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Eleven cases of newborns with acrania and macroscopically diagnosed anencephaly were neuropathologically examined. They presented changes in which 1 group corresponded to the diagnosis of aprosencephaly. In the second group, the development of prosencephalic structures was more advanced. The pathomechanism of the observed anomalies was analyzed in relation to data provided by molecular-genetic classification of nervous system malformations, but that did not exclude the influence of eventual extrinsic factors.

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The ability of the specific immune response of organisms is determined by the possibility of synthesis, transport and presentation of the major histocompatibility complex class II (MHC II) molecules on the surface of antigen-presenting cells. MHC II molecules are responsible for the binding, transport and presentation of a foreign antigen to helper T lymphocytes. They also stimulate the multiplication of specific B lymphocytes and determine the type of antibodies produced. The expression of MHC II molecules on the cellular surface of the spinal cord in cervical, thoracic, lumbar and sacral regions was studied on 30 normal human foetuses between 11 and 22 weeks of gestation (GW) and 9 foetuses with genetic defects (Down syndrome, mucopolysaccharidosis, mucoviscidosis or Nori's syndrome) between 17 and 22 GW. The immunocytochemical presence of MHC II molecules was found in all regions of the spinal cord in both groups of foetuses, normal and pathological, during the whole interval under study. The molecules were dispersed in the grey and white matter of the spinal cord and located most frequently on the surface of cells, near the central canal and blood vessels. These cells corresponded morphologically and immunocytochemically with amoeboid and ramified microglia. No differences in MHC II expression between the spinal cord regions or between normal foetuses and those with genetic defects were noted. It seems likely that such an early occurrence of MHC II expression in the spinal cord of foetuses with normal development, as well as the absence of abnormalities in this expression in foetuses with genetic defects, may indicate the significant role of these molecules in the immunological protection of the foetus and thus ensuring normal embryogenesis.

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Immunohistochemistry (IHC) and ultrastructural study were performed on 19 demented autopsy cases of sporadic Alzheimer's disease (AD). Semiquantitative IHC assessment of the pathological changes, according to the criteria of the Consortium to Establish a Registry of Alzheimer's Disease (CERAD) and the Consortium on Dementia with Lewy Bodies, showed morphological hallmarks of AD in 18 demented patients. It was found that 11 of these cases fulfilled criteria for "pure" AD, whereas the remaining 7 cases, with mixed findings, Lewy bodies (LBs) and Lewy-related dystrophic neurites, neuritic plaques (NP) and sometimes neurofibrillary tangles (NFT), met the criteria for Lewy body variant of Alzheimer's disease (LBV). One case with brain stem and cortical LBs but without NP and NFT was finally diagnosed as a pure form of dementia with Lewy bodies (DLB). Regional distribution and semiquantitative assessment frequency of alpha-synuclein-immunoreactive LBs, tau-immunoreactive NFT and beta-amyloid immunoreactive senile plaques, were compared between LBVand AD. Ultrastructural examination confirmed the filamental structure of cortical LBs. In conclusion, IHC study including antibody to alpha-synuclein, the sensitive marker for Lewy bodies, revealed the coexistence of brain stem and cortical LBs and pathological features of AD in a great part of dementia cases. Patients with mixed, LBs, NP and sometimes NFT pathology, fulfilled neuropathological CERAD criteria for LBV. Semiquantitative comparative IHC study, according to LBs- and NFT-scores and CERAD NP-scores showed in the LBV group a significantly lower frequency of NFT coexisting with neocortical LBs than in the group with pure form of AD.

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Antigen-presenting cells (APCs) that show the expression of major histocompatibility complex (MHC) class II molecules in adult persons are related to an early phase of immunological response. These molecules are responsible for the binding, transport, and presentation of a foreign antigen to helper T lymphocytes and determine the type of antibodies produced. They also stimulate the multiplication of specific B lymphocytes and participate in the elimination of autoreactive lymphocytes and maturation of T lymphocytes. Cells with MHC II molecules expressed on their surface were observed in the frontal and temporal lobes of 30 brains of human fetuses with normal development between gestation weeks (GW) 11 and 22. MHC II expression was noted during the whole interval under study. Its immunocytochemical localization was noted on the surface of the cerebral meninges cells, in the choroid plexus of the lateral ventricle and blood vessel lumen, and in ameboid microglia (AM) and ramified microglia (RM) cells in both cerebral lobes of the human fetus. The expression of MHC II that occurred on the cells of the central nervous system (CNS) already in GW 11 may be evidence not only of an early capability of immunological protection of the fetal nervous system, but also of a significant role potentially played by this system in normal embryogenesis. Despite continuous controversy over the cellular lineage of microglia origin, the expression of MHC II on AM and RM cells indicates its mesodermal origin, as in other APCs.

