Serum Tau Protein Levels Research Articles

Comparison of Serum Neurofilament Light Chain and Tau Protein Levels in Cases with Autism Spectrum Disorder and Their Healthy Siblings and Healthy Controls.

: There is a growing interest among clinicians and researchers in identifying potential biomarkers associated with autism. Neurofilament light chain (NfL) and Tau protein, which are proteins associated with neurodegeneration and neuroaxonal degeneration, are particularly promising potential biomarker candidates in this field. : In this study, we compared serum NfL (sNfL) and serum Tau (sTau) levels in Autism spectrum disorder (ASD) patients, their healthy siblings (HS), and healthy controls (HC), aimed to investigate their relationship with ASD severity. Our study included 43 ASD-diagnosed participants, 43 HS participants and 42 HC participants. Clinical characteristics of the participants were assesed by Kiddie Schedule for Affective Disorders and Schizophrenia, Childhood Autism Rating Scale, Aberrant Behavior Checklist, and Strengths and Difficulties Questionnaire. Serum samples were subjected to analysis via enzyme-linked immunosorbent assay to quantitatively measure the levels of NfL and Tau protein. : sNfL levels in the ASD group were significantly higher than both of the control groups. Regarding sTau levels, no significant difference was found between study and control groups. In addition, NfL and Tau levels were not significantly correlated with ASD symptom severity. : Our findings may indicate that the sNfl levels associated with neuroaxonal damage may constitue a potential clinical biomarker rather than being an endophenotype phenomena.

Correlation analysis between the amniotic fluid contamination and clinical grading of neonatal hypoxic–ischemic encephalopathy and biomarkers of brain damage

BackgroundAmniotic fluid contamination (AFC) is a risk factor for neonatal hypoxic ischemic encephalopathy (HIE); however, the correlation between AFC level and the incidence and clinical grading of HIE, in addition to relevant biomarkers of brain damage, have not been assessed.MethodsThis single-center observational study included 75 neonates with moderate-to-severe HIE. The neonates with HIE were divided into four subgroups according to the AFC level: normal amniotic fluid with HIE group (NAF-HIE), I°AFC with HIE group (I°AFC-HIE), II°AFC with HIE group (II°AFC-HIE), and III°AFC with HIE group (III°AFC-HIE). The control groups consisted of 35 healthy neonates. The clinical grading of neonatal HIE was performed according to the criteria of Sarnat and Sarnat. Serum tau protein and S100B were detected by enzyme-linked immunosorbent assay kits. Correlations of serum tau protein and S100B were evaluated using the Pearson correlation analysis.Results(1) The incidence of neonatal HIE in the NAF-HIE group was 20 cases (26. 7%), I°AFC-HIE was 13 cases (17.3%), II°AFC-HIE was 10 cases (13.3%), and III°AFC-HIE was 32 cases (42. 7%). The incidence of moderate-to-severe HIE in the I°–III°AFC-HIE groups was 73.3% (55/75). (2) In 44 cases with severe HIE, 26 cases (59.1%) occurred in the III°AFC-HIE group, which had a significantly higher incidence of severe HIE than moderate HIE (p < 0.05). In NAF-HIE and I°AFC-HIE groups, the incidence of moderate HIE was 45.2% and 29.0%, respectively, which was higher than that of severe HIE (X2 = 9.2425, p < 0.05; X2 = 5.0472, p < 0.05, respectively). (3) Serum tau protein and S100B levels in the HIE groups were significantly higher than in the control group (all p < 0.05), and were significantly higher in the III°AFC-HIE group than in the NAF-HIE and I°AFC-HIE groups (all p < 0.05). (4) Serum tau protein and S100B levels in the severe HIE group were significantly higher in the moderate HIE group (all p < 0.05). (5) Serum tau protein and S100B levels were significantly positively correlated (r = 0.7703, p < 0.0001).ConclusionAmong children with severe HIE, the incidence of III°AFC was higher, and the levels of serum tau protein and S100B were increased. AFC level might be associated with HIE grading.

