Wyniki wyszukiwania

1

Biologia molekularna chorob poliglutaminowych

100%

Owecki M., Kozubski W.

Postępy Higieny i Medycyny Doświadczalnej

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2002

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tom 56

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nr 6

779-788

2

Serum VEGF levels in migraine patients

81%

Michalak S., Wegrzyn D., Losy J., Kozubski W.

Acta Neurobiologiae Experimentalis

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2009

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tom 69

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nr 1

Introduction: Migraine is a known risk factor for ischemic stroke. Recent studies have shown endothelial dysfunction in migraine patients. The aim of this study was to examine the levels of circulating Vascular Endothelial Growth Factor (VEGF) during interictal period. Material and methods: We included in the study 52 migraineurs (aged 37.9 ± 9.6 years). All patients satisfi ed criteria of IHS for the diagnosis of migraine. The control group was represented by 34 healthy subjects (aged 28.9 ±7.0 years). Serum VEGF, Macrophage Infl ammatory Protein-1 (MIP-1) and tumor necrosis factor (TNF) were analyze by means of ELISA. Results: The level of circulating VEGF was decreased (<0.05) during interictal period of migraine patients (281.53 ± 180.37 pg/ml) comparing to controls (441.80 ± 295.93 pg/ml). There were no differences (P>0.05) between TNF concentration in migraineurs and controls (median, min.ñmax.: 2.04; 0.49ñ18.6 and 2.14; 0.49ñ8.97, respectively). Similarly, serum MIP-1 did not showed differences (P>0.05) between both groups (migraineurs: 0.0; 0.0ñ285.25 and controls: 0.0; 0.0ñ333.54 pg/ml). Serum VEGF correlated with MIP-1 (rS=0.7684, P<0.05) and TNF level (rS=0.4791, P<0.05). Conclusion: Migraineurs have decreased serum VEGF concentration, which may be related endothelial dysfunction and responsible for increased risk of stroke. Both TNF and MIP may be involved in regulatory processes of VEGF production.

3

The expression of Tumor Necrosis Factor-aipha in migraineurs macrophages

81%

Michalak S., Wegrzyn D., Kozubski W.

Acta Neurobiologiae Experimentalis

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2006

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tom 66

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nr 4

4

Serum S-100 protein and Neuron Specific Enolase in patients with onconeuronal antibodies

81%

Michalak S., Osztynowicz K., Kozubski W.

Acta Neurobiologiae Experimentalis

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2006

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tom 66

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nr 4

5

Profil przeciwciał onkoneuronalnych u chorych z neurologicznymi zespołami paranowotworowymi

81%

Michalak S. R., Osztynowicz K., Kozubski W.

Diagnostyka Laboratoryjna

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2007

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tom 43

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nr 3

6

Analysis of mutation in SPR and HTRA2 genes in patients with Parkinson’s disease

71%

Polrolniczak A., Dorszewska J., Florczak-Wyspianska J., Owecki M., Kozubski W.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr 1

