Oxyhemoglobin Concentration and Oxygen Uptake Signal During Recovery From Exhaustive Exercise in Healthy Subjects-Relationship With Aerobic Capacity.

This proof of concept study is dedicated to the quantification of the short-term recovery phase of the muscle oxygenation and whole-body oxygen uptake kinetics following an exhaustive cycling protocol. Data of 15 healthy young participants (age 26.1 ± 2.8 years, peak oxygen uptake 54.1 ± 5.1 mL∗min-1∗kg-1) were recorded during 5 min cool down-cycling with a power output of 50 W on an electro-magnetically braked cycle ergometer. The oxygen uptake (VO2) signal during recovery was modeled by exponential function. Using the model parameters, the time (T1/2) needed to return VO2 to 50% of VO2 peak was determined. The Hill's model was used to analyze the kinetics of oxyhemoglobin concentration (Sm, %), non-invasively recorded by near-infrared spectroscopy (NIRS) over the M. vastus lateralis. Analysis of the Pearson correlation results in statistically significant negative relationships between T1/2 and relative VO2 peak (r = -0.7). Relevant significant correlations were determined between constant defining the slope of VO2 decrease (parameter B) and the duration of the anaerobic phase (r = -0.59), as well as between Hill's coefficient and average median Smmax for the final 2 min of recovery. The high correlation between traditional variables commonly used to represent the cardio-metabolic capacity and the parameters of fits from exponential and Hill models attests the validity of our approach. Thus, proposed descriptors, derived from non-invasive NIRS monitoring during recovery, seem to reflect aerobic capacity. However, the practical usefulness of such modeling for clinical or other vulnerable populations has to be explored in studies using alternative testing protocols.

Removal of the Sinusoidal Transorbital Alternating Current Stimulation Artifact From Simultaneous EEG Recordings: Effects of Simple Moving Average Parameters.

Alternating current stimulation is a promising method for the study and treatment of various visual neurological dysfunctions as well as progressive understanding of the healthy brain. Unfortunately, due to the current stimulation artifact, problems remain in the context of analysis of the electroencephalography (EEG) signal recorded during ongoing stimulation. To address this problem, we propose the use of a simple moving average subtraction as a method for artifact elimination. This method involves the creation of a template of the stimulation artifact from EEG signal recorded during non-invasive electrical stimulation with a sinusoidal alternating current. The present report describes results of the effects of a simple moving average filtration that varies based on averaging parameters; in particular, we varied the number of sinusoidal periods per segment of the recorded signal and the number of segments used to construct an artifact template. Given the ongoing lack of a mathematical model that allows for the prediction of the "hidden" EEG signal with the alternating current stimulation artifact, we propose performing an earlier simulation that is based on the addition of artificial stimulation artifact to the known EEG signal. This solution allows for the optimization of filtering parameters with detailed knowledge about the accuracy of artifact removal. The algorithm, designed in the MATLAB environment, has been tested on data recorded from two volunteers subjected to sinusoidal transorbital alternating current stimulation. Analysis of the percentage difference between the original and filtered signal in time and frequency domain highlights the advantage of 1-period filtration.

Plasma adiponectin array in women with Alzheimer's disease.

Introduction Alzheimer's disease (AD) is a progressive and irreversible neurodegenerative disease. Typical features of AD include memory loss, social dysfunction and physical impairment. Although the pathological findings in the central nervous system are well established, the etiological factors are poorly known. Recent studies suggested the role of metabolic disturbances in the development of AD neurodegeneration. Adiponectin, an anti-inflammatory and metabolism regulating factor, was linked to AD. Aim The aim was to examine whether adiponectin fractions combined with insulin/insulin resistance-associated metabolic parameters correlate with AD progression. Material and methods The study comprised 98 women: 27 with moderate to severe AD, 31 with AD at early stage and 40 healthy controls, matched for age and BMI. To evaluate memory impairment, the MMSE was performed. Plasma total adiponectin and its high-, medium- and low molecular weights were measured with ELISA. Anthropometric, clinical and metabolic parameters were assessed. Correlations between adiponectin array and measured parameters were evaluated. Results In comparison to the controls, enhanced levels of total and medium molecular weight adiponectin characterized AD individuals. In AD, we found correlations between adiponectin array, and anthropometric and biochemical parameters. After adjustment to BMI, a significant increase of the total adiponectin and high- and medium molecular weight fractions was observed. A negative correlation between low molecular weight adiponectin and MMSE was found. Conclusions Our results indicate a possible link between adiponectin variations and AD. We hypothesize that changes in adiponectin profile observed in AD result from compensatory mechanism against neuropathological processes, as well as from adiponectin homeostasis impairment.

