Glial Fibrillar Acidic Protein Research Articles

Performance of glial fibrillary acidic protein (GFAP) and ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) biomarkers in predicting CT scan results and neurological outcomes in children with traumatic brain injury (BRAINI-2 paediatric study): protocol of a European prospective multicentre study

IntroductionIn light of the burden of traumatic brain injury (TBI) in children and the excessive number of unnecessary CT scans still being performed, new strategies are needed to limit their...

Inhibition of Adult Neurogenesis in Male Mice after Repeated Exposure to Paracetamol Overdose.

Paracetamol, or acetaminophen (N-acetyl-para-aminophenol, APAP), is an analgesic and antipyretic drug that is commonly used worldwide, implicated in numerous intoxications due to overdose, and causes serious liver damage. APAP can cross the blood-brain barrier and affects brain function in numerous ways, including pain signals, temperature regulation, neuroimmune response, and emotional behavior; however, its effect on adult neurogenesis has not been thoroughly investigated. We analyze, in a mouse model of hepatotoxicity, the effect of APAP overdose (750 mg/kg/day) for 3 and 4 consecutive days and after the cessation of APAP administration for 6 and 15 days on cell proliferation and survival in two relevant neurogenic zones: the subgranular zone of the dentate gyrus and the hypothalamus. The involvement of liver damage (plasma transaminases), neuronal activity (c-Fos), and astroglia (glial fibrillar acidic protein, GFAP) were also evaluated. Our results indicated that repeated APAP overdoses are associated with the inhibition of adult neurogenesis in the context of elevated liver transaminase levels, neuronal hyperactivity, and astrogliosis. These effects were partially reversed after the cessation of APAP administration for 6 and 15 days. In conclusion, these results suggest that APAP overdose impairs adult neurogenesis in the hippocampus and hypothalamus, a fact that may contribute to the effects of APAP on brain function.

Immunohistochemical, functional, and anatomical evaluation of patients with idiopathic epiretinal membrane

PurposeThe main purpose of this study was to perform an immunohistochemical, functional, and anatomical evaluation of patients with idiopathic epiretinal membrane (ERM).MethodsTwenty-four specimens of idiopathic ERM from 24 consecutive patients who underwent 23 G pars plana vitrectomy for ERM and internal limiting membrane (ILM) peeling at the San Juan University Hospital in Alicante (Spain) in 2019 were analyzed. All patients underwent a complete ophthalmological examination including measurement of best corrected visual acuity (BCVA) and macular analysis by spectral-domain optical coherence tomography (SD-OCT) at the time of diagnosis and 3 months after surgery. Specific glial fibrillar acid protein antibodies (GFAP) and S100 calcium-binding protein β (S100β) immunostaining markers were used to identify the macroglial component of the ERM, Müller cells, and astrocytes. Ionized calcium-binding adapter molecule 1 protein (Iba1) antibodies were used as specific markers for inflammatory cells, such as microglia and macrophages.ResultsMean preoperative BCVA measured with Snellen chart was 0.3 and 0.6 preoperatively and at 3 months after surgery, respectively. SD-OCT identified 15 patients (62.5%) with a disruption of the outer retinal hyperreflective bands. The immunohistochemical study showed the presence of Müller cells in almost all cases (91.6%), as well of abundant microglia and macrophages. Microglia and macrophages were more frequently present in earlier stages of ERM. Microglia were present in ERM independently of the outer retinal hyperreflective bands integrity as measured by SD-OCT. A greater presence of macrophages was found in those ERMs with no outer retinal hyperreflective band disruption.ConclusionsMüller cells seem to be the most frequent cell group in ERMs, with also presence of microglia cells and macrophages. Astrocytes were more frequently found in early stages of ERMs. Microglia and macrophages were most frequent in ERMs with early stage (1, 2, or 3) than in advanced stages (4).