Tau protein hyperphosphorylation in children with cerebral palsy with sleep disorders

Aims: In this study, we aimed to evaluate the relationship between sleep disorder and serum tau protein levels in children with cerebral palsy.&#x0D; Methods: The sample was selected among children aged 6-10 years who applied to our physical medicine and rehabilitation outpatient clinic. In order to evaluate sleep quality, the Pittsburgh Sleep Quality Index (PSQI) questionnaire was recorded by asking parents of all participants. Children with CP who had a Pittsburgh Sleep Quality Index value above 5 were determined as the sleep disorder group. We recruited 27 children with CP and sleep disorders in the first patient group (Group 1), 27 children with CP but without sleep disorders in the second group (Group 2). The third group (Group 3), which was the healthy group, included 27 children without any disease. We also recorded the age of children at diagnosis, risk factors for CP (premature, prolonged birth, etc.), CP type, gross motor function classification system (GMFCS), botox application, orthoses usage, maternal age at birth, and additional problems. We measured total tau protein (T-tau) and phosphorylated tau protein (P-tau) levels in blood samples through a double-antibody sandwich enzyme-linked immunosorbent assay (ELISA). The correlation between tau protein and PSQI values was examined.&#x0D; Results: Maternal age (p=0.001), gross motor function classification system (GMFCS) (p=0.001), and pittsburgh sleep quality index (PSQI) (p=0.001) were significantly higher in the group with sleep disorders. There was a statistically significant difference between the groups in terms of serum T-Tau and P-tau protein levels (T-tau p=0.003, P-tau p=0.004). In the group sleep disorders, PSQI was significantly correlated with T-tau (r=0.499) and P-tau (r=0.473).&#x0D; Conclusion: This study shows that tau protein levels are higher in CP patients with sleep disorders than in participants without sleep disorders. In the correlation analyzes, a positive and significant correlation was observed between PSQI values and T-tau and P-tau in sleep disorders groups, and no correlation was found in without sleep disorders.

The Early Prognostic Value and Optimal Time of Measuring Serum and Cerebrospinal Fluid Tau Protein for Neurologic Outcomes in Postcardiac Arrest Patients Treated with Targeted Temperature Management.

Neuroprognostication of cardiac arrest patients remains a challenge. We evaluated the early prognostic value and optimal time of measuring serum and cerebrospinal fluid (CSF) tau protein levels to predict neurologic outcome in postcardiac arrest patients treated with targeted temperature management (TTM). We also evaluated the cutoff values in predicting poor outcomes. Patients treated with TTM following cardiac arrest, from May 2018 to June 2019, were included in the study. Serum and CSF tau levels were obtained and compared immediately, at 24, 48, and 72 hours after return of spontaneous circulation (ROSC). The area under the receiver-operating characteristic curve (AUROC) and the Delong method were used to identify the cutoff values of serum and CSF tau protein levels in predicting poor outcomes at each interval. Of 38 patients enrolled, 16 experienced poor outcomes. Both serum and CSF tau levels were consistently higher in the poor outcome group than in the good outcome group. The AUROCs of serum and CSF tau protein were not significantly different at each time point. Immediately after ROSC, sensitivities of both serum and CSF tau protein levels were 31.25% at 100% specificity and increased to 86.6% and 73.3%, respectively, at 72 hours. This study demonstrates that serum and CSF tau protein levels could be used as valuable predictors of neurologic outcomes in postcardiac arrest patients treated with TTM. The early optimal time for measuring the serum and CSF tau protein levels was determined to be 72 hours after ROSC.

The study of Tau and phospho Tau protein levels in attention deficit and hyperactivity disorder

Background/aim Attention deficit and hyperactivity disorder (ADHD) is a widespread neurodevelopmental disorder that begins in childhood and has negative consequences throughout adult life. The etiology and pathogenesis of ADHD are still unclear. Tau protein is a soluble microtubule-related protein expressed by neurons and localized in the cytoplasm as well as axons. Tau protein provides stability of microtubule in two ways: phosphorylation and isoforms. The excessive phosphorylation of Tau separates the protein from the microtubule, thus making it unstable. In this study, we aimed to investigate whether there is a relationship between serum Tau protein and phospho Tau (p-Tau181) levels and ADHD occurrence.Materials and methods This study included 26 male children aged 7–12 years with newly diagnosed ADHD, who had previously not used any medication for ADHD, and 26 male healthy children. Serum Tau and p-Tau181 concentrations were performed by enzyme-linked immunosorbent assay (ELISA). Results In patients, the Tau levels were not significantly different from those of the controls; the p-Tau181 levels were significantly higher than those of the controls. Conclusion We concluded that high p-Tau181 might be associated with the progression of ADHD and cognitive changes in ADHD.