Antimicrobial Resistance Patterns in Women with Positive Urine Culture: Does Menopausal Status Make a Significant Difference?

Aim. Urinary tract infection (UTI) is considered one of the most common bacterial infections in women. The aim of this study was to investigate the types of uropathogens present, as well as the degree of antimicrobial drug resistance seen among premenopausal (n = 2748) and postmenopausal (n = 1705) women with uncomplicated UTI. Methods. Urinary samples (n = 4453) collected from women with UTI were analyzed in terms of uropathogens present. These were considered as positive if bacterial growth was ≥105 colony forming units (CFUs)/mL. Susceptibility and resistance testing for commonly used antibiotics was subsequently assessed. Results. The most common uropathogens cultured from urine samples were Escherichia coli (65.5%), followed by Enterococcus faecalis (12.2%), Klebsiella pneumoniae (4.7%), and Proteus mirabilis (4.2%). The resistance to ampicillin exceeded 40%, independently of menopausal status. Of note, resistance to ciprofloxacin exceeded 25% among postmenopausal patients. Moreover, resistance of all uropathogens to commonly used antimicrobials was significantly higher in postmenopausal women. Conclusion. Due to the high resistance rate, ampicillin, ciprofloxacin, and the trimethoprim/sulfamethoxazole combination should be avoided in treating postmenopausal women affected by UTI without being indicated by initial urine culture report. Finally, cephalexin and cefuroxime are promising alternatives as initial treatment in postmenopausal women.

Association between Cerebrospinal Fluid Biomarkers for Alzheimer's Disease, APOE Genotypes and Auditory Verbal Learning Task in Subjective Cognitive Decline, Mild Cognitive Impairment, and Alzheimer's Disease.

In the course of Alzheimer's disease (AD), early pathological changes in the brain start decades before any clinical manifestation. The concentration levels of AD cerebrospinal fluid (CSF) biomarkers, such as amyloid-ß1-42 (Aß1-42), total tau (T-tau), and phosphorylated tau (P-tau), may reflect a cerebral pathology facilitating an early diagnosis of the disease and predicting a cognitive deterioration. The aim of this study was to estimate the prevalence of AD CSF biomarkers in those individuals with a subjective cognitive decline (SCD), a mild cognitive impairment (MCI), and Alzheimer's dementia (AD-D), together with the relationships between the biomarkers, an APOE ɛ4 presence, and a verbal episodic memory performance. We included 252 patients from the memory clinic with a diagnosis of SCD (n = 85), MCI (n = 87), and AD-D (n = 80). A verbal episodic memory performance level was assessed and was based on a delayed recall trial from the 10-word list of an auditory verbal learning task (AVLT). We found that the patients with more severe cognitive impairments had significantly lower levels of Aß1-42 and higher levels of T-tau and P-tau. This pattern was also typical for the APOE ɛ4 carriers, who had lower levels of Aß1-42 than the noncarriers in the AD-D and MCI groups. The levels of T-tau and P-tau were significantly higher in the APOE ɛ4 carriers than in the noncarriers, but only in the MCI patients. The AVLT performance in the whole study samples was predicted by age, Aß1-42, and the T-tau CSF biomarkers, but not by the APOE genotyping.

Hypertension in patients with Alzheimer's disease--prevalence, characteristics, and impact on clinical outcome. Experience of one neurology center in Poland.

The aim of the study was to evaluate hypertension (HT) prevalence, characteristics, and impact on clinical outcome in patients with Alzheimer's disease (AD). We evaluated 701 patients with AD (249 males, 452 females, and mean age 74.9 ± 7.5 years). As a group representing general population matched with regard to age, education level, and place of residence, we included 762 subjects (438 males, 324 females, and mean age 74.7 ± 4.4 years) from the Polish National Multicenter Health Survey (WOBASZ) studies. The patients with AD were characterized by lower systolic blood pressure (BP) and diastolic BP values (134 ± 21 vs. 151 ± 23 mm Hg, P < .001 and 77 ± 11 vs. 86 ± 12 mm Hg, P < .001, respectively) as well as lower HT prevalence (66% vs. 78.6%, P < .001) compared with the WOBASZ group. In long-term follow-up of AD group, HT and BP levels were not associated with the decline in cognitive functions nor the increased risk of death. Patients with AD were characterized by lower prevalence of HT and other vascular risk factors. BP levels and HT had no impact on clinical outcome.

