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Biomedical subjects

M Barcikowska

Publications and source records attributed to M Barcikowska.

At least 55 records · Page 3Linked to original sources
PubMed1994

The second layer neurones of the entorhinal cortex and the perforant path in physiological ageing and Alzheimer's disease.

The hippocampal formation was studied in 5 brains of younger (29 to 52 years of age) and 6 brains of elderly (61 to 89 years of age) subjects without signs of dementia, as well as in 11 brains of patients with Alzheimer's disease (65 to 91 years of age). The 8-microns-thick sections were stained either with cresyl violet, Weil method or with immunocytochemical methods for amyloid (4G8) and neurofibrillary tangles (Tau-1). Cell bodies, senile plaques and tangles were counted in all brains. In brains of patients with Alzheimer's disease a significant neuronal loss (about 56%) was observed in the second layer of the entorhinal cortex. The tangles/neurones ratio was very high (62.79.1%) in this layer. A great number of senile plaques were present in the whole hippocampal formation, especially in the molecular layer of the dentate gyrus (22.91.5 plaques/mm2) which is the termination zone of the perforant path. It seems therefore, that pathological alterations in Alzheimer's disease disrupt the main input to the hippocampal formation. In "physiological" ageing we did not observe changes in the density of neurones, although single tangles and plaques were found in all hippocampal areas. In elderly individuals 3.81.3% of neurones of the second layer revealed neurofibrillary pathology; a few plaques were found in various areas of the hippocampal formation. These observations may suggest only a slight decrease in number of neurones in the hippocampal formation. However, these changes cause a slight impairment of memory and learning often found in elderly individuals without dementia.

Adult↗
PubMed1994

[Mossbauer spectroscopy of iron in substantia nigra in Parkinson disease and controls].

Mössbauer spectroscopy was used to study iron content, its redox state and binding sites in substantia nigra from parkinsonian and control brains. Measurements performed on fresh frozen samples demonstrated the presence of ferric iron only, both in disease and control. We found no difference in the total amount of iron in substantia nigra between the disease and control. Mössbauer spectra observed at 4.1 K in fresh frozen samples were different from those obtained in formalin fixed samples. In the fresh frozen samples only ferritin like iron was observed, whereas in the formalin fixed samples also non-ferritin iron was detected. It seems that in formalin fixed brains, during years, iron is released from ferritin and bound to an iron chelator or formalin.

Aged↗
PubMed1993

Microglia is a component of the prion protein amyloid plaque in the Gerstmann-Sträussler-Scheinker syndrome.

The microglial cell has been demonstrated as component of the cerebral amyloid plaque of Alzheimer's disease. Involvement of microglia in plaques of another cerebral amyloidosis, the Gerstmann-Sträussler-Scheinker syndrome (GSS), has found little attention. We examine here the presence of microglia in GSS plaques by immunohistochemistry and transmission electron microscopy. Paraffin sections from five brains of patients with GSS were immunolabelled with antibodies against prion protein, A4/beta amyloid protein, ferritin, leukocyte common antigen, HLA-DR, CD 68, and the MAC387 epitope for microglia and monocytes/macrophages; microglia was also labelled with the Ricinus communis agglutinin-1 lectin. Such (immuno)labelling demonstrated many delicate cell processes and occasional somata within and around prion protein plaques in all GSS brains. Microglial immunoreactivity was strongest with anti-ferritin and variable with anti-macrophage antibodies. Ultrastructural examination of brain tissue from one autopsy and one biopsy of GSS identified microglial cells in close proximity of amyloid plaque fibrils. Our observations demonstrate microglia as an important component of the amyloid plaque in GSS and suggest a major role for microglia in processing and deposition, or at least organization, of prion protein amyloid. Thus, plaques in both transmissible and non-transmissible cerebral amyloidoses seem to develop via similar pathogenetic mechanisms, irrespective of differences in etiology and molecular composition of the amyloid.

Brain↗
PubMed1993

Paraneoplastic subacute sensory neuronopathy. Clinical-pathological study.

We report 2 cases of subacute sensory neuropathy (SSN) in small cell cancer of the lung. In both cases motor disturbances were caused by motor neuropathy and neuropathy as well. In both cases we observed altered immunoreactivity of the nervous tissue, suggesting the participation of humoral immunity in the tissue damage.

Antibody Formation↗
PubMed1992

Ubiquitin expression in globose tangles in the locus coeruleus in brains of patients with Alzheimer's and Parkinson's diseases.