Diagnosis of Parkinson’s disease (PD) is often problematic because clinically it can be difficult to distinguish idiopathic PD from the other extrapyramidal disorders. It is known, that PD is caused either by environmental and genetic factors . Genetic mutations are the cause of familial form of PD and include genes PARK1-PARK18. The etiology of sporadic PD (SPD) is still not clear, but it is currently assumed that genetic susceptibilities, may be involved. It is suggested, that in pathogenesis of the SPD beside SNCA and PARK2 genes, may be involved also SPR (sepiapterin reductase gene) [PARK3] and HTRA2 (HTRA serine peptidase 2 gene)[PARK13] genes. The HTRA2 gene, also known as Omi, was found to be associated with PD in German population. However, some studies have indicated that some variants of HTRA2 may not be related to PD. SPR gene, which is located in the PARK3 linkage region is inconsistently associated with a risk of PD but significance of mutations in this gene as well as HTRA2 in PD is still not clear. The aim of the study was the analysis of the frequency of T637A/G SPR as well G421T, G1195A and C1210T mutations in HTRA2 gene in Polish patients with PD and in control group. Peripheral blood was collected from 89 patients with PD clinical diagnosis (42F and 47M, the avr. age 62 ± 10.15 years), and from 113 healthy donors (79F and 7M, the avr. age 55.5 ± 9.54 years). Genomic DNA was isolated using standard protocols. Genotyping was performed by PCR/RFLP using specific primers and restriction enzymes (SsiI, MboII, MvaI, MspI) and sequencing. The SPR gene analysis detected T637A mutation in 3 (3%) PD patients compared to 2 (2%) persons in the control group. Moreover, mutations G421T and G1195A of HTRA2 gene have been identified in 3 (3%) [G421T – 1%, G1195A – 2%] patients with PD and none of controls. Analysis of C1210T HTRA2 mutation detected no mutated variant both in PD patients group and in control group. It was also observed that the stage of the disease was 1–2 in Hoehn and Yahr scale and response to L-dopa was good in patients with T637A SPR and G421T, G1195A HTRA2 mutations. It was also observed some tendency for depression manifestation in PD patients with T637A SPR mutation. It can be concluded, that mutations of SPR and HTRA2 genes probably may be one of the risk factor for manifestation of PD. Thus, the results of this study suggest that analysis of T637A SPR and G421T, G1195A HTRA2 genes mutations may be an additional diagnostic and prognostic factor in PD patients in the future.

7

The activity of serum paraoxonase and level of conjugated dienes in stroke patients

61%

Michalak S., Kazimierski R., Hellmann A., Wencel-Warot A., Kocialkowska D., Kozubski W.

Acta Neurobiologiae Experimentalis

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2009

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tom 69

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nr 1

Paraoxonase (PON) protects low-density lipoproteins from oxidation. Gln192Arg genotype of PON was identifi ed as a risk factor for stroke. The aim of our study was to evaluate the activity of the esterase and concentration of conjugated dienes (CD) in the early phase of stroke and its clinical signifi cance. Material and methods: The PON activity and conjugated dienes (CD) concentrations were analyzed within fi rst 24 hours after stroke onset by means of spectrophotometric methods. Results: We included into the study 424 persons [403 ischemic stroke (IS) patients, aged 67 ± 12 and 21 patients with IS secondary hemorrhagic transformation (SHT), aged 69 ± 11 and 12 age-matched healthy controls]. The PON activity was lower in SHT patients (13.2; interquartile range 2.3ñ67.1 U/L) comparing to IS patients (63.7; 40.2ñ145.9 U/L) and controls (42.34; 38.98ñ57.44 U/L) (P<0.05). There was no signifi cant difference in CD concentration between IS and SHT patients (P>0.05). Multiple regression analysis revealed correlations between CD concentration and Barthel index in IS and SHT, and between PON activity and Barthel index in HT patients. Conclusion The serum PON activity in early phase of stroke was signifi cantly lower in SHT than in IS patients. PON activity showed correlation with clinical outcome in SHT patients whereas CD concentrations correlated with the outcome in both IS and SHT groups.

8

Znaczenie biomarkerów aktywności choroby w długofalowej ocenie chorych na stwardnienie rozsiane leczonych interferonem beta

61%

Michalak S., Pietrzak A., Osztynowicz K., Tokarz-Kupczyk E., Wygladalska-Jernas H., Kozubski W.

Diagnostyka Laboratoryjna

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2017

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tom 53

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nr 1A

9

Beta-cells specific antibodies in neurological autoimmune disorders

61%

Michalak S., Jernas L., Tokarz-Kupczyk E., Wygladalska H., Osztynowicz K., Kozubski W.

Acta Neurobiologiae Experimentalis

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2006

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tom 66

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nr 4

10

The APOE genotype and the plasma expression of microRNA-107, -132 and -138 in patients with Alzheimer's disease-preliminary study

61%

Prendecki M., Florczak-Wyspianska J., Lagan-Jedrzejczyk U., Plociennik A., Kozubski W., Dorszewska J.

Acta Neurobiologiae Experimentalis

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2015

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tom 75

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nr Supl.

