Cerebral small vessel disease (CSVD) is the most common, chronic and progressive vascular disease. The changes affect arterioles, capillaries and small veins supplying the white matter and deep structures of the brain. It is the most common incidental finding on brain scans, especially in people over 80 years of age. Magnetic resonance imaging (MRI) plays a key role in the diagnosis of CSVD. The nomenclature and radiological phenotypes of CSVD were published in 2013 based on the unified position of the so-called Centres of Excellence in Neurodegeneration. The disease is characterized by a diverse clinical and radiological picture. It is primarily responsible for stroke incidents, gait disturbances, depression, cognitive impairment, and dementia in the elderly. The CSVD contributes to about 20% of strokes, including 25% of ischemic strokes and 45% of dementias. Common causes of CSVD include arteriosclerosis, cerebral amyloid angiopathy (CAA), genetic small vessel angiopathy, inflammation and immune-mediated small vessel diseases, and venous collagenosis. There is no causal treatment and management is mainly based on combating known risk factors for cardiovascular disease (CVD).

The potential role of microbiological factors such as Chlamydia pneumoniae (ChP) in the pathogenesis of neurodegenerative disorders, including Alzheimer's disease (AD) and vascular dementia (VD), has been suggested, but the correctness of this hypothesis still needs to be tested. In this study the appearance of ChP in the cerebrospinal fluid (CSF) of 57 AD and 21 VD patients and in 47 controls (CG) as well as the influence of ChP on the levels of tau protein and Abeta42 were investigated. The frequency of ChP occurrence in the AD patient group (43.9%) was significantly higher (p < 0.001) than in the control group (10.6%). In the case of VD patients, 9.5% of this group was positive for ChP. The presence of ChP DNA in the CSF of patients with AD significantly increases the occurrence of this disease (odds ratio = 7.21). Cerebrospinal fluid Abeta42 levels were significantly lower in patients with AD than in the CG (p < 0.001). Cerebrospinal tau protein was significantly higher in AD vs. CG (p = 0.007). However, no relationships between the presence of the bacterium in CSF and the level of either tau or Abeta42 protein were observed. In conclusion, we may suspect that testing for the presence of ChP in CSF, along with the tau and Abeta42 markers, may be used in the clinic diagnosis of AD.

Background. Cerebral venous thrombosis (CVT) is a rare condition which constitutes 0.5-1% of all strokes. The clinical and radiological picture of CVT is non-specific and can mimic other disorders.

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

Background. Gliomas are a heterogenous group of tumors that show the same histological features but differ in their behavior. Gliomas are characterized by biological aggressiveness and extensive infiltrative growth into surrounding healthy brain tissue. Objectives. In this study we estimated CD44v6 and E-cadherin expression and correlation between CD44v6 and E-cadherin in relation to glioma malignancy. We also analyzed simultaneous expression of CD44v6 and E-cadherin in the same tumor sample in order to determine the biological tumor behavior. Material and Methods. Expression of CD44v6 and E-cadherin was evaluated on ninety-two formalin-fixed paraffin-embedded glioma tissue blocks using immunohistochemistry (IHC). Results. CD44v6 expression was found in 71.6% of gliomas. There was a statistically significant difference between the frequency of positive cases for CD44v6 expression in low (grade I) vs. high (grade IV) as well as in grade I vs. grade II of glioma malignancy (p = 0.001). E-cadherin membrane staining was observed in 28.8% of gliomas. No significant differences were observed between E-cadherin expression and grade of gliomas (p > 0.05). However, re-expression of E-cadherin was found in grade II gliomas. In this group, E-cadherin expression was revealed in 43.3% of the cases. In order to define the relationship between CD44v6 expression and E-cadherin, we analyzed the simultaneous expression of CD44v6 and E-cadherin in the same glioma sample in the whole group and in respect to the degree of glioma malignancy. A positive correlation between studied biomarkers was observed in the analyzed gliomas (p = 0.004) but a simultaneous expression of CD44v6 and E-cadherin revealed no significant differences in respect to glioma malignancy. Conclusions. Our results showed that the level of E-cadherin might reflect different biological features of gliomas, whereas CD44v6 is associated with tumor cell malignancy. The simultaneous presence of CD44v6 and E-cadherin in a set of low-grade gliomas indicates that both these molecules might strengthen cell migration and may be a hallmark of glioma invasive growth (Adv Clin Exp Med 2014, 23, 5, 827-834).