Serum Tau Protein Research Articles

Serum Amyloid Biomarkers, Tau Protein and YKL-40 Utility in Detection, Differential Diagnosing, and Monitoring of Dementia.

Introduction: The diagnosis and treatment of dementia is one of the greatest challenges in contemporary health care. The widespread use of dementia biomarkers would improve the quality of life of patients and reduce the economic costs of the disease. The aim of the study was to evaluate the usefulness of proteins related to the Alzheimer's disease pathogenesis—amyloid beta isoform (Aβ) and total tau protein (t-tau), as well as the quite recently discovered marker YKL-40 in the most common types of dementia.Methods: 60 dementia (AD—Alzheimer's disease, VaD—vascular dementia, MxD—mixed dementia) and 20 cognitively normal subjects over 60 years old were examined. Subjects with dementia of etiology different than AD or VaD and with neoplastic or chronic inflammatory diseases were excluded. Concentrations of Aβ40, Aβ42, t-tau, and YKL-40 were measured in serum using ELISA kits on admission and after 4 weeks of inpatient treatment. ANOVA and Tukey's test or Dunn's test were used to perform comparison tests between groups. Correlations were measured using Pearson's coefficient. Biomarker diagnostic utility was assessed with ROC analysis.Results: YKL-40 differentiates between cognitively normal and mild dementia patients with 85% sensitivity and specificity and t-tau with 72% sensitivity and 70% specificity. YKL-40 and t-tau concentrations correlate with each other and with the severity of clinically observed cognitive decline.Conclusions: YKL-40 is a sensitive and specific biomarker of early dementia and, to a lesser extent, of dementia progression, however, many comorbidities may influence its levels. In such conditions, less specific but still reliable t-tau may serve as an alternative marker. Obtained results did not confirm the diagnostic utility of amyloid biomarkers.

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.

Oral and Periodontal Health in Patients with Alzheimer's Disease and Other Forms of Dementia - A Cross-sectional Pilot Study.

Systemic inflammation is characteristic for the pathogenesis of Alzheimer's disease (AD) and is responsible for the accumulation of its disease-specific Tau-protein and β-amyloid plaques. Studies focusing on an association with periodontitis showed worse periodontal conditions in patients with dementia, but until now, no study has investigated the differences between AD and other forms of dementia (noAD/DEM). Expecting severe periodontal disease in AD, the aim of this pilot-study was to compare the periodontal and dental status in patients with either AD or noAD/DEM. Twenty patients recently diagnosed with AD and 20 with noAD/DEM between the ages of 50 and 70 years were recruited at the Department of Neurology, University Hospital, Münster, Germany and clinically examined at the Department of Periodontology, School of Dental Medicine, Münster, Germany. Neuropsychological testing, levels of Tau-protein and β-amyloid in serum and liquor were used to distinguish between both groups. Dental and periodontal parameters such as clinical attachment loss (CAL), probing pocket depth (PPD), bleeding-on-probing (BOP), radiographic bone loss, full-mouth plaque score (FMPS), and missing and restored teeth were recorded. Periodontitis was diagnosed in all patients. Patients with AD presented mean BOP of 54.7 ± 31.1% and radiographic bone loss of 42.5 ± 25.3%; the mean BOP of those with noAD/DEM was 52.0 ± 23.7% and radiographic bone loss was 40.9 ± 32.3%. There was also no statistically significant difference regarding other periodontal and dental parameters. Both patients with AD and noAD/DEM had periodontal disease. Consequently, patients with all forms of dementia (AD/other) need special dental care to improve periodontal and oral health.

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.
 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 <0.05.
 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 <0.05) and there was no difference in mean serum tau levels between groups with and without cognitive impairment.
 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.
 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 <0.05.
 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 <0.05) and there was no difference in mean serum tau levels between groups with and without cognitive impairment.
 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.

Mutation in microtubule-associated protein tau MAPT coding gene and its correlation with Alzheimer’s disease

Alzheimer's disease (AD) is a progressive irreversible neuronal dysfunction characterized by progressive memory loss along with neuropsychiatric symptoms and a decline in daily activities. Disturbances in microtubule-associated protein tau (MAPT) gene expression result in disruption of the neuronal cytoskeleton and formation of neurofibrillary tangles. The study aims are to highlight the correlation between MAPT gene's exons mutations and AD. Beside the possibility of utilizing serum's tau protein concentration as an indicator for AD due to the accumulation of intracellular neurofibrillary filaments of highly phosphorylated Tau in AD patient's brain. DNA had been extracted from participant's blood that divided into three groups 30 participants in each ,AD patients ,Positive family history and healthy or control groups. The results of this research showed that serum's Tau protein concentration in AD patient group was significantly higher than healthy control and positive family history group and according to this result serum's tau concentration could be utilized as a good indicator for AD .Beside mutation in each 1,9 and 13 exons had been identified by PCR product analysis utilizing specific primers for each , Amplification PCR products in exon (1) showed 428bp band in AD patients group does not exist in 26.66% and in positive family history for AD group does not exist in 23.33%, In exon (9) PCR product of 604bp band in AD patients group does not exist in 53.33%, and in positive family history group does not exist in 43.33%. While amplification PCR product of exon 13 showed 299bps band in all healthy control and positive family history but not in AD patient group instead it band in 263bp had been appeared in 36.66%. These results confirmed the important role of tau protein and its coding gene in the pathology of AD.