BACKGROUND AND AIMS: Alzheimer’s disease (AD) is a multifactorial disease conditioned by genes (70%) and environment (30%), characterized by brain deposition of amyloid-β and neurofibrillary tangles. An involvement of over 20 genes (including APOE) and dozens of microRNAs (e.g. miR-107) has been previously described in the pathogenesis of AD. APOE has 3 common variants: protective – ε2, neutral – ε3 and pathogenic – ε4. The miR-107, associated with amyloid cascade, seems to be a promising AD plasma biomarker, whose downregulation has been demonstrated in the early stage of the disease. Though miR-132 has been linked with apoptosis of neurons and miR-138 with tau hyperphosphorylation, their role in AD remain unclear, and neither of these miRNA has been previously associated with APOE. The aim of the study was the analysis of APOE genotypes and the expression of three miRNAs: miR-107, -132, -138 in patients with AD and in control subjects, both related and unrelated to AD cases. METHODS: The DNA from 100 subjects (aged 47–83), including 42 patients with AD and 15 related and 43 unrelated controls of the same age was genotyped by “mismatch primer” qPCR. The subsequent expression analysis of miR-107, -132 and -138 in the plasma of ten subjects was performed by qPCR. RESULTS: Our study have shown that the miR-107 was significantly downregulated in AD patients (P<0.05) comparing to related controls, but did not reach significance as compared to unrelated controls. The downregulation of miR-132 was not statistically significant as compared to related and unrelated subjects. Expression of miR-138 in AD was decreased only as compared to relatives. Subsequently, the presence of two APOE ε4 alleles in AD patient and at least one ε4 copy in the controls was associated with altered expression of the analyzed miRNAs. CONCLUSIONS: It appears that in the course of AD the expression of miR-107, -132 and -138 depends on the APOE genotype.

11

The interpretation of oligoclonal bands based on artiÞ cial neuronal networks

61%

Szulc M., Dybizbanski T., Jurkowlaniec A., Losy J., Michalak S., Rybarczyk A., Kozubski W.

Acta Neurobiologiae Experimentalis

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2009

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tom 69

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nr 1

The examination of oligoclonal bands (OCB) in cerebrospinal fl uid (CSF) is important for the diagnosis of multiple sclerosis, however the correlation between quality, number and disease progression is uncertain. The aim of this study was to test the automatic system, for detection and identifi cation of OCB. The patterns of OCB, obtained from isoelectrofocusing of CSF proteins, were scanned with the use of fl atbed scanner. Next, for each of the scanned images, the selected features of the pattern were extracted by the means of the image processing algorithms, and arranged into the feature vector. That created the ìsignatureî of the image that was subsequently analyzed by classifi er based on the Artifi cial Neural Networksí. The result was the positive (P), negative (N) or ìuncertainî (U) classifi cation of the bandsí pattern. We have used database of the 225 samples, manually classifi ed by the expert, that formed the training set for the classifi er with the equal number of positive and negative results. Among 20 samples (10P/10N) used in the testing phase of the system 17 were classifi ed correctly, 3 were ìuncertainî, no false results was obtained. The system is implemented in the MATLAB environment. The future work focus on designing the system that would be able not only to classify the OCB patterns, but also to possibly cluster the images into the groups with common parameters.

12

Substantia nigra hyperechogenicity in Polish patients with Parkinson’s disease

61%

Ambrosius W., Michalak S., Owecki M., Lukasik M., Florczak-Wyspianska J., Kozubski W.