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In adults, under physiological conditions proteins of the major histocompatibility complex, class II (MHC II) molecules are synthesized and then presented on the surface of the cells known under a common name as antigen presenting cells (APCs). Dendritic cells (DCs), microglia, macrophages, ameboid microglia and lymphocytes B are qualified as APCs. The aim of present study was to evaluate the expression of MHC II molecules in the central nervous system (CNS) and hematopoietic organs during the fetal development. Observations were made on the cerebral occipital lobe, cerebellum, thymus, spleen and liver of 30 normal human fetuses, between 11 and 22 week of gestation (GW). Histological, histochemical and immunohistochemical techniques were used to identify cells with expression of MHC II molecules. In the brain, MHC II molecules were detected on macrophages/ameboid microglia in meninges, choroid plexus and single cells of ramified microglia in deeper layers of the cortex and white matter. In the other organs besides macrophages and dendritic cells, MHC II molecules were also immunopositive in thymic epithelial cells, and in the spleen and liver also in other cells of stroma and lobule. The expression of MHC II molecules on so extensive population of cells, at an early stage of the fetal development, may evidence their significant involvement in histogenesis and morphogenesis. It seems that in adults the complex of MHC II with protein is originated from the foreign antigen. On the contrary, during normal fetal development the complex of MHC II with protein origins most probably from the fetus own structures.

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A fetal, cryopreserved ventral mesencephalic rat tissue was grafted into striatum of 143 healthy adult rats, applying two different forms, solid tissue block or cell-suspension. The fetal tissue was preserved in liquid nitrogen for 30-80 days. For transplantation stereotaxic placement technique was employed. The controls were subjected to sham transplantation. The survival of transplanted dopaminergic cells in rat striatum was evaluated by means of histological and immunocytochemical methods (TH-tyrosine hydroxylase) 1, 3, 7, 14 and 21 days after transplantation. The host cellular reaction against the graft and sham-lesion was examined. Glial fibrillary acidic protein (GFAP) was used for the visualization of astroglial reaction and ferritin for microglia. The occurrence of T-lymphocytes was also assessed using W3/13 antibodies. Electron microscopy was utilized as well in the evaluation. It was found that fetal cells of cryopreserved rat mesencephalon transplanted into adult rat striatum in two different models survive and mature similarly. The host cellular reaction against the graft was nonspecific and similar to that found in the control groups. Over a posttransplantation period of 21 days no graft rejection was observed in any of the experimental groups.

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The aim of the study was to find out whether differences in morphology and time-sequence of microglia appearance in course of development of the phylogenetically different structures of the central nervous system (CNS) in normal human fetus do exist. An attempt was also made to evaluate quantitatively the development of microglial cells in comparison to astroglia, taking into account their role in the structural and immunological maturation of the CNS. The study was performed on CNS tissue of frontal lobes, mesencephalon and cerebellum from 72 fetuses between 8 and 22 week of gestation (GW). Histochemical and immunohistochemical reactions were used as basic study methods. A quantitative evaluation of developing microglia and astroglia in all investigated structures was performed by counting the mean number of cells per 1 mm2. Morphological and ultrastructural patterns of the three basic types of microglia; ameboid, ramified active and ramified resting, were characterized. It was indicated that they emerge at the same time in all structures under study, except the ameboid microglia arising earlier in the mesencephalon. A quantitative evaluation revealed that the number of ameboid microglial cells decreased slightly in an early stage of fetal development. The number of ramified microglial cells between 11 and 22 GW increased in all structures. The highest values of ramified microglia were found in mesencephalon, and the lowest in white matter of cerebellum. The number of astroglial cells exceeded the increase in ramified microglia by several times in all structures.