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.

Plasma tau protein and Aβ42 level as markers of cognitive impairment in patients with Parkinson's disease.

Parkinson's disease (PD) is a progressive neurodegenerative disorder with a characteristic clinical picture. Apart from classical movement disorders, a significant role is also played by non-motor symptoms, in particular cognitive impairments, which have a significant impact on the quality of life of the patients. Tau protein and amyloid beta are well-known non-specific biomarkers in Alzheimer's disease (AD). The study assessed the practical value of determining tau protein and amyloid beta (Aβ42) in the blood serum of patients with PD and their relationship with cognitive impairments, radiographic image and the used dose of L-DOPA. The neuropsychological assessment was carried for 64 patients with PD. The levels of amyloid beta 1-42 (Aβ42) and tau proteins in serum were also measured. The Aβ42 level in the serum was statistically higher in patients with longer duration of the disease (p < 0.05) and those who were taking a higher dose of L-DOPA (p < 0.05). The average level of tau protein in the serum was slightly lower in the study groups than in the control group and showed no statistical significance. No correlation was found between the levels of tau protein and Aβ42 and the results of neuropsychological tests. Tau protein correlated with hippocampal atrophy (p < 0.05). Serum levels of Aβ42 and tau protein in PD may be a useful marker for the assessment of cognitive impairments. The role of L-DOPA in the process of dementia in PD remains unclear.

Serum tau as a predictor for neurological outcome after cardiopulmonary resuscitation

AimWe evaluated serum tau protein as biomarker for poor neurological outcome over an extended observation period in patients after successful cardiopulmonary resuscitation (CPR) treated with mild therapeutic hypothermia (MTH) or normothermia (NT). MethodsThis is a retrospective analysis of a prospective observational study including 132 patients after successful CPR. Serum tau was determined in 24 h intervals for up to 168 h after CPR. Patients were treated with MTH targeting a temperature of 33 °C for 24 h or NT according to current guidelines. Neurological outcome was assessed with the Cerebral Performance Categories Scale (CPC) at hospital discharge. ResultsForty-three percent of the patients were treated with MTH. Serial serum tau levels (pg/ml) showed a peak between 72–96 h after CPR (159 (IQR 27–625). Patients with poor neurological outcome (CPC 3–5) at hospital discharge (n = 68) had significantly higher serum tau levels compared to patients with good neurological outcome at 0–24 h (164 (48–946) vs. 69 (12–224); p = 0.009), at 24–48 h (414 (124–1049) vs. 74 (0–215); p < 0.001), at 48–72 h (456 (94–1225) vs. 69 (0–215); p < 0.001) and at 72–96 h (691 (197–1173) vs. 73 (0–170); p < 0.001). At 72–96 h the AUC to predict poor neurological outcome was 0.848 (95% CI: 0.737–0.959). Serum tau levels were not significantly different between patients with MTH and NT in multivariate analysis after adjusting for clinical relevant covariates. ConclusionSerum tau showed highest values and the best prognostic discrimination of poor neurological outcome at 72–96 h after CPR. Prolonged elevation may indicate ongoing axonal damage in patients with hypoxic encephalopathy.

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.

Serum and saliva total tau protein as a marker for relapsing-remitting multiple sclerosis

Multiple sclerosis (MS) is considered as motor and sensory function loss, which results from demyelination and following axonal lesion. Tau protein interferes in the construction and stabilization of microtubules that are needed for axonal transport. We hypothesize that the level of tau protein alters in MS, so we examined the level of total tau protein in serum, stimulated and unstimulated saliva as a suitable biomarker for detecting of relapsing-remitting MS. A case-control study was carried out in 30 healthy women and 30 who suffer MS and were hospitalized in Imam Reza hospital, Tehran, Iran. Total tau protein level was assayed in serum and stimulated and unstimulated whole saliva. Total tau protein was expressed at a lower level in serum of MS patients compared to control groups. The serum total tau protein level negatively correlated with EDSS. There was no significant difference in saliva total tau protein between MS and healthy individuals. Moreover, there was no significant correlation between saliva and serum total tau protein and between saliva total tau protein and EDSS. The serum level of tau protein is lower in MS and it may be considered as a potential biomarker in Multiple sclerosis. However, it seems that tau protein in the saliva isn’t a suitable biomarker for detection of MS.