Relationship of Serum Tau Levels with Cognitive Functions and Factors Affecting The Cognitive Function Decrease in Parkinson's Disease Patients

Introduction: Cognitive impairment is a non-motor symptom of Parkinson's disease (PD) which occurs as the disease progresses and affects quality of life. Many efforts have been developed in early detection of cognitive disorders, one of which is the examination of tau protein biomarkers, where the tau protein that undergoes pathological changes to form neurofibrillary tangles (NFTs) is found in Alzheimer's disease and PD and plays a role in cognitive impairment. However, the role of tau in PD is still controversial. This study aims to assess the relationship between serum tau levels and cognitive function and the factors that affect cognitive function in PD patients.&#x0D; Methods: This cross-sectional design was conducted at the RSUP DR. M Djamil Padang. During the period March to August 2020, 62 research subjects were obtained. Cognitive function examination was carried out by using the MoCA-Ina test and examination of serum tau levels using the Elisa method. The relationship between categorical variables was tested by Chi square and differences in serum tau levels in the group with and without cognitive impairment were tested with the Mann Whitney test, considered statistically significant if the p value &lt;0.05.&#x0D; Results: With Moca Ina examination, it was found that 67.7% of patients had impaired cognitive function. The mean serum tau level was 198.004 ± 162.69 ng / L.There was a significant relationship between education level and degree of disease with cognitive function (p &lt;0.05) and there was no difference in mean serum tau levels between groups with and without cognitive impairment.&#x0D; Conclusion: There is a significant relationship between education level and degree of disease with cognitive function and there is no difference in mean serum tau protein levels between the cognitive impaired group and the cognitive normal group.

Relationship of Serum Tau Levels with Cognitive Functions and Factors Affecting The Cognitive Function Decrease in Parkinson's Disease Patients

Introduction: Cognitive impairment is a non-motor symptom of Parkinson's disease (PD) which occurs as the disease progresses and affects quality of life. Many efforts have been developed in early detection of cognitive disorders, one of which is the examination of tau protein biomarkers, where the tau protein that undergoes pathological changes to form neurofibrillary tangles (NFTs) is found in Alzheimer's disease and PD and plays a role in cognitive impairment. However, the role of tau in PD is still controversial. This study aims to assess the relationship between serum tau levels and cognitive function and the factors that affect cognitive function in PD patients.&#x0D; Methods: This cross-sectional design was conducted at the RSUP DR. M Djamil Padang. During the period March to August 2020, 62 research subjects were obtained. Cognitive function examination was carried out by using the MoCA-Ina test and examination of serum tau levels using the Elisa method. The relationship between categorical variables was tested by Chi square and differences in serum tau levels in the group with and without cognitive impairment were tested with the Mann Whitney test, considered statistically significant if the p value &lt;0.05.&#x0D; Results: With Moca Ina examination, it was found that 67.7% of patients had impaired cognitive function. The mean serum tau level was 198.004 ± 162.69 ng / L.There was a significant relationship between education level and degree of disease with cognitive function (p &lt;0.05) and there was no difference in mean serum tau levels between groups with and without cognitive impairment.&#x0D; Conclusion: There is a significant relationship between education level and degree of disease with cognitive function and there is no difference in mean serum tau protein levels between the cognitive impaired group and the cognitive normal group.

Differential longitudinal changes of neuronal and glial damage markers in anorexia nervosa after partial weight restoration

Atrophic brain changes in acute anorexia nervosa (AN) are often visible to the naked eye on computed tomography or magnetic resonance imaging scans, but it remains unclear what is driving these effects. In neurological diseases, neurofilament light (NF-L) and tau protein have been linked to axonal damage. Glial fibrillary acidic protein (GFAP) has been associated with astroglial injury. In an attempt to shed new light on factors potentially underlying past findings of structural brain alterations in AN, the current study investigated serum NF-L, tau protein, and GFAP levels longitudinally in AN patients undergoing weight restoration. Blood samples were obtained from 54 acutely underweight, predominantly adolescent female AN patients and 54 age-matched healthy control participants. AN patients were studied in the severely underweight state and again after short-term partial weight restoration. Group comparisons revealed higher levels of NF-L, tau protein, and GFAP in acutely underweight patients with AN compared to healthy control participants. Longitudinally, a decrease in NF-L and GFAP but not in tau protein levels was observed in AN patients upon short-term partial weight restoration. These results may be indicative of ongoing neuronal and astroglial injury during the underweight phase of AN. Normalization of NF-L and GFAP but not tau protein levels may indicate an only partial restoration of neuronal and astroglial integrity upon weight gain after initial AN-associated cell damage processes.