Plasma ADRD Biomarkers are Altered in COVID‐19 ICU Survivors

AbstractBackgroundLong Covid, which features cognitive symptoms in some people, affects an estimated 23.3 million Americans. Older adult survivors of COVID‐19‐associated critical illness are more likely to experience the cognitive symptoms of Long Covid, including deficits in attention, memory, and executive functioning. We sought to evaluate Alzheimer’s disease and related dementia (ADRD) plasma biomarkers in pilot study of older ICU survivors of COVID‐19‐related critical illness and non‐COVID critical illness.Method17 ICU survivors (13 COVID‐19, 4 non‐COVID) underwent clinical and cognitive testing, a blood sample, and a structural MRI approximately 2 months after ICU discharge. Plasma from the blood sample was extracted, and SIMOA assays were used to measure Aβ42, Aβ40, glial fibrillar acidic protein (GFAP), neurofilament light chain (NfL), and phosphorylated tau (pTau181). Structural MRI scans were processed using Freesurfer version 6 to measure brain atrophy (mean global cortical thickness). Plasma analyte values over three standard deviations outside the mean of the whole group were excluded (1 NfL and 1 pTau). Two‐sample t‐tests were used to compare plasma analytes between ICU groups. Pearson or Spearman correlation models were used to evaluate the relationship of target analytes with brain volumes. Covariates were tested but did not change the results.ResultSignificantly lower Aβ42/40 ratio and Aβ42 levels were observed in COVID‐19 ICU survivors relative to non‐COVID ICU survivors (Figure 1). Across all participants Aβ42/40 ratio was not associated with mean global cortical thickness, while NfL and GFAP levels were negatively associated with cortical thickness (Figure 2). However, when limited to only the COVID‐19 ICU survivors, a more ADRD‐like pattern was observed, with a trend for a positive association of Aβ42/40 ratio with cortical thickness and negative association of GFAP and NfL with cortical thickness (Figure 3).ConclusionCognitive impairment in COVID‐19 critical illness may be related to ADRD pathophysiology. Future studies in larger samples of COVID‐19 ICU survivors, as well as those with Long Covid symptoms with a history of mild to moderate COVID‐19 infection are needed to better understand these relationships.

Serum biomarker levels predict disability progression in patients with primary progressive multiple sclerosis

BackgroundWe aimed to investigate the potential of serum biomarker levels to predict disability progression in a multicentric real-world cohort of patients with primary progressive multiple sclerosis (PPMS).MethodsA total of 141...

Changes in the cerebral cortex and thyroid in the simulation of cerebral hypoperfusion and its combination with physical exercise

Cerebral hypoperfusion, as the main mechanism of age-associated diseases, is widespread, which leads to decreased work capacity in the most qualified segment of employees. The study aimed to analyze compensatory and adaptive reactions of the cerebral cortex, thyroid gland, and blood in cerebral hypoperfusion and its combination with short-term physical activity. Chronic cerebral hypoperfusion was modeled by permanent bilateral occlusion of the common carotid arteries. The study included 280 rats, of which 112 were subjected to daily short-term swimming as a model of rehabilitation measures. On days 1, 6, 8, 14, 21, 28, 35, 60, and 90 after surgery, the animals were subjected to the Morris water maze and open field tests. Histological sections of the brain and thyroid gland were examined. The concentrations of the active products of thiobarbituric acid, nitrites, and L-arginine in blood plasma were measured. The results showed that changes in the cerebral cortex and thyroid gland in the cerebral hypoperfusion model were characterized by a general stage: days 18, hypothyroid condition and death of cortical cells, cerebral hemispheres, predominantly neurons; weeks 23, stabilization, transition to the euthyroid condition, accompanied with thyrocyte desquamation, folliculogenesis, perifollicular hemocapillaries fullness, decreased functional activity of neurons, and astrocyte activation; weeks 45, incomplete adaptation, which is characterized by neurons approaching the vessels of the hemocirculatory channel and satellites sinking into the cytoplasm of neurons. Mosaicism of thyroid blood filling was also observed. After 3 months, degenerative changes in the cells of the cerebral cortex of the cerebral hemispheres appear, including a decrease in the numerical density of neurons and immunoreactive cells of glial fibrillar acid protein and a hyperthyroid state with signs of decompensation: plasmorrhagia and desquamation of the thyroid epithelium. Daily 15-min exercise with cerebral hypoperfusion demonstrated a neuroprotective effect, slowed down the progression of hypoxic and neurodegenerative changes, and reduced the concentration of nitrites and malondialdehyde in the blood and the levels of neuronal nitric oxide synthase in immunoreactive neurons.

Expression of Cytoskeletal Proteins (GFAP, Vimentin), Proapoptotic Protein (Caspase-3) and Protective Protein (S100) in the Epileptic Focus in Adults and Children with Drug-Resistant Temporal Lobe Epilepsy Associated with Focal Cortical Dysplasia.