Occupational metals exposure and cognitive performance among foundry workers using tau protein as a biomarker

IntroductionHuman exposure to heavy metals is a potential risk for developing cognitive impairment. Aluminum (Al) foundry is one of industries that involve occupational exposure to different metals. Aim of the workto evaluate the cognitive performance of Aluminum foundry workers in relation to different metals exposure. Materials and methodsa cross sectional study conducted on 75 Al foundry workers and 75 non-occupationally exposed subjects as controls. Personal interview with specially designed questionnaire, Assessment of cognitive functions done using Montreal cognitive assessment (MocA), Stress, depression and sleep were also assessed. Serum levels of Aluminum (AL), Lead (Pb), manganese (Mn), Zinc (Zn) and tau protein were measured. ResultsExposed group showed significant increase in serum levels of Aluminum, lead, Manganese and tau protein, p value < 0.005 (mean ± SD 0.56 ± 0.18, 22.3 ± 5.01, 42.04 ± 7.4, 1.53 ± 0.58 Vs 0.36 ± 0.11, 13.4 ± 1.29, 39.4 ± 4.4, 1.03 ± 0.44 respectively) with significant decrease of zinc level compared to control (mean ± SD 46.4 ± 5.2 Vs 88.8 ± 6.04, p value 0.005). There was a significant decrease MocA scores among exposed population, (mean ± SD 24.4 ± 3.4 compared to 28.4 ± 1.3 in non exposed, p value < 0.005). which was affected by serum levels of lead, aluminum, manganese and tau protein (β −0.165, −8.958, −.286, −2.341 respectively and p < 0.005).Stress scores was higher in exposed workers than control but not affecting cognitive performance. Conclusionoccupational exposure to metals can cause cognitive dysfunction which may be subtle, so there is a need for formal cognitive testing at baseline, and on regular intervals during working period. Serum tau protein could be used as a prognostic biomarker for the hazardous effect of occupational exposure to these metals on the neuronal cells.

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.

Serum tau concentration after diving - an observational pilot study.

Increased concentrations of tau protein are associated with medical conditions involving the central nervous system, such as Alzheimer's disease, traumatic brain injury and hypoxia. Diving, by way of an elevated ambient pressure, can affect the nervous system, however it is not known whether it causes a rise in tau protein levels in serum. A prospective observational pilot study was performed to investigate changes in tau protein concentrations in serum after diving and also determine their relationship, if any, to the amount of inert gas bubbling in the venous blood. Subjects were 10 navy divers performing one or two dives per day, increasing in depth, over four days. Maximum dive depths ranged from 52-90 metres' sea water (msw). Air or trimix (nitrogen/oxygen/helium) was used as the breathing gas and the oxygen partial pressure did not exceed 160 kPa. Blood samples taken before the first and after the last dives were analyzed. Divers were monitored for the presence of venous gas emboli (VGE) at 10 to15 minute intervals for up to 120 minutes using precordial Doppler ultrasound. Median tau protein before diving was 0.200 pg·mL⁻¹ (range 0.100 to 1.10 pg·mL⁻¹) and after diving was 0.450 pg·mL⁻¹ (range 0.100 to 1.20 pg·mL⁻¹; P = 0.016). Glial fibrillary acidic protein and neurofilament light protein concentrations analyzed in the same assay did not change after diving. No correlation was found between serum tau protein concentration and the amount of VGE. Repeated diving to between 52-90 msw is associated with a statistically significant increase in serum tau protein concentration, which could indicate neuronal stress.

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.

Expression of telomere repeat binding factor 1 and TRF2 in Alzheimer’s disease and correlation with clinical parameters

ABSTRACTObjective: The objective of this study was to investigate the expression of serum telomere repeat binding factor 1 (TRF1) and TRF2 in patients with Alzheimer’s disease (AD) and their correlation with clinicopathological features.Methods: Fifty AD subjects and 50 healthy controls were enrolled in this study. Enzyme-linked immunosorbent assay (ELISA) was used to determine the expression of TRF1 and TRF2 in the peripheral blood plasma. Correlation analysis was used to evaluate the correlation between the protein expression and AD clinical parameters.Results: The expression of TRF1 in peripheral blood serum of AD patients was significantly higher than that of the control group (t = 5.533, P < 0.01) and TRF2 was lower than the control group (t = 2.627, P = 0.010). The expression of TRF1 was positively correlated with the history of coronary heart disease (Spearman’s r = 0.298，P = 0.035). The expression of TRF1 and TRF2 was positively correlated with age (Pearson’s r1 = 0.830，P1 < 0.01；Pearson’s r2 = 0.942，P2 < 0.01), BMI (Pearson’s r1 = 0.791，P1 < 0.01；Pearson’s r2 = 0.941，P2 < 0.01), Aβ42 (Pearson’s r1 = 0.765，P1 < 0.01；Pearson’s r2 = 0.926，P2 < 0.01) and Tau protein (Pearson’s r1 = 0.648，P1 < 0.01；Pearson’s r2 = 0.691，P2 < 0.01) in blood serum of AD patients. However, there was no significant difference between both proteins expression and the history of hypertension, diabetes or stroke.Conclusion: TRF1 and TRF2 may be both specific to peripheral blood serum of AD, and may be related to the development of AD.