A preliminary study about neurofilament light chain and tau protein levels in psoriasis: Correlation with disease severity.

BackgroundStudies investigating cognitive dysfunction in psoriatic patients remain inconclusive.ObjectiveTo investigate the risk of cognitive decline in plaque‐type psoriasis patients.MethodsSerum neurofilament light chain (NFL) and tau protein concentrations in 45 patients with plaque‐type psoriasis and forty‐five healthy controls were measured by enzyme‐linked immunosorbent assay (ELISA).ResultsMean homeostasis model assessment (HOMA‐IR) values (6.82 vs 3.25) and serum levels of insulin (28.19 vs 15.71), NFL (5.74 vs 1.98), and tau (348.17 vs 207.30) in patients with psoriasis were found to be significantly higher than those of in healthy controls. There was a significant positive correlation between NFL and tau (r = .257, P = .015). There was significant correlation between NFL, tau and PASI (r = .310, P = .040) and (r = .383, P = .010), respectively. Significant correlations between NFL and insulin, TC, HDL‐C, TG, VLDL‐C, and BMI were found. NFL (9.38 vs 3.08) and tau (439.28 vs 281.58) concentrations and PASI values (23.94 vs 14.18) in patients with disease onset before 40 years were significantly higher than that of the patients with disease onset after 40 years. C‐reactive protein (CRP) was significantly correlated with BMI (r = .449, P < .001), LDL‐C (r = .240, P = .026), TG (r = .244, P = .024), and VLDL‐C (r = .241, P = .025) in patients with psoriasis.ConclusionsIncreased serum NFL and tau protein levels and the presence of positive correlations between NFL, tau protein and PASI score show cognitive decline risk may be higher in moderate‐to‐severe psoriasis.

Serum levels of tau protein increase according to the severity of the injury in DAI rat model.

Traumatic brain injury (TBI) in the form of diffuse axonal injury (DAI) is difficult to diagnose in the early phase of the injury. Early diagnosis of DAI may provide opportunity for developing treatment and management strategies. Tau protein has been demonstrated to increase in the early phase of TBI with high diagnostic accuracy in patients with DAI. We tested the biological plausibility of tau protein using a rat DAI model by evaluating the association between serum tau levels and the severity of brain injury.DAI was induced in animals using the Marmarou model.After a survival of 60 minutes, rats were anesthetized and sacrificed after obtaining blood samples (5ml) from the heart. Eighteenratswereemployedin the present studyand were randomly subjected to sham-operated control (n=4), mild DAI (n=7), and severe DAI (n=7). Of seven severe DAI rats, two rats that had focal injury caused by skull fracture were excluded in the measurement of tau protein level. The serum levels of tau protein in the rat DAI model were found to increase significantly and consistently according to the severity of the injury.Rats with DAI showed significantly higher serum levels of tau protein compared to sham rats; the severe DAI rats had higher levels of tau than moderate DAI and sham rats (sham vs. mild, P=0.02; mild vs. severe, P=0.02). In conclusion, serum tau protein levels may be useful as a biomarker for diagnosing and estimating the severity of DAI in the early phase.

Associations between serum tau, neurological outcome, and cognition following traumatic brain injury.

To investigate the dynamic change in the serum Tau protein early after acute traumatic brain injury (TBI) and its association with neurological outcome and cognitive function. Around 229 patients with acute TBI and 30 healthy subjects were evaluated for the serum levels of Tau protein on 1, 3, 5, 7, and 14 days after TBI. The relationships of the serum levels of Tau protein and initial GCS and GOS at 6 months post-injury were also analyzed. Further, 95 TBI patients were assessed with their cognitive function with Montreal cognitive assessment (MoCA) score. Serum Tau was significantly higher in patients with TBI at 1, 3, 5, 7, and 14 days. The serum Tau at each point was significantly lower respectively in the patients with mild TBI than that in medium and severe TBI. The serum Tau was significantly lower in patients with good outcome compared to the poor outcome group. The early serum Tau was negatively correlated with both GCS and GOS. In the TBI group, 39 (41%) out of 95 patients developed cognitive dysfunction assessed by MoCA. Tau protein at day 1, 3, and 5 after TBI was significantly correlated with cognitive dysfunction at 6 months after TBI. Acute Tau associations with neurological outcomes and cognition may implicate white matter damage and neuronal degeneration. Serum Tau may be used as a reliable biological marker for early diagnosis and cognitive recovery following TBI.