Plasma leptin levels and free leptin index in women with Alzheimer's disease.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by irreversible and progressive loss of memory and other cognitive functions. Controversies still exist on the precise mechanisms contributing to neurodegeneration. Obesity and disturbances in metabolic homeostasis are thought to be AD risk factors. Adipokine leptin has receptors in the brain, also in the regions related to AD. Leptin may protect against AD. The aim was to assess leptin and soluble leptin receptor levels in plasma as well as free leptin index (FLI) in correlation with metabolic status of women diagnosed with Alzheimer's disease. Eighteen women with moderate to severe stage of AD, 40 women with AD at early stage, and 42 female controls, matched for age and body mass index, participated in the study. Leptin and soluble leptin receptor levels were measured with RIA and IRMA, respectively. Then, FLI was calculated. In addition, metabolic parameters (lipid profile, glucose and insulin concentrations, HOMA-IR) were estimated. Clinical and anthropometric data were collected. The Mini-Mental State Examination (MMSE) as a cognitive impairment measurement was performed. Correlations with both leptin and FLI, and MMSE, clinical and biochemical parameters were evaluated. Leptin levels and FLI were significantly lower and leptin receptor concentrations were higher in AD subjects when compared with the controls. In AD group leptin, soluble leptin receptor and FLI correlated with selected metabolic parameters but not with MMSE. We conclude that alterations in leptin, leptin receptor, and FLI were the most intensified in advanced AD. However, these results did not correlate with dementia stage measured with MMSE. Therefore, further intensive research is needed to explain the mechanisms involved in this phenomenon.

Agraphia in patients with frontotemporal dementia and parkinsonism linked to chromosome 17 with P301L MAPT mutation: dysexecutive, aphasic, apraxic or spatial phenomenon?

OBJECTIVES: Patients with frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) may be agraphic. The study aimed at characterizing agraphia in individuals with a P301L MAPT mutation. METHODS: Two pairs of siblings with FTDP-17 were longitudinally examined for agraphia in relation to language and cognitive deficits. RESULTS: All patients presented with dysexecutive agraphia. In addition, in the first pair of siblings one sibling demonstrated spatial agraphia with less pronounced allographic agraphia and the other sibling had aphasic agraphia. Aphasic agraphia was also present in one sibling from the second pair. CONCLUSION: Agraphia associated with FTDP-17 is very heterogeneous.

A novel MAPT mutation, G55R, in a frontotemporal dementia patient leads to altered Tau function.

Over two dozen mutations in the gene encoding the microtubule associated protein tau cause a variety of neurodegenerative dementias known as tauopathies, including frontotemporal dementia (FTD), PSP, CBD and Pick's disease. The vast majority of these mutations map to the C-terminal region of tau possessing microtubule assembly and microtubule dynamics regulatory activities as well as the ability to promote pathological tau aggregation. Here, we describe a novel and non-conservative tau mutation (G55R) mapping to an alternatively spliced exon encoding part of the N-terminal region of the protein in a patient with the behavioral variant of FTD. Although less well understood than the C-terminal region of tau, the N-terminal region can influence both MT mediated effects as well as tau aggregation. The mutation changes an uncharged glycine to a basic arginine in the midst of a highly conserved and very acidic region. In vitro, 4-repeat G55R tau nucleates microtubule assembly more effectively than wild-type 4-repeat tau; surprisingly, this effect is tau isoform specific and is not observed in a 3-repeat G55R tau versus 3-repeat wild-type tau comparison. In contrast, the G55R mutation has no effect upon the abilities of tau to regulate MT growing and shortening dynamics or to aggregate. Additionally, the mutation has no effect upon kinesin translocation in a microtubule gliding assay. Together, (i) we have identified a novel tau mutation mapping to a mutation deficient region of the protein in a bvFTD patient, and (ii) the G55R mutation affects the ability of tau to nucleate microtubule assembly in vitro in a 4-repeat tau isoform specific manner. This altered capability could markedly affect in vivo microtubule function and neuronal cell biology. We consider G55R to be a candidate mutation for bvFTD since additional criteria required to establish causality are not yet available for assessment.

The prion protein M129V polymorphism: longevity and cognitive impairment among Polish centenarians.