Folia Morphologica

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2014

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tom 73

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nr 3

Background: Hyperechogenicity of the substantia nigra (SN) measured by transcranial sonography (TCS) is a characteristic feature observed in patients with Parkinson’s disease (PD). To our knowledge, no SN hyperechogenicity data are available for Polish population. Moreover most of studies come from few centres, which used the one type of ultrasound device. The main aim of the study was to investigate the association between PD and SN hyperechogenicity measured by sonographic machine, not assessed so far. Materials and methods: In this study cross-sectional study SN hyperechogenicity was evaluated in 102 PD patients and 95 control subjects. Midbrain was visualised by Aloka Prosound 7 ultrasound device. SN area measurement, the relation to the clinical features of PD, inter- and intra-observer reliability were evaluated. Results: We confirmed that SN echogenicity is significantly increased in PD patients compared to control subjects (p < 0.001). The area under curve for PD patients vs. controls was 0.93. Receiver operating characteristic analysis indicated a cut-offs for SN echogenicity at 0.19 cm² with accuracy equal to 90%, specificity — 86% and sensitivity — 93.7%. The SN hyperechogenicity was not related to PD clinical findings. Reliability was good if an experienced sonographer performed the SN measurements. Conclusions: This study shows that the SN abnormality observed by TCS is a specific feature, which can be helpful in the process of PD diagnosing. (Folia Morphol 2014; 73, 3: 267–271)

13

Homocysteine, cysteine and gluthatione in epileptic patients treated with antiepileptic drugs

61%

Bugaj R., Urbanska N., Dorszewska J., Sniezawska A., Przedpelska-Ober E., Kozubski W.

Acta Neurobiologiae Experimentalis

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2011

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tom 71

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nr 1

Today, epilepsy is regarded as the most common neurological disease. AEDs pharmacotherapy, used to treat patients with epilepsy affect plasma concentrations of sulfur amino acids: Hcy, Cys and GSH. These are the main intracellular thiols, whose anabolic and catabolic pathways are closely linked. Through transsulfuration of Hcy arises Cys, who further participates in the synthesis of GSH. It has been shown that the increase of plasmatic Hcy in patients with epilepsy taking AEDs can be affected by a number of factors including diet, type of pharmaceutical preparations taken, the duration of treatment, and genetic factors. The study group consisted of 63 patients with idiopathic epilepsy, 28 women and 35 men, aged from 18 to 65. Among patients with epilepsy 55 people, 24 women and 31 men, aged from 18 to 65 were treated with various AEDs, and 8 patients, 4 women and 4 men, aged between 18 and 65 were before the inclusion the anticonvulsant therapy. A preliminary analysis in our studies was conducted on 38 people from the control group, 28 women and 10 men, aged from 22 to 67, without symptoms of dementia or any other neurological disorders. The concentration to sulfur amino acids (Hcy, Cys, GSH) in plasma has been identified by HPLC (high performance liquid chromatography) with electrochemical detection. The analysis was performed in Thermo Hypersil BDS C18 column (250x4, 6x5 µm) using phosphate buffer with 12.7% acetonitrile as mobile phase for the determination of Hcy and GSH, and phosphate buffer with 10% acetonitrile as buffer mobile phase for the determination of Cys. Studies show that AEDs pharmacotherapy in patients with epilepsy leads to a significant increase in Hcy- treated in polytherapy, especially in the application of VPA and the long-term treatment. In addition, in patients with epilepsy treated with VPA in monotherapy, plasma Cys concentration is significantly reduced. Moreover, it was observed that long-term AEDs treatment and mild HHcy (Hcy>16 µmol/l) in patients with epilepsy leads to a significant increase in GSH concentration. It can be assumed that patients with epilepsy using AEDs are exposed to high oxidative stress, which is an index for the observed higher concentrations of GSH, the main intracellular antioxidant. It also seems that only the combined supplementation of vitamins B and FA in patients with epilepsy treated with AEDs may contribute to the effective regulation of Hcy- the risk factor for vascular diseases.

14

Polymorphisms of the PARK2 gene and Parkin protein levels in patients with Parkinson’s disease

61%

Dorszewska J., Debek A., Oczkowska A., Florczak-Wyspianska J., Owecki M., Kozubski W.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr 1