Association between Elevated Serum Tau Protein Level and Sepsis-Associated Encephalopathy in Patients with Severe Sepsis.

Sepsis-associated encephalopathy (SAE) is a common complication of sepsis. It is imperative to recognize, diagnose, and effectively manage SAE at the early stages. The aim of this study was to evaluate the potential of using the serum tau protein level in the diagnosis of SAE and the prediction of SAE outcomes. This was a retrospective and observational study. The patients included in this study were diagnosed with severe sepsis or septic shock. The serum tau protein level was measured using a commercial enzyme-linked immunosorbent assay. The association between the level of serum tau protein and SAE was assessed by multiple logistic regression analysis. One hundred nine patients with severe sepsis were enrolled during a period of two years. Of the 109 enrolled patients, 27 developed SAE. The serum tau protein level was significantly higher in the patients with SAE than that of the non-SAE group. The serum tau protein level and the sequential organ failure assessment (SOFA) score were independent factors that were associated with SAE. The combined use of the serum tau protein level with the SOFA score improved the accuracy in distinguishing SAE from non-SAE patients. A cutoff value serum tau protein level of 75.92 pg/mL had 81.1% sensitivity and 86.1% specificity in predicting the 28-day mortality in patients with severe sepsis. We identified a close association between the serum tau protein level with the appearance of SAE in patients with severe sepsis. The serum tau protein level can be useful in the prediction of poor outcomes in patients with sepsis.

Observational study of long-term persistent elevation of neurodegeneration markers after cardiac surgery

Surgery and anesthesia induce inflammatory changes in the central nervous system, which ultimately lead to neuronal damage concomitant with an increase in the level of neurodegeneration markers. Despite some experimental data showing prolonged activation of the immune system post-surgery, no study has determined the extent of long-term elevation of neurodegeneration markers. The purpose of this study was to investigate the serum levels of tau protein, ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1), neurofilament light (NF-L), and glial fibrillary acidic protein (GFAP) after elective cardiac surgery with the implementation of cardiopulmonary bypass (CPB). The serum levels of these markers from 30 patients were compared longitudinally to the baseline (pre-surgery or t0), at 24 hours (t+24), at 7 days (t+7d), and at 3 months (t+3m). The secondary outcome was the production of macrophage-colony stimulating factor (M-CSF) and tumor necrosis factor-α (TNF-α) in vitro by isolated monocytes in response to lipopolysaccharide (LPS) as the measure of immune system activation. The tertiary outcome was the serum level of C-reactive protein (CRP), serum amyloid P (SAP), and α-2-macroglobulin (A2M). Serum levels of tau protein increased 24 hours after surgery (p = 0.0015) and remained elevated at 7 days (p = 0.0017) and three months (p = 0.036). Serum levels of UCH-L1 peaked at 24 hours (p = 0.00055) and normalized at 3 months. In vitro secretion of M-CSF by LPS-stimulated peripheral monocytes, but not TNFα, correlated highly (r = 0.58; p = 0.04) with persistent elevation of serum tau levels at 3 months. The serum CRP and SAP increases correlated with tau post-CPB levels significantly at 3 months. We demonstrated that elevation of serum tau levels at 24 hours, 7 days, and 3 months after heart surgery is concomitant with some traits of inflammation after CPB. The elevation of tau several weeks into recovery is significantly longer than expected.

Serum tau protein level in patients with long-term consequences of the mild brain traumatic injury

Objective — to study the content of tau protein in blood serum of the patients with long‑term consequences of the mild brain traumatic injury.Methods and subjects. We examined 47 patients aged 22 — 53 years with long‑term consequences of the mild brain traumatic injury with the mean age 47.22 ± 8641 years (14 women, 29.78 % and 33 men, 70.22 %). In this study the serum tau protein level was measured by immunofluorescent method using monoclonal primary and secondary mice antibodies (Sigma) with the consequent measurements of the fluorescent glow with immunofluorescence microscope «Olympus» BX41 (Japany). Data was compared to healthy controls (n = 30, with mean age 27.5 ± 8.33 years) and neurological controls (patients with partial epilepsy, n = 58 with mean age 38.62 ± 9.43 years).Results. Received data showed us that the clinical course of long‑term consequences of the mild brain traumatic injury in patients after mild brain contusion in their anamnesis (38.29 %) was associated with the elevated tau protein serum level (p &lt; 0.05) 0.97 ± 0.01 ОD, healthy controls demonstrated 0.061 ± 0.02 and neurological controls 0.374 ± 0.27) as a marker of axonal impairment, that is important for clinic, prognosis and outcome in the formation of long‑term consequences of brain trauma and these should be counted in the future patients treatment. Clinical and neurological examinations of the patients with long‑term consequences of the mild brain traumatic injury have revealed the presence of multiple neurological manifestations which could indicate the damage of mesencephalic and brain stem structures.Conclusions. The features of the clinical course and formation of long‑term consequences of the mild brain traumatic injury is accompanied by axonal impairment of brain that is reflected in increased serum tau levels.