The European Commission of the International League Against Epilepsy (ILAE) has identified glial mechanisms of seizures and epileptogenesis as top research priorities. The aim of our study was to conduct a comparative analysis of the expression levels of cytoskeletal proteins (glial fibrillar acidic protein (GFAP) and vimentin), protective protein S100, and proapoptotic caspase-3 protein in patients with drug-resistant epilepsy (DRE) associated with focal cortical dysplasia (FCD). We aimed to investigate how the expression levels of these proteins depend on age (both in children and adults), gender, and disease duration, using immunohistochemistry. Nonparametric statistical methods were employed for data analysis. In the epileptic focus area of the cortex and white matter in patients with FCD-associated temporal lobe DRE, a higher level of expression of these proteins was observed. Age and gender differences were found for vimentin and S100. In the early stages of disease development, there was a compensatory sequential increase in the expression of cytoskeletal and protective proteins. In patients with DRE, depending on the disease duration, patterns of development of neurodegeneration were noted, which is accompanied by apoptosis of gliocytes. These results provide insights into epilepsy mechanisms and may contribute to improving diagnostic and treatment approaches.

Study protocol for investigating the clinical performance of an automated blood test for glial fibrillary acidic protein and ubiquitin carboxy-terminal hydrolase L1 blood concentrations in elderly patients with mild traumatic BRAIN Injury and reference values (BRAINI-2 Elderly European study): a prospective multicentre observational study

IntroductionTwo blood brain-derived biomarkers, glial fibrillar acidic protein (GFAP) and ubiquitin carboxy-terminal hydrolase L1 (UCH-L1), can rule out intracranial lesions in patients with mild traumatic brain injury (mTBI) when assessed...

Early autoimmunity and outcome in virus encephalitis: a retrospective study based on tissue-based assay

To explore the autoimmune response and outcome in the central nervous system (CNS) at the onset of viral infection and correlation between autoantibodies and viruses.MethodsA retrospective observational study was conducted...

Evaluation of Microglia Activation Neuroinflammation and Neuronal Loss Presence in Experimentally Generated Rat Autism Model with Propionic Acid

Objective: This study was conducted to determine the behavioral disorders and neuroinflammation that occur in the rat model of autism. Materials and methods: A total of 25 rats, 20 of which were working and 5 were control group, were used in the study. The scores of the rats were recorded by performing a behavioral test before and after the application. A single dose of propionic acid (4 µl, 0.26 M solution) and (4 µl) saline were administered to the brain right ventricles of the rats in the working group and control group, respectively. Hippocampus tissue was obtained after the sacrification process on the 21st day of the rats and examined. Results: Dystrophic changes with small, pycnotic and hyperchromatic nuclei of neurons in the cerebral cortex and hippocampal region were detected in histopathological studies. It was determined that the primitive cell layer thickness of the working group decreased significantly, and their density increased due to irregular chromatolysis in neurons and abnormal Nissl granule distribution. It was determined that the number of glial fibrillar acid protein positive cells increased significantly in the cerebral cortex and hippocampal region in propionic acid applied rats. Conclusion: Propionic acid crosses the blood brain barrier. As a result, neuroinflammation, microglial activation and loss of myelin are observed in the brain.

Intraoperative transfusion is a risk factor for cerebral injury after cardiac surgery in children: a prospective observational study