Parkinson’s disease (PD) is one of the most common degenerative diseases of the extrapyramidal system, the frequency of which increases with age. It is now believed that the causes of PD are environmental and genetic factors. Important genetic factors resulting in PD are mutations in the PARK2 gene, which may affect the level of Parkin. The aim of the study was conducted on 234 individuals of the Polish population: 89 patients diagnosed with PD, 32 patients diagnosed with Parkinson’s syndrome and 113 individuals from the control group without neurological symptoms and characteristics of dementia. As a result of the methods of analysis demonstrated the following: G930C mutation of exon 8 in the PARK2 gene, which was analysed by performing PCR-RFLP. Detection of deletion of exon 2 using PCR. Whereas the evaluation of mutations within exon 11 in PARK2 gene was performed using HRM method and sequencing. Also performed to measure the concentration of Parkin’s plasma in blood using ELISA method. The study results no presence of the deletion of exon 2 in the PARK2 gene in any individual study. At the same time, it was almost 3-times higher frequency of G930C mutation in exon 8 PARK2 in patients with PD and almost 6-times higher incidence of mutation G1281 A in exon 11 of PARK2 in PD patients compared with controls. At the same time, in the present study demonstrated that the presence of mutations in 8 and 11 exon of PARK2 gene does not appear to be associated with the generate of Parkin’s plasma concentration. Genotype-fenotype study in the PARK2 gene can constitute intravital diagnostic tests in patients with PD, as well as in patients diagnosed with Parkinson’s syndrome in the course of a degenerative disease.

15

An evaluation of the reproducibility of the measurement of the intima-media thickness of carotid arteries

61%

Kazmierski R., Niezgoda A., Guzik P., Lukasik M., Ambrosius W., Kozubski W.

Folia Morphologica

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2003

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tom 62

|

nr 1

The intima-media thickness (IMT) of carotid arteries was demonstrated to be a reliable measure for early stages of atherosclerosis. B-mode ultrasound may be used to measure carotid IMT. The measurements of the IMT of the carotid artery (CA) conducted by different investigators can be comparable and enable the implementation of clinical trial successfully while maintaining a high reproducibility value. The objective of the study was to evaluate the reproducibility of the measurements made by the same investigator on two separate occasions (intraobserver variability) and the reproducibility of the off-line measurements between four sonographers in our laboratory (interobserver variability). The IMT of CA in 25 subjects (15 post stroke and 10 healthy persons) was investigated with the use of high-resolution ultrasonography. The CA subdivided into the common, bulbs and internal segments were scanned twice with a 3-week interval. Additionally three other readers with different levels of experience and skills in ultrasonography were asked to perform the same measurements in duplicate with at least a 3-week interval between. A high concurrence for intraobserver variability was detected with a correlation coefficient ranging from 0.92 to 0.95; p < 0.0001, and maximal bias 0.019 mm. Interobserver variability for all four readers also demonstrated a high correlation coefficient ranging from 0.72 to 0.83; p < 0.0001, and the maximal bias of measurements did not exceed 0.08 mm. The analogue measurements performed by the team demonstrate a reliable reproducibility in terms of the results of morphologic measurements. The differences obtained in the study were less than the error of the method (i.e. 0.1 mm) and should not influence clinical decision-making. Additionally, this study demonstrated that interobserver concurrence increases with the increasing experience of the investigators.

16

Carotid intima-media thickness better differentiates between groups of stroke patients and persons without cerebrovascular disease than other conventional and novel risk factors

61%

Kazmierski R., Watala C., Podsiadly E., Dorszewska J., Adamczewska-Goncerzewicz Z., Tylewska-Wierzbanowska S., Kozubski W.

Folia Morphologica

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2004

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tom 63

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nr 3

When measured by ultrasound, the morphological markers of carotid atherosclerosis such as intima-media thickness (IMT) and cross-sectional plaque area have been associated with the risk of ischaemic stroke. We set out to determine whether the morphological parameters of the carotid arteries made it possible to better differentiate between groups of older atherothrombotic stroke patients and persons without cerebrovascular disease than conventional and novel risk factors of stroke. Of the total number of 623 persons examined, 54 stroke patients (mean age 63.3 years) and 74 controls without cerebrovascular disease (mean age 66.3 years) fulfilled the inclusion criteria for this investigation and were enrolled in the case-control study. After adjustment for age, gender and education level, the strongest associations were found between stroke and carotid IMT [odds ratio (OR) = 10.6; 95% confidence interval (CI): 4.3–26.9] and plaque area (OR = 5.4; 95%CI: 2.3–13.1). Other risk factors showed weaker associations with stroke occurrence. Of the clinical risk factors, a significant association was found between stroke and coronary heart disease (OR = 3.5; 95%CI: 1.2–10.2), hypertension (OR = 3.2; 95%CI: 1.5–7.2) and smoking (OR = 2.7; 95%CI: 1.1– –6.4). From the laboratory-derived risk factors a significant association was found between stroke and triglyceride levels (OR = 4.4; 95%CI: 1.9–10.0), and an inverse correlation was observed between stroke occurrence and HDL-cholesterol level (OR = 0.4; 95%CI: 0.2–0.8). The carotid IMT and plaque area, measured with the use of ultrasonography, showed a better correlation with stroke occurrence than currently recognised clinical and biochemical risk factors. The intima-media thickness and plaque area of the carotid arteries could be useful parameters in the development of strategies to identify patients at high risk of atherothrombotic ischaemic stroke.