The locus coeruleus belongs to brain areas exhibiting remarkable neuronal loss already during physiological aging and very early neurofibrillary tangles. We performed a semiquantitative, immunocytochemical study focused on the expression of ubiquitin in neurofibrillary tangles in the locus coeruleus as compared with the central superior nucleus. The locus coeruleus exhibited later ubiquitin expression in the neurofibrillary tangles, a lower percentage of ubiquitinated tangles and more frequently granular cytoplasmic staining with Tau-1 than the central superior nucleus. These results suggesting different, probably delayed, processing of Tau protein in the locus coeruleus might contribute additionally to cell injury in this area.

Aged↗
PubMed1992

Tubulovesicular structures in Creutzfeldt-Jakob disease.

By electron microscopy tubulovesicular structures (TVS) have been consistently observed in brain tissue of transmissible spongiform encephalopathies such as natural and experimental scrapie, bovine spongiform encephalopathy and experimentally induced, but not naturally occurring, Creutzfeldt-Jakob disease (CJD). For the first time we report here the presence of TVS in human brains with CJD as detected by transmission electron microscopy. TVS were observed in all three CJD specimens (two biopsies, one autopsy), but they were rare and were found only in one or two location(s) per grid. TVS were seen in distended pre- and postsynaptic terminals and measured approximately 35 nm in diameter; they were smaller and of higher electron density than synaptic vesicles. Their occurrence in all types of transmissible spongiform encephalopathies irrespective of the affected host and the strain of the infectious agent suggests their biological significance.

Aged↗
PubMed1992

Immunohistochemical study of a case with progressive supranuclear palsy without ophthalmoplegia.

A case of progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome; PSP) with parkinsonism and absence of gaze palsy or mental changes is reported. Neuropathological examination, apart from typical changes, showed, lack of midbrain tegmentum demyelination, marked loss of Purkinje cells and presence of hyalin-like bodies in individual neurons of the substantia nigra. Immunostaining against tau-1 protein revealed the prevalence of a diffuse reaction in locus coeruleus neurons; reflecting either different ability of these cells to accumulate straight filaments, or a various time sequence of neurofibrillary tangles formation. Ferritin immunohistochemistry demonstrated widespread microglial cell proliferation, confirming further the generalized character of CNS pathology in PSP.

Aged↗
PubMed1992

Peripheral nervous system alterations in small cell lung cancer. Clinico-pathological study.

Small cell lung cancer (SCLC) is one of the most malignant tumors, especially often associated with nonmetastatic neurological disorders, corresponding to paraneoplastic neurological syndromes. The pathogenesis of which is unknown, however, mostly attributed to autoimmune processes. The aim of the study was to determine the pattern of the peripheral nervous system damage in SCLC. To provide further data contributing to the pathomechanism underlying these syndromes, immunocytochemical studies were initiated. Autopsy material was collected from 47 cases of SCLC. All these patients were examined clinically. The sections from the cervical, thoracic and lumbosacral segments of the spinal cord with spinal roots and dorsal root ganglia were taken. For immunohistochemistry following antisera were used: GFAP, MBP, IgG, IgM, ferritin, ubiquitin, alpha 1-antichymotrypsin, alpha 2-macroglobulin, C3 and C5b9 complement fractions. In 18 patients peripheral nervous system disturbances were diagnosed neurologically, 21 of cases presented neuromuscular disorders by emg. Among the nonmetastatic lesions most often a damage of dorsal root ganglia was observed (in 33 cases). Degeneration of the spinal roots was absent only in 8 cases. In 21 cases degenerative changes of motor neurons within anterior horn were present. In no case ubiquitin-positive inclusion bodies within the motor neurons could be found. In 8 cases extravasation of the IgG with diffuse labeling of the grey matter was observed. IgM immunoreactivity was markedly less frequently present, C5b9 complement fraction immunoreactivity was also confined only to cases with peripheral nervous system disturbances. Therefore, our preliminary data seem to confirm the participation of humoral immunity in paraneoplastic syndrome pathogenesis.

Adult↗
PubMed1992

Cerebellar granular layer degeneration in small cell lung cancer: paraneoplastic cerebellopathy or artifact?