INTRODUCTION: Donor blood components are able to initiate a systemic inflammatory response syndrome (SIRS) and potentiate neuroinflammation with subsequent cerebral damage. OBJECTIVE: To study the effect of transfusion on the development of cerebral damage during the surgical correction of congenital heart defects in children. MATERIALS AND METHODS: 78 patients aged from 1 to 78 months, weighing from 3.3 to 21.5 kg, were studied. All patients underwent correction of a septal defect under cardiopulmonary bypass. All patients were divided to group 1 — without the use of transfusion and group 2 — with the use of red blood cell transfusion. Cerebral damage markers (S-100-β protein, neuron-specific enolase (NSE) and glial fibrillar acidic protein (GFAP)) and SIRS (interleukins 1 (ILb-1), 6 (IL-6), 10 (IL-10) and tumor necrosis factor alpha (TNF-α) were studied. Markers ware studied at three control points: 1 — before the start of surgery, 2 — immediately after end of cardiopulmonary bypass, 3 — 16 hours after the end of the operation. RESULTS: The peak concentration of most markers in the blood in both groups of patients was noted at the 2nd control point. The concentration of all markers of cerebral damage was significantly higher in the transfusion group at the 2nd control point: S-100-β protein (ng/ml) — 509.90 [379.30–871.70] and 717.10 [517.90–1195.33] (р = 0.024); NSE (ng/ml) — 17.55 [11.19–26.41] and 34.05 [17.06–44.90] (р = 0,023); GFAP (ng/ml) — 0.1190 [0.1135–0.1245] and 0.1231 [0.1138–0.1493]. Correlations were found between markers of cerebral damage and SIRS, the strongest of which was the relationship between NSE and TNF-α at the 3rd control point — Rho = 0.43 (p = 0.0001). A correlation of S-100-β protein with transfusion volume was observed at the 2nd (Rho = 0.48, p = 0.00065) and 3rd control points (Rho = 0.36, p = 0.01330). CONCLUSIONS: The influence of the fact of transfusion and the dose of red blood cell on the development of cerebral damage during cardiac surgery in children has been proven.

Clinical characteristics and short-term outcomes of autoimmune encephalitis in adults

To characterize clinical, paraclinical features and short-term outcomes in different types of autoimmune encephalitis (AE) in a one-center cohort of Russian patients, as well as to evaluate the frequency and significance of the joint expression of antineuronal and anti-glial antibodies (Abs) in AE. Forty-one patients were diagnosed with AE at the Research Center of Neurology from November 2020 to December 2022. Demographic, clinical characteristics, results of laboratory tests, MRI of brain, treatment and outcomes of disease were analyzed. The analysis of Abs to glial antigens (myelin-oligodendrocyte glycoprotein - MOG, glial fibrillar acidic protein - GFAP, aquaporin 4 - AQP-4) was performed by indirect immunofluorescence assay (Euroimmun, Germany). In 24 (58.5%) patients was established definite AE, confirmed by specific Abs detection; in 2 (4.9%) - definite limbic encephalitis, in 15 (36.6%) - seronegative probable AE (including 3 cases of Hashimoto's encephalitis). GFAP-Abs in cerebrospinal fluid (CSF) were detected only in two patients - with clinical and MRI-picture of autoimmune GFAP-astrocytopathy (A-GFAP-A). GFAP- and MOG-Abs in the blood were detected in 25.7% and 6%, respectively, AQP-4-Abs were not detected. There were no correlations between co-expression with glial Abs and clinical characteristics. Systemic and antithyroid Abs were present in 15% and 31%, respectively. Paraneoplastic AE accounted for 22%. For the first time in the Russian population, 2 cases of A-GFAP-A, 6 cases of AE associated with COVID-19 were described. The most common first syndrome were epileptic seizure (34%), psychiatric (29%) and cognitive (14%) disorders. Relapses of AE was observed in 22%. Inflammatory changes in CSF were detected in 41%, focal changes on MRI in 68%. First-line immune therapy was performed in all patients, 85% of cases received pulse therapy with methylprednisolone. Second-line immune therapy (rituximab or cyclophosphamide intravenously) was performed in 19.5%, 78% of patients achieved significant improvement during treatment (scores ≤2 on the modified Rankin scale). The results allow us to consider COVID-19 as a trigger of AE. The absence of detection of GFAP-Abs in CSF in patients with other types of AE contributes to the confirmation of the specificity of GFAP-seropositivity of CSF for the diagnosis of A-GFAP-A. The expression of GFAP- and MOG-Abs in AE can serve as confirmation of the immuno-mediated etiology of the disease, which is especially important for the AE diagnosis in the absence of antineuronal Abs.