17

The activities of AChE and BChE in rat brain are related to behaviour disturbances in the course of experimental breast cancer

51%

Michalak S., Szulc M., Wieczorek M., Medon M., Luczak L., Rybarczyk A., Gorka M., Ambrosius W., Osztynowicz K., Kozubski W.

Acta Neurobiologiae Experimentalis

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2006

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tom 66

|

nr 4

18

Polymorphism of MTHFR, MTR and MTHFD1 as related to the oxidative DNA damage, and the level of thiols in Alzheimer's and Parkinson’s diseases

51%

Florczak J., Dorszewska J., Rozycka A., Kempisty B., Chojnacka K., Jaroszewska-Kolecka J., Trzeciak W. H., Kozubski W.

Acta Neurobiologiae Experimentalis

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2006

|

tom 66

|

nr 4

19

SNCA, PARK2 and LRRK-2 mutations in Polish patients with sporadic Parkinson’s disease

51%

Polrolniczak A., Dorszewska J., Florczak J., Owecki M., Rozycka A., Rubis B., Jagodzinski P. P., Kozubski W.

Acta Neurobiologiae Experimentalis

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2011

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tom 71

|

nr 1

Parkinson’s disease (PD) is one of the most common neurodegenerative disorders in Poland. Although the genetic basis of familial PD is now well established, the majority of PD is sporadic and occurs without a clear mode of inheritance. The etiology of sporadic PD remains unknown, but it is currently assumed that genetic susceptibilities may be involved. The observation that mutations in α-synuclein (SNCA), parkin (PARK2)and leucine-rich repeat kinase 2 (LRRK2) genes are common in familial PD and increasing evidence supporting a direct role for PARK2 and LRRK-2 in sporadic both early- and late-onset disease make those genes a particularly compelling candidate for intensified investigation. The aim of the study was analysis and identification of SNCA, PARK2 and LRRK-2 mutation in Polish patients with sporadic PD. Peripheral blood was collected from 34 patients with sporadic PD clinical diagnosis (the average age 58 years), and 22 patients with the other neurological diseases (the average age 55 years) as well as from 25 healthy donors (the average age 60 years). Genomic DNA was isolated using standard protocols. SNCA mutations analysis was performed to exclude one of the familial forms of PD. Restriction-enzyme digestion of polymerase-chain reaction (PCR) amplified genomic DNA fragment of SNCA exon 3 detected no G88C mutation. PCR-amplification of parkin exons 2 and 4 also detected no exon deletion. Moreover exon 41 of LRRK-2 gene as well as exons 4, 7 and 11 of PARK2 gene was screened using realtime PCR/HRM and exon sequencing. None of the patients as well as control subjects tested had mutation of LRRK2 gene. These results are consistent with previous reports in the Polish population Mutation in tested exons of PARK2 gene were identified in 20,6% patients with sporadic PD, 4,5% patients with the other neurological disorders and 4,0% control subjects. All detected mutations were heterozygous. One of the PD patients had two mutations in PARK2 gene (G1281A, G601A). It can be concluded, that both G88C SNCA and G2019S LRRK-2 mutations as well as deletion of 2 and 4 exon of parkin gene are rare causes of PD in Poland. Moreover point mutation in PARK2 seems to be associated with sporadic PD in polish population. Thus, the results of this study suggest that screening for PARK2 mutations may be a component of genetic testing for sporadic PD.