The PRNP gene encodes the cellular isoform of prion protein (PrP (c) ). The M129V polymorphism influences the risk of prion diseases and may modulate the rate of neurodegeneration with age. We present the first study of the polymorphism among Polish centenarians. In the control group (n = 165, ages 18 to 56 years) the observed M129V genotype frequencies agreed with those expected according to the Hardy-Weinberg equilibrium (MM, MV, VV): 43%, 44%, 13% (HWE p > 0.05). Among centenarians (n = 150, ages 100 to 107) both homozygotes were more common than expected and HWE was rejected: 46%, 37%, 17% (expected 42%, 46%, 13%; HWE p = 0.025). This finding is consistent with a higher mortality rate among heterozygotes. However, the observed allele and genotype frequencies did not differ significantly between the oldest-old and the young controls. The genotypic frequencies were not related to severe cognitive impairment among the centenarians.

APBB2 genetic polymorphisms are associated with severe cognitive impairment in centenarians.

APBB2 gene encodes for ß-amyloid precursor protein-binding family B member 2, (APBB2, FE65-like, FE65L1), an adaptor protein binding to the cytoplasmatic domain of ß-amyloid precursor protein (ßAPP). Over-expression of APBB2 promotes formation of ß-amyloid (Aß), the main constituent of senile plaques. Polymorphisms within APBB2 gene have been proposed as candidate risk factors for Alzheimer's disease. However, their association with longevity has never been investigated. Here we present the first attempt to analyze APBB2 polymorphisms in centenarians. We used a PCR-RFLP method to analyze two intronic nucleotide substitutions: hCV1558625 (rs17443013) and rs13133980. We found no differences in genotype or allele distribution between centenarians and young controls. After stratification of centenarians upon their cognitive performance, the APBB2 rs13133980 G allele was over-represented in centenarians with severe cognitive impairment compared to individuals without this disability. Also the hCV1558625-rs13133980 AG haplotype increased relative risk for severe cognitive impairment in centenarians. Our results support the concept of APBB2 polymorphism association with cognitive performance in the oldest age.

Identification of a late onset Alzheimer's disease candidate risk variant at 9q21.33 in Polish patients.

Late onset Alzheimer's disease (LOAD) accounts for about 95% of all Alzheimer's disease cases. While the APOE ε4 variant seems to have unparalleled influence on increased LOAD risk, it does not explain all of the heritability of LOAD. In this study, we present the application of a cost-effective, pooled DNA genome-wide association study (GWAS) to uncover genetic risk variants associated with LOAD in Polish women diagnosed with either mild cognitive impairment (MCI) or well-defined LOAD. A group of 141 patients (94 LOAD and 47 MCI), as well as 141 controls, were assayed using Affymetrix Genome-Wide Human SNP 6.0 arrays. Allele frequency distributions were compared using χ(2)-tests, and significantly associated SNPs at p < 0.0001 with a proxy SNP were selected. GWAS marker selection was conducted using PLINK, and selected SNPs were validated on DNA samples from the same cohort using KASPar Assays. In addition, to determine the genotype of APOE variants (rs429358, rs7412), a multiplex tetra-primer amplification refractory mutation system was applied. The GWAS revealed nine SNPs associated with MCI and/or LOAD. Of these, the association of seven SNPs was confirmed by genotyping of individual patients. Furthermore, the APOE ε4 appeared to be a risk variant for LOAD, while the APOE ε3 showed a protective effect. Multivariate analysis showed association between rs7856774 and LOAD, independently from the effect of APOE variation. Pooled DNA GWAS enabled the identification of a novel LOAD candidate risk variant, rs7856774 (9q21.33), tagging a possible genomic enhancer affecting proximal transcribed elements including DAPK1 gene.

Discrete movements of foot epithelium during adhesive locomotion of a land snail.

During the adhesive locomotion of land snails a series of short dark transverse bands, called pedal or foot waves, is visible ifa moving snail's ventral surface is observed through a sheet of glass. Moreover, the mucus secreted from the pedal glands and some pedal epithelial cells forms a thin layer which acts as a glue augmenting adherence, while also acting as a lubricant under the moving parts of the snail's foot. The relationships between velocity and the frequency of pedal waves as well as changes in the volume of small air bubbles under foot waves were analyzed by means of digital recordings made through a glass sheet on which the snails were moving. On the ventral surface of a moving snail foot, the adhering parts of the foot constituted about 80% of the total area, while several moving parts only about 20%. The single moving region of the foot (the pedal wave) amounted to about 3% of snail length. The epithelium in the region of the pedal wave was arched above the substrate and was also more wrinkled than the stationary epithelium, which enabled the forward motion of each specific point of epithelium during the passage of a pedal wave above it. The actual area of epithelium engaged by a pedal wave was at least 30% greater than the area of the epithelium as recorded through a glass sheet. In the region of the pedal wave, the tiny subepithelial muscles acting on the epithelium move it up in the front part of the wave, and then down at the end of the wave, operating vertically in relation to the substrate. In the middle part of the wave, the epithelium only moves forward. In summary, during the adhesive locomotion of snails, the horizontal movement of the ventral surface epithelium proceeds as temporally separate phases of upward, forward and downward movement.

