were significantly higher in patients with severe neurological symptoms; the difference did not reach a clinical significance. Further studies are needed in order to reveal the validity of tau protein for detecting neurological injuries in patients with CO toxicity.

Avidity of anti-neurocytoskeletal antibodies in cerebrospinal fluid and serum

Antibodies have different avidities that can be evaluated using modified enzyme-linked immunosorbent assay (ELISA) techniques. We determined levels and avidities of antibodies to light (NFL) and medium (NFM) subunits of neurofilaments and tau protein in serum and cerebrospinal fluid (CSF) from 26 patients and anti-tau antibody levels and their avidities in 20 multiple sclerosis (MS) patients and 20 age- and sex-matched controls. Each sample was analyzed using both standard ELISA and also using a similar ELISA protocol with the addition of urea. The avidities of anti-neurocytoskeletal antibodies were higher in the CSF than those in serum (anti-NFL, p < 0.0001; anti-tau, p < 0.01; anti-NFM, n.s.). There was no relationship between avidities in serum and CSF for individual anti-neurocytoskeletal antibodies. We did not observe the relationship among the avidities of various anti-neurocytoskeletal antibodies. The avidities of anti-tau antibodies in the CSF were significantly higher in the MS patients than those in the controls (p < 0.0001). The study demonstrates the differences in avidities of CSF or serum neurocytoskeletal antibodies measured as the urea resistance by ELISA method. Avidity determination of anti-neurocytoskeletal antibodies could contribute to the evaluation of the immunological status of patients.