ЛАБОРАТОРНЫЕ БИОМАРКЁРЫ ПОВРЕЖДЕНИЯ ГОЛОВНОГО МОЗГА ПРИ САХАРНОМ ДИАБЕТЕ

Objective: This review outlines the literature data on the main laboratory biomarkers of brain damage in diabetes mellitus (DM) type I and II. Neurospecific proteins: S-100 protein, neurospecific enolase, glial fibrillar acidic protein, myelin basic protein, and brain-derived neurotrophic factor (BDNF) are considered specific markers of cerebral dysfunction in DM. Emphasis is placed on pro-inflammatory cytokines (IL-1, IL-6, tumor necrosis factor-α, C-reactive protein), as blood biomarkers, the increase of which indicates brain damage in DM type I and II. High concentrations of adipokines, inflammatory mediators of adipose tissue, are a reliable laboratory sign of brain damage in this endocrinopathy. Advanced glycation end products (AGEs), as pathogenic metabolites of oxidative stress (OS), detected in blood in high concentration, can act as indicators of cognitive deficit in DM. Increased concentration of autoantibodies to some neuroreceptors (dopamine, glutamate) may serve as specific laboratory biomarkers of brain damage in DM type I. Further searches of new laboratory biomarkers of brain dysfunction are needed in order to improve the diagnosis of cerebral insufficiency in DM Keywords: Diabetes mellitus, biomarkers, brain damage, neurospecific proteins, adipokines.

Chapter 14 - Motor symptoms in nonparaneoplastic CNS disorders associated with neural antibodies

Motor symptoms are common, and sometimes predominant, in almost all nonparaneoplastic CNS disorders associated with neural antibodies. These CNS disorders can be classified into five groups: (1) Autoimmune encephalitis with antibodies against synaptic receptors, (2) cerebellar ataxias associated with neuronal antibodies that mostly target intracellular antigens. (3) Stiff-person syndrome and progressive encephalomyelitis with rigidity and myoclonus which have antibodies against glutamic acid decarboxylase and glycine receptor, respectively. Both diseases have in common the presence of predominant muscle stiffness and rigidity. (4) Three diseases associated with glial antibodies. Two present motor symptoms mainly due to the involvement of the spinal cord: neuromyelitis optica spectrum disorders with aquaporin-4 antibodies and myelin oligodendrocyte glycoprotein antibody-associated disease. The third disorder is the meningoencephalitis associated with glial fibrillar acidic protein antibodies which frequently also presents a myelopathy. (5) Two antibody-related diseases which are characterized by prominent sleep dysfunction: anti-IgLON5 disease, a disorder that frequently presents a variety of movement disorders, and Morvan syndrome associated with contactin-associated protein-like 2 antibodies and clinical manifestations of peripheral nerve hyperexcitability. In this chapter, we describe the main clinical features of these five groups with particular emphasis on the presence, frequency, and types of motor symptoms.

Coherence of the electroencephalogram and peripheral markers of nerve tissue damage in depressive disorders

To evaluate the coherence parameters of the electroencephalogram and the level of peripheral markers of nerve tissue damage in patients with depressive disorders. Thirty patients with a diagnosis from a cluster of mood disorders: affective disorder within a single depressive episode and recurrent depressive disorder were examined. A control group consisted of 30 healthy individuals, comparable in sex and age to the main group. The bioelectric activity of the brain was recorded and analyzed with the calculation of the averaged coefficients of intra- and interhemispheric coherence. The concentration of calcium-binding protein S100b, the main protein of myelin MBP and glial fibrillar acid protein GFAP was determined in blood sera by solid-phase enzyme immunoassay. Patients with depressive disorders showed signi cantly lower coefficients of interhemispheric coherence of alpha (p=0.003), beta (p=0.042) and theta rhythms (p=0.041), as well as intrahemispheric coherence of alpha rhythm in the left (p=0.016) and right hemispheres (p=0.026), beta rhythm in the right hemisphere (p=0.034) compared to the control group. Patients with depressive disorders showed a higher concentration of MBP compared to the control group (p=0.008). Additionally, we identified statistically significant correlations between EEG coherence coefficients and serum markers in patients with depressive disorders. The results clearly confirm the presence of inflammatory changes in the brain in patients with depression, which is reflected in structural and functional changes.