TOMM40 rs10524523 polymorphism's role in late-onset Alzheimer's disease and in longevity.

Recently, it has been reported that TOMM40 variable-length poly-T sequence polymorphism (rs10524523) in combination with APOE alleles (E2, E3, E4) significantly influences late-onset Alzheimer's disease (LOAD) age of onset. In a group of 414 LOAD patients, 173 centenarians and 305 neurologically healthy individuals, we investigated the impact of TOMM40 poly-T tracts on LOAD incidence, age of onset, and longevity. TOMM40 allelic variants were classified into four categories: short (S; 14-16T), long a (La; 20-22T), long b (Lb; 26-30T), and very long (VL; 31-39T). Our results demonstrate that La and Lb share similar characteristics in affecting LOAD risk, thus for some analyses they were combined into L category. We observed significantly lower frequency of VL allele (p < 0.0001) and significantly higher frequency of L alleles in the LOAD patients compared to the control individuals (p < 0.0001). S/S, S/VL, and VL/VL genotypes and VL-E2, S-E3, VL-E3 haplotypes are significantly associated with lower LOAD risk. VL-E3 haplotype carriers significantly more frequently developed LOAD when they were ≥79 years old. Additionally, S/L genotype is associated with a significantly increased LOAD risk (p < 0.0001). We conclude that in the carriers of TOMM40-APOE haplotypes comprising E4 allele, the TOMM40 rs10524523 allele does not play substantial role in establishing LOAD risk. Nevertheless, TOMM40 L allele increases the risk when E4 is absent. Finally, L allele, as well as genotypes (S/L, V/L) and haplotypes (L-E3, L-E4) comprising L significantly reduce the likelihood of living up to 100 years.

Inflammatory bowel disease - is there something new in the immunological background?

In the present paper we correlate clinical data, as well as histopathological, immunohistochemical and molecular biology methods, with the occurrence of both forms of inflammatory bowel disease (IBD) i.e. ulcerative colitis and Crohn's disease. We found that patients with a history of Epstein-Barr virus (EBV) or cytomegalovirus (CMV) infections, as well as steroid treatment, had increased susceptibility to the development of IBD. The diagnosis of IBD was confirmed by histopathology. Previous infections by EBV and CMV, as well as M. tuberculosis, were proved by PCR-based techniques and in situ hybridization. We found PCR-proved latent viral infections in 30-50% of the IBD patients we studied. However, we were unable to prove the presence of viral antigens by immunohistochemistry for EBV or CMV. We found positive correlations between the presence of anti-CMV IgG, as well as PCR-positive results for M. tuberculosis with an ulcerative colitis diagnosis. Additionally, up to 80% of IBD patients used steroids, which was found to be correlated with a diagnosis of Crohn's disease. Our data may support the theory that IBD could be related to previous viral infections and the use of steroids.

Association between genetic and environmental factors and the risk of Alzheimer's disease.

The only well confirmed genetic risk factor for sporadic Alzheimer's disease (AD) is the possession of apolipoprotein E (APOE) epsilon4 allele. As it contributes to 40-70% of AD cases, a large proportion of genetic variance may be determined by additional loci. Our aim was to estimate how reported genetic factors (APOE, NOS3, MTHFR) interact to increase the risk for AD and combine them with environmental factors (homocysteine, vitamin B12, cholesterol). Genotyping was performed in 154 AD patients and 176 healthy controls. Levels of homocysteine, vitamin B12 and cholesterol were assessed in subgroups of 100 AD patients and 100 controls. We found a difference in APOE epsilon4 and NOS3 G/G distribution between groups (p<0.005). Plasma total homocysteine was increased and vitamin B12 decreased in AD patients (p<0.001). The influence of APOE epsilon4 and NOS3 G alleles on the risk of AD was independent of homocysteine, vitamin B12 levels and MTHFR status.