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Quantitative changes associated with the differentiation of microglial and astroglial cells in 48 fetal mesencephalons between 8 and 22 week of gestation (GW) were studies. Using lectin (RCA-1) labelling, two morphological types of RCA-1 positive cells, ameboid microglia (AM) and ramified microglia (RM) were identified on the basis of the cell body shape and the configuration of cytoplasmic processes. Astrocytes (AS) were identified by immunocytochemical labelling of GFAP. Measurements of microglial and astroglial cells were carried out in mesencephalon tectum and tegmentum under the microscope in sequential segments corresponding to equal sized non-overlapping areas. The quantitative data about concerning the number and percentage distribution of AM, RM and AS from each of the grid-quartiles were analyzed. The study revealed a time-sequence of appearance, characteristic pattern of distribution along perpendicular and longitudinal axes originating from aqueduct and changes in percent distribution of both types of microglial cells and astrocytes. Ameboid type of microglia was already present in 8 GW fetus in tectum (22.5 cells/mm2) and in tegmentum (10.2 cells/mm2). During the fetal development the number of AM peaked about 8-9 GW in tectum, accounting for 29 cells/mm2 close to aqueduct, and about 11-12 weeks in tegmentum, reaching 10.2-11 cells/mm2 close to aqueduct. As the fetus development advanced, the number of AM cells both in tectum and tegmentum was slowly dropped down reaching about 1.0 cells/mm2 in 20-22 GW. The ramified microglial cells as well as astroglial cells emerged in the fetal mesencephalon after 11 GW. A quantitative study also revealed a rapid increase in the density of RM in 13-16 GW (6.3 cells/mm2-close to aqueduct) and AS cells in 13-16 GW (36 cells/mm2-close to aqueduct) and later a decrease in cell number was observed. Similarly to AM, changes in the number of RM and AS cells were stabilized to about 20-22 GW. The percentage distribution of each type of microglia and astrocyte cells both in tectum and tegmentum differed markedly during the fetus development depending on the localization along the axes.

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Forty human primary brain astrocytoma tumours (anaplastic and non anaplastic) were subjected to correlative light and electron microscopic studies of microglia in tumour tissue and in its surroundings. It was found that a great number of microglia cells were present in the all types of astrocytomas. In the non anaplastic tumours (fibrillary, protoplasmic, gemistocytic) ramified microglia mostly was observed. In glioblastomas and anaplastic astrocytomas the greatest number of ameboid microglia and very rarely ramified microglial cells were found. It is suggested that the differences between the various kinds of astrocytomas determine the difference in the type of microglial reaction. It is assumed that this might be caused by the differences in secreting some factors by these tumour astrocytes.

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A primary lymphoma in the left temporal lobe of the brain in a 66-year old man is presented. The brain tumor was diagnosed on the basis of clinical symptoms (temporary dizziness, mixed aphasia and right hemiparesis) and repeated CT scanning of the brain. The patient with diagnosed malignant, non-operative brain tumor underwent a series of radiotherapy and steroidtherapy. The patient died twelve months after the first signs and symptoms had occurred. A general autopsy did not reveal any neoplasmatic changes. A macroscopic neuropathological examination showed large tumor's mass in the left temporal lobe which was not separated clearly from its surrounding. A microscopic examination included histopathological (HE, Kanzler-Arendt, Perdrau, PATH, PAS) and immunocytochemical techniques (GFAP, anti-galactocerebroside, LCA, CD45RO, OPD4, CD20). It was found that the examined brain tumor was B-cell malignant lymphoma with the presence of T-cells. Since no changes were revealed in internal organs, the tumor was diagnosed as a primary brain lymphoma.

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A fetal, cryopreserved ventral mesencephalic rat tissue was transplanted into striatum of healthy adult rats. A stereotactic apparatus was used for transplantation of solid tissue blocks. The survival of transplanted dopaminergic cells in rat striatum was evaluated by means of histological and immunocytochemical methods (TH - thyrosine hydrolase) 1, 3, 7, 14, and 21 days after transplantation. The cellular reaction of the host to graft and to sham-lesion was examined. Glial fibrillary acidic protein (GFAP) was used for the visualization of astroglial reaction and ferritin for microglia. It was found that fetal cells of cryopreserved rat ventral mesencephalon transplanted into adult rat striatum survive though, in a small number. Cellular reactions of the host to both graft of dopaminergic cells and sham-lesion are similar to glial scar and are nonspecific.

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