Administration of dutasteride in animal models of retinitis pigmentosa

AbstractPurpose: Retinitis pigmentosa (RP) describes a large group of hereditary retinopathies. It mainly affects the rods. However, once the rods have degenerated, the cones, also die, leading to complete blindness. Although, the mutations that cause RP have been identified in different genes, the mechanisms that cause the death of photoreceptor cells are still unknown. Gonadal hormones may play a protective role in RP. Our research group has shown that oral administration of progesterone to RP mice significantly conserves the number of photoreceptors. 5α‐reductase inhibitors (such as dutasteride (DUT)) are approved treatments for androgenic alopecia. Modulation or inhibition of 5α‐reductase activity increases the levels of the neuroprotective steroid progesterone and 17β‐estradiol. The purpose of this study was to administer DUT to RP mice. This may be another form of increasing progesterone levels in the retina and therefore, may be neuroprotective.Methods: Animals were treated in accordance with the ARVO statement for the use of animals. rds mice were treated intraperitoneally with DUT and euthanized on day 21. Haematoxylin–eosin, cell death, and rod and cone immunohistochemistry were performed to determine if DUT was able to delay photoreceptor death. Immunohistochemical techniques were used to study changes in retinal microglia (Iba‐1) and macroglial cells. Neuronal nitric oxide synthase (nNOS) was also quantified.Results: DUT increased photoreceptor survival in rds mice. An increase in iba‐1 positive cells was found in rds retinas and DUT normalized the number, migration and the length and number of branches in these cells. DUT decreased GFAP (glial fibrillar acid protein) expression. We have also observed a slightly increase in nNOS expression in rds mice. DUT administration was also able to decrease nNOS expression.Conclusions: DUT may be used to improve cell survival, to ameliorate retinal micro and macroglial activation as well as alterations in nNOS in RP.

Perioperative Changes in Serum Concentration of Glial Fibrillar Acid Protein and Delayed Cognitive Recovery: an Experimental Observational Study

A number of studies have found an association between the increased concentration of glial fibrillar acid protein (GFAP) in blood serum in patients with various types of brain damage (ischemic stroke, traumatic brain injury, neurodegenerative and neuro-oncological diseases), as well as with a rapid decline in cognitive functions in elderly people with initially normal cognitive abilities.The objective: to identify the relationship between delayed cognitive recovery and changes in serum GFAP concentration in the perioperative period in patients operated for various oncological diseases.Subjects and Methods. The study included 30 patients who underwent surgical treatment for prostate cancer, colorectal cancer and pancreatic cancer under combined general anesthesia.The inclusion criteria were the expected duration of the operation over 300 minutes and the age over 60 years. GFAP was determined in plasma by enzyme immunoassay before anesthesia, the next day after surgery and on the 4th–5th day. Neuropsychological testing was performed before surgery and on the 4th–5th postoperative day. Delayed cognitive recovery was defined as a decrease in the composite z-score of more than one standard deviation (SD) compared to the preoperative assessment.Correlation analysis was performed between changes in the composite z-score (in absolute values) and the difference in GFAP concentration between the outcome and the first postoperative day, the outcome and the 4th–5th postoperative day and the first and 4th–5th postoperative days.Results. In five cases (16.6%), a decrease in the composite z-score > 1 SD was revealed indicating a delayed cognitive recovery. In the remaining 25 (83.4%) patients, changes in the composite z-score were less than one standard deviation. The median concentration of GFAP in patients with delayed cognitive recovery was 0.13 [0.1; 0.14] before surgery, 0.12 [0.09; 0.14] the day after surgery and 0.16 [0.05; 0.19] on the 4th–5th day after surgery. In patients without cognitive impairment, the concentration of GFAP was 0.15 [0.125; 0.184] before surgery, 0.15 [0.121; 0.163] 24 hours after surgery and 0.13 [0.079; 0.151] on the 4th–5th day after surgery. The correlation values between changes in the composite z-score and the difference in GFAP concentrations were: between the outcome and the first postoperative day – rs = 0.107, p = 0.37, outcome and the 4th–5th postoperative day – rs = 0.134, p = 0.37, the first and 4th‒5th postoperative days – rs = 0.21, p = 0.37.Discussion. There was no statistically significant difference in GFAP levels between patients with delayed cognitive recovery and patients without cognitive impairment. There was also no correlation between the difference in GFAP concentrations in plasma before surgery and 24 hours after, before surgery and on the 4th–5th day of the postoperative period and the composite z-score.Conclusions. The use of GFAP to predict cognitive decline associated with surgical treatment of colorectal cancer, prostate cancer and pancreatic cancer under general anesthesia is not yet possible.