20

Oxidative DNA damage and level of thiols as related to polymorphisms of MTHFR, MTR, MTHFD1 in Alzheimer's and Parkinson's diseases

51%

Dorszewska J., Florczak J., Rozycka A., Kempisty B., Jaroszewska-Kolecka J., Chojnacka K., Trzeciak W. H., Kozubski W.

Acta Neurobiologiae Experimentalis

|

2007

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tom 67

|

nr 2

Neurodegenerative diseases, such as Alzheimer's disease (AD) and Parkinson's disease (PD), are accompanied by increased levels of 8-oxo-2'deoxyguanosine (8-oxo2dG) and alterations in levels of homocysteine (Hcy), methionine (Met), and cysteine (Cys). Hcy may undergo remethylation due to involvement of MTHFR, MTR and MTHFD1 proteins. Present studies are aimed at determination of 8-oxo2dG, Hcy, Met, and Cys in AD and PD patients as well as in control groups, using HPLC/EC/UV, as well as estimation, by restriction analysis, frequency of following gene polymorphisms: MTHFR (C677T, A1298C, G1793A), MTHFD1 (G1958A), and MTR (A2756G). In AD there were significant differences of the levels of only Cys (GG, MTHFR, G1793A) and Met/Hcy (AA, MTHFD1, G1958A) whereas in PD there were more significant differences of the levels of thiols: Hcy [MTHFR: CT (C677T) and GG (G1793A); MTR, AG (A2756G)], Met [MTR, AA (A2756G)], Cys [MTR, AG (A2756G)], and Met/Hcy [MTHFR: CC, CT (C677T) and AA (A1298C), and GG (G1793A); MTHFD1 AA (G1958A); MTR AA (A2756G)]. Significant differences in the levels of Cys/Hcy, MTHFD1 GA (G1958) were varied between AD and PD groups. The results indicate that of the enzymes studied only polymorphisms of folate-dependent enzyme MTHFD1 have pointed to significant differences in intensity of turnover of circulating thiols between AD and PD patients.

Ograniczanie wyników

Biologia molekularna chorob poliglutaminowych

Serum VEGF levels in migraine patients

The expression of Tumor Necrosis Factor-aipha in migraineurs macrophages

Serum S-100 protein and Neuron Specific Enolase in patients with onconeuronal antibodies

Profil przeciwciał onkoneuronalnych u chorych z neurologicznymi zespołami paranowotworowymi

Analysis of mutation in SPR and HTRA2 genes in patients with Parkinson’s disease

The activity of serum paraoxonase and level of conjugated dienes in stroke patients

Znaczenie biomarkerów aktywności choroby w długofalowej ocenie chorych na stwardnienie rozsiane leczonych interferonem beta

Beta-cells specific antibodies in neurological autoimmune disorders

The APOE genotype and the plasma expression of microRNA-107, -132 and -138 in patients with Alzheimer's disease-preliminary study

The interpretation of oligoclonal bands based on artiÞ cial neuronal networks

Substantia nigra hyperechogenicity in Polish patients with Parkinson’s disease

Homocysteine, cysteine and gluthatione in epileptic patients treated with antiepileptic drugs

Polymorphisms of the PARK2 gene and Parkin protein levels in patients with Parkinson’s disease

An evaluation of the reproducibility of the measurement of the intima-media thickness of carotid arteries

Carotid intima-media thickness better differentiates between groups of stroke patients and persons without cerebrovascular disease than other conventional and novel risk factors

The activities of AChE and BChE in rat brain are related to behaviour disturbances in the course of experimental breast cancer

Polymorphism of MTHFR, MTR and MTHFD1 as related to the oxidative DNA damage, and the level of thiols in Alzheimer's and Parkinson’s diseases

SNCA, PARK2 and LRRK-2 mutations in Polish patients with sporadic Parkinson’s disease

Oxidative DNA damage and level of thiols as related to polymorphisms of MTHFR, MTR, MTHFD1 in Alzheimer's and Parkinson's diseases