Serum kynurenic acid positively correlates with cardiovascular disease risk factor, homocysteine: a study in stroke patients.

KYNA, an antagonist of ionotropic glutamate receptors and alpha7 nicotinic receptors, has been found as well in the brain as in the periphery. The altered metabolism of KYNA, especially its deficiency, can lead to the enhanced glutamate-mediated excitotoxicity, and was suggested to be a factor contributing to the development of neurodegeneration and seizures. Elevated serum concentration of homocysteine is considered to be an independent risk factor of atherosclerosis and is an emerging risk factor of cognitive dysfunction and stroke. In the present study, serum level of KYNA, homocysteine and other biochemical parameters were assessed in patients at early (up to 24 h after infarct) stage of stroke. Serum KYNA and homocysteine levels were similar in control (N = 26) and stroke (N = 24) groups. KYNA level correlated positively with the level of homocysteine in control and in stroke group, with p = 0.018; r = 0.462 and p = 0.027; r = 0.451, respectively. In control group, KYNA correlated positively also with age (p = 0.007; r = 0.514) and with creatinine level (p = 0.002; r = 0.581). In stroke group, serum KYNA correlated positively with creatinine (p = 0.001; r = 0.644) and with urea level (p < 0.001; r = 0.716). Homocysteine level correlated inversely with folate level in control (p = 0.01; r = -0.499) but not in stroke group (p = 0.13; r = -0.317). Serum homocysteine in stroke group correlated positively also with age (p = 0.001; r = 0.6401), and with urea level (p = 0.017; r = 0.4813). Clinical significance of the association between serum KYNA and homocysteine levels requires further investigation.

CYP46: a risk factor for Alzheimer's disease or a coincidence?

Excess cholesterol is removed from the brain via hydroxylation mediated by cholesterol 24S-hydroxylase (CYP46). Although serum and cerebrospinal fluid (CSF) concentrations of 24S-hydroxycholesterol are altered during the progress of Alzheimer's disease, studies carried out to date in different populations on the association of CYP46 gene polymorphisms and risk of AD have been inconclusive. In this report, we analyzed CYP46 polymorphisms in 215 Polish AD cases and 173 healthy individuals. A fragment of CYP46 intron 2 was amplified by PCR reaction and sequenced. We discovered a new single nucleotide substitution in CYP46 intron 2, but found no difference in particular genotype or allele frequencies between AD patients and controls. However, the GG genotype of the known rs754203 polymorphic site might be a risk factor for AD, especially in APOE varepsilon4 carriers. Interestingly, in AD patients the rs754203 G allele was more frequent in males than in females. However, considering the extreme divergence of results obtained by different authors, a clear connection between the CYP46 gene and AD is questionable.

The E318G substitution in PSEN1 gene is not connected with Alzheimer's disease in a large Polish cohort.

Mutations in the presenilin 1 (PSEN1) gene are known to cause nearly 50% of early-onset, familial Alzheimer's disease (AD) cases. To determine whether E318G mutation is related causally to AD in the Polish population E318G mutation frequency was assessed using PCR-RFLP method in a total of 659 subjects: 256 AD patients, 210 healthy, age-matched control subjects, 100 Parkinson's disease patients and 93 centenarians. When the mutation frequencies were compared to healthy controls, no significant differences between the groups were found. It could be concluded that E318G mutation is not related causally to AD in the Polish population, either as a risk factor or a disease causing mutation.

Plasma homocysteine level and the course of ischemic stroke.

Increased level of homocysteine (Hcy) in blood seems to influence negatively the course of ischemic stroke (IS), the possible mechanism of this action could be acceleration of oxidative stress. The aim of this study is to assess the influence of Hcy level in patients with IS on the prognosis 3 months after the stroke onset. 75 patients aged 68.27 +/- 12.62 years, with the diagnosis of first ever IS were examined. Patients with the symptoms corresponding with TACS at the beginning of stroke and with diminished level of consciousness were not included. The level of Hcy over 15 micromol/l was assessed as mild hiperhomocysteinemia (MHcy). 74 (98.7%) patients were assessed 3 months after IS onset in the Rankin scale. Recovery was assessed, according to Rankin Scale: good recovery (GR) 0-2, bad recovery (BR) 3-5 and death. MHcy was seen in 9 (14.5%) with GR and in 8 (66.7%) with BR (P = 0.0005). MHcy increases the risk of BR 11.78 times (95% CI 2.93-47.42).