A novel cell-free intrathecal approach with PRP for the treatment of spinal cord multiple sclerosis in cats

BackgroundMultiple sclerosis (MS) is a progressive autoimmune demyelinating disease of the central nervous system. To date, there is no effective therapy for it. Our study aimed to determine the potential role of platelet-rich plasma (PRP) in the treatment of MS in cats.MethodsThe current study was conducted on 15 adult Persian cats that were divided into three groups: control negative, control positive (ethidium bromide (EB)-treated group), and PRP co-treated group (EB-treated group intrathecally injected with PRP on day 14 post-spinal cord injury). PRP was obtained by centrifuging blood on anticoagulant citrate dextrose and activating it with red and green laser diodes. The Basso–Beattie–Bresnahan (BBB) scores were used to assess the motor function recovery on days 1, 3, 7, 14, 20, and 28 following 14 days from EB injection. Moreover, magnetic resonance imaging (MRI) analysis, histopathological investigations, transmission electron microscopy (TEM) studies, and immunohistochemical analysis were conducted, and the gene expressions of nerve growth factors (NGFs), brain-derived neurotrophic factors (BDNF), and stromal cell-derived factors (SDF) were evaluated.ResultsOur results indicated that PRP had a significant ameliorative effect on the motor function of the hindlimbs as early as day 20 and so on. MRI revealed that the size and intensity of the lesion were significantly reduced in the PRP co-treated group. The histopathological and TEM investigations demonstrated that the PRP co-treated group had a significant improvement in the structure and organization of the white matter, as well as a high remyelination capacity. Furthermore, a significant increase in myelin basic protein and Olig2 immunoreactivity as well as a reduction in Bax and glial fibrillar acidic protein immune markers was observed. NGFs were found to be upregulated by gene expression.ConclusionAs a result, we concluded that the intrathecal injection of PRP was an effective, safe, and promising method for the treatment of MS.

Role of soluble fractalkine, GFAP and CD163 in cognitive functions after open heart surgery in diabetic and non-diabetic patients

Purpose: In this study, the relationship between postoperative cognitive functions and serum fractalkine, Glial Fibrillar Acidic Protein (GFAP) and Cluster of differentiation 163 (CD163) levels in diabetic and non-diabetic patients after open heart surgery was evaluated. Methods and Materials: This research was planned prospectively as observational clinical study. Cognitive functions, fractalkine, GFAP and CD163 levels were evaluated with preoperative day 1 and postoperative day 7 in 44 patients. Minimental test (MM) was used to evaluate cognitive functions. Results: A positive correlation was found between preoperative CD163 concentrations and postoperative MM test scores in non-diabetic patients (r=0.536, p=0.010). There was also a positive correlation between postoperative CD163 concentrations and postoperative MM Test scores in non-diabetics (r=0.461, p=0.031). In diabetic patients, a positive correlation was found between preoperative and postoperative GFAP concentrations (r=0.792, p

Time-Course Changes in Oxidative Stress and Inflammation in the Retinas of rds Mice: A Retinitis Pigmentosa Model

(1) Background: Retinitis pigmentosa (RP) is characterized by progressive photoreceptor death. A Prph2Rd2 or an rds mouse is an RP model that closely reflects human RP. The objective of this study was to investigate the relationship of rod and cone death with oxidative stress and inflammation in rds mice. (2) Methods: The retinas of control and rds mice on postnatal days (PN) 11, 17, 21, 28, 35, and 42 were used. Oxidative damage to macromolecules, glutathione (GSH and GSSG), GSH synthesis enzymes, glial fibrillar acidic protein (GFAP), ionized calcium-binding adapter molecule 1 (Iba1), and cluster of differentiation 68 (CD68) was studied. (3) Results: The time sequence of oxidative stress and inflammation changes in rds mice occurs as follows: (i) At PN11, there is a small increase in photoreceptor death and in the microglial cells; (ii) at PN17, damage to the macromolecules is observed; (iii) at PN21, the maximum photoreceptor death rate is detected and there is an increase in GSH-GSSG and GFAP; (iv) at PN21, the microglial cells are activated; and(v) at PN28, there is a decrease in GSH synthesis enzymes. (4) Conclusions: These findings contribute to the understanding of RP physiopathology and help us to understand whether oxidative stress and inflammation are therapeutic targets. These findings contribute to our understanding that, in RP, oxidative stress and inflammation evolution and their relationship are time-dependent. In this sense, it is important to highlight that both processes are potential therapeutic targets in this disease.