Coronavirus disease 2019 poses a global challenge to healthcare and society in the early 21 st century. We report neuropathological changes in 52 patients aged between 22 years and 88 years (median 58 years) who were infected with the CoV-2 coronavirus. Patients died under various circumstances and had various pre-existing diseases. The inclusion criteria for this study were: positive result for the nasopharyngeal swab for SARS-CoV-2 RNA, diagnosis of pneumonia of SARS-CoV-2 or nucleoproteins of SARS-CoV-2 in pulmonary tissue confirmed by immunohistochemical methods (IHC). Samples from all brain structures and lung specimens were taken for histopathological examinations. Brain and pulmonary samples were stained typically with histological and immunohistochemical methods and small tissue fragments were examined with the transmission electron microscope (TEM). The light and electron microscopy examination confirmed the numerous neuropathological changes in the brains of the patients infected with the CoV-2. Many of these changes were caused by pre-existing diseases of patients and/or by necessary treatment. However, vascular lesions and the inflammatory process seem to be characteristic of the CoV-2 infection. In all of the structures of 52 brains of patients, damage of the vessel walls and morphological feature of the damage to the blood-brain barrier were observed. Lymphocytic and microglial infiltrates, both perivascular and diffuse, were also observed. Hence, the brain changes due to COVID-19 infection, could be called COVID-19 cerebral angiopathy with diffuse inflammation.

Introduction: Adult neurogenesis includes proliferation and differentiation of progenitor cells as well as their migration and maturation. In the adult human brain, two neurogenic regions, the hippocampal dentate gyrus (DG) and the subventricular zone (SVZ) of lateral ventricles, have been identified. In the dentate gyrus, three types of transcriptionally active cells and in the subventricular zone, four types of transcriptionally active cells, including GFAP-positive neural stem cells (NSCs), have been differentiated. Material and methods: The aim of the study was to identify and compare density of neurogenic cells between two study groups of patients (7 men, 7 women, mean age 70 ± 6.03) with ischemic stroke and with hemorrhage (6 men, 2 women, mean age 64.75 ± 12.23) and the control group of patients (6 men, 2 women, mean age 64 ± 10.95) free of neuropathologic changes who died suddenly within less than 10 min. Results: In both groups, in the hippocampal dentate gyrus and in the subventricular zone of lateral ventricles, the presence of single GFAP-positive neural stem cells and the transcriptionally active cells labelled with phosphorylated histone H3 Ser-10 (p-Histone H3 Ser-10)/neural progenitor cells (NPCs), was observed. The quantitative analysis of cells with p-Histone H3 Ser-10 expression in the hippocampal DG revealed significant differences between the hemorrhage and control groups (p = 0.001, test t). However, in the SVZ, it showed a statistically significant decrease in the density of transcriptionally active cells in the group of patients with ischemic stroke (p = 0.001, test t). A distinct decrease in the density of transcriptionally active cells, proportional to the length of the patients' hospitalization, was observed. Conclusions: Hypoxia belongs to pathomechanic factors responsible for ischemic stroke, which can induce neurogenesis. However, hypoxia along with ischemia and other factors implicated in ischemic stroke, such as the patient's age or duration of ischemia can have a decisive influence on the decrease in the density of transcriptionally active cells in this pathologic process.

Introduction: Kufor-Rakeb syndrome (KRS) is a rare autosomal recessive neurodegenerative disorder manifesting as juvenile-onset atypical parkinsonism with pyramidal signs, supranuclear gaze palsy, dementia and characteristic minimyoclonus, with a notable phenotype variability. The responsible gene ATP13A2 was also associated with hereditary spastic paraplegia, uncomplicated early-or late-onset parkinsonism and a form of neuronal ceroid lipofuscinosis. We present clinical and ultrastructural findings in a 28-year-old woman with novel biallelic ATP13A2 mutations. Material and methods: An ultrastructural study of the skin and muscle sample was carried out. Sequence analysis of all protein coding exons and exon-intron boundaries of genes was performed on patient's genomic DNA. A proprietary oligonucleotide-selective sequencing method was used for capturing genomic targets and sequencing was performed using Illumina sequencing system. Results: The patient presented with juvenile-onset progressive parkinsonian syndrome and cognitive deterioration, accompanied by mild spastic paraplegia, supranuclear gaze palsy, cerebellar syndrome, peripheral neuropathy and fine myoclonus. Plentiful and varied osmiophilic deposits were found in skin and muscle biopsy. Sequence analysis identified two novel heterozygous variants in ATP13A2: a nonsense variant c.2209C>T, p.(Gln737*) and a 2-bp deletion c.2366_2367delTC, p.(Leu789Argfs*15) causing a frameshift leading to a premature stop codon. Oral levodopa treatment was initiated resulting in marked improvement of bradykinesia, rigidity, speech and swallowing. Conclusions: We report two novel ATP13A2 pathogenic mutations, further expanding the phenotype of Kufor-Rakeb syndrome with the unusual features of ataxia and polyneuropathy. We thoroughly describe ultrastructural findings and document a meaningful response to levodopa.

A b s t r a c t Maternal ethanol consumption during pregnancy may cause foetal alcohol syndrome (FAS). Our experiments of ethanoltreated female rats were based on the FAS model in humans; therefore, the results obtained may help explain the clinical mechanism of the disease development. The ultrastructural examination of the cerebellar cortex of ten-day-old rat pups of ethanol-treated dams during pregnancy (group IA), pregnancy and lactation (group IIA), and lactation (group IIIA) revealed that alcohol administration leads to a delayed maturation of Purkinje cells. This was most strongly manifested in the pups of dams treated with ethanol during pregnancy and lactation. Moreover, this study showed degenerative changes in Purkinje cells as well as in granular layer cells in all experimental groups. There was a difference in

A b s t r a c tWe report the case of an 84-year-old