Study on serum Tau protein level and neurodevelopmental outcome of placental abruption with neonatal hypoxic-ischemic encephalopathy

Objective: The aim of this study was to explore differences in serum Tau protein levels and neurodevelopmental prognoses of placental abruption or umbilical cord around neck with hypoxic-ischemic encephalopathy (HIE).Methods: Forty neonates with moderate/severe HIE divided into placental abruption with HIE group (placental abruption with hypoxic-ischemic encephalopathy (PA-HIE) group) (n = 18) and umbilical cord around the neck with HIE group (umbilical cord around the neck with hypoxic-ischemic encephalopathy (UCAN-HIE) group) (n = 22). Healthy term newborns comprised the control group (n = 35). Serum Tau protein levels were measured using an enzyme-linked immunosorbent assay 24 hours (3.50 hours [1.00–24.00]) after birth. Neurodevelopment outcomes were assessed based on the Gesell Developmental Scale at 9 months of age.Results: Serum Tau protein levels were significantly higher in 40 cases (1013 pg/ml [538.04–1190.42]) than in the control group (106.41 pg/ml [64.55–154.71], p = .0001). Serum Tau protein levels in the PA-HIE group (1024.46 pg/ml [657.88–1190.42]) were significantly higher than those in the UCAN-HIE group (892.78 pg/ml [538.04–1179.50], p = .0149). The development quotient score in the PA-HIE group (67.0 [47.0–90.0]) was significantly lower than that in the UCAN-HIE group (81.5 [52.6–100.0]) (p = .0028). The component ratio of neurodevelopmental retardation in the PA-HIE group (44.45%) was significantly higher than that in the UCAN-HIE group (22.73%) (X2 = 13.3138, p = .0013).Conclusions: Compared with the UCAN-HIE group, the serum Tau protein level and the component ratio of neurodevelopmental retardation were significantly higher in the PA-HIE group.

Targeting Higher Levels of Tau Protein in Ukrainian Patients with Wilson's Disease.

IntroductionWilson’s disease (WD) is a rare genetic disorder of copper metabolism in which impaired copper homeostasis may enhance amyloid aggregation and trigger neurodegeneration. Tau protein is a highly soluble microtubule-associated phosphoprotein that plays a significant role in microtubule stabilization; it is also a critical component of neurotoxic degenerative mechanisms. Tau has been shown to be involved in neuronal degeneration and axonal damage, and impaired copper metabolism has been shown to be involved in copper intoxication and thus associated with the processes of neurodegeneration and cellular damage. We have therefore investigated tau protein as a potential marker of axonal impairment and neurodegeneration.MethodsPatients with WD (n = 47; mean age ± standard deviation [SD] 30.19 ± 7.87 years; mean disease duration : 10.06 ± 3.9 years) and healthy controls (HC; n = 30; mean age 29.6 ± 4.73 years) were tested for serum tau protein levels using an enzyme-linked immunosorbent assay method. All patients were receiving a stable penicillamine dose as ongoing therapy.ResultsPatients with WD had a higher mean tau protein level than did the HC (221.7 ± 135.1 vs. 71.14 ± 20.56 pg/mL, p < 0.0001). Patients with WD also had abnormally high serum tau protein levels (t statistic 6.047, 95% confidence interval − 218.2 to − 95.86) in both the cerebral and hepatocerebral forms of WD, with patients having the cerebral form showing a tendency toward higher tau levels. We found that tau protein did not differ according to gender, disease duration, age at disease onset, ceruloplasmin serum level and copper serum level.ConclusionThis study provides novel data revealing that high tau protein levels in WD patients could be a potential biomarker for axonal impairment and possible neuronal damage due to tau protein, leading to neurodegeneration in WD.

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.

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.

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.