The aim of our study was to ascertain whether granular cell degeneration represents uniquely an artifactual or a supravital event in patients with oat cell carcinoma. The material includes 52 cases of small cell lung cancer (SCLC). Formalin fixed and paraffin embedded representative cerebellar slides were stained routinely (HE, Klüver-Barrera), and some of them served as material for immunohistochemical study. The following antibodies were used: anti-ferritin, anti-GFAP, anti-IgG and anti-C3 complement fraction. Finally 5 cases out of our material could be diagnosed as paraneoplastic cerebellar degeneration (PCD), on the basis of lack of metastases within the CNS and concomitant intensive loss of Purkinje and granule cells. Clinically the cerebellar syndrome was disclosed in 3 cases. In the granular layer prevalence of microglial cell reaction was noted. GFAP-labeled astroglia were not demonstrated in the same intensity. Antisera to the C3 complement fraction showed moderate staining of Purkinje cell cytoplasm and in some cases also of granule cells. IgG immunostaining was disclosed in Purkinje cell cytoplasm and in 4 cases also in granule cell nuclei. The immunopathological changes presently observed and glial cell proliferation could be evidence for a nonartifactual origin of PCD.

Adult↗
PubMed1992

beta-Amyloid deposits within the cerebellum of persons older than 80 years of age.

The cerebellum, frontal cortex, hippocampal and parahippocampal regions of 100 patients older than 80 years, most of whom had died of stroke, were examined. Eighteen percent were diagnosed as clinically demented. On the specimens labeled previously with Thioflavin S and Bielschowsky method, immunohistochemical studies were performed with Fab (antigen-binding fragment) of the anti beta-amyloid antibody 4G8. Positive amyloid immunoreactivity was observed in the cerebrum in 71 of 100 cases, Cerebella of 31 subjects of 71 with cerebral amyloidosis also revealed amyloid deposits. They appeared in various morphological forms, such as diffuse plaques and focal subpial deposits, as well as classical and primitive neuritic plaques. Cases with amyloid in the cerebellum alone were not observed. Beta-amyloid deposits in the cerebellum were associated with a significant number of beta-amyloid plaques in the cerebrum, which showed other Alzheimer-type pathology, also in individuals without clinical symptoms of dementia. There was no correlation either between cerebellar amyloid deposits and clinical cerebellar symptoms or between the presence of diabetes mellitus, arterial hypertension, and neuropathological changes. A clear association of microglial cells with amyloid deposits in the cerebellum was demonstrated. In our experience, LN-1 and RCA-1 were not as suitable for formalin-fixed paraffin-embedded tissue, as was anti-ferritin. Negative staining for tau-1 and positive staining for anti-ubiquitin characterized neurites within primitive and classical plaques. No neurofibrillary pathology was detected in the cytoplasm of cerebellar neurons when we used anti tau-1 labeling.

Aged↗
PubMed1992

Creutzfeldt-Jakob disease with tubulovesicular structures: an ultrastructural study.

Tubulovesicular structures (TVS) have been consistently observed in brain tissue of the transmissible spongiform virus encephalopathies such as natural and experimental scrapie, bovine spongiform encephalopathy and experimentally induced Creutzfeldt-Jakob disease (CJD). TVS were recently demonstrated in 3 cases of naturally occurring CJD. We report here the presence of TVS in another human brain with CJD, as detected in all 3 specimens by thin section electron microscopy. Their occurrence in all types of spongiform encephalopathies, irrespective of the affected host and the strain of infectious agent, emphasizes their biological significance.

Astrocytes↗
PubMed1991

Tubulovesicular structures in human and experimental Creutzfeldt-Jakob disease.

Tubulovesicular structures (TVS) have been consistently observed in brain tissue of animals with transmissible spongiform encephalopathies such as natural and experimental scrapie, bovine spongiform encephalopathy, and experimental Creutzfeldt-Jakob disease (CJD). In this communication we demonstrate for the first time the presence of TVS in natural CJD. TVS were detected in all 3 CJD specimens. However, they were rare and were found only in one or two locations per grid. They were seen in distended pre- and postsynaptic terminals and measured approximately 35 nm in diameter, and they were smaller and of higher electron density than synaptic vesicles. Their occurrence in all types of spongiform encephalopathies irrespective of the affected host and the strain of infectious agent emphasizes their biological significance.

Animals↗
PubMed1991

Phagocytosis of beta/A4 amyloid fibrils of the neuritic neocortical plaques.

Immunocytochemistry using monoclonal antibodies to beta/A4 protein was applied to study the macrophages involved in the removal of amyloid deposits. The material examined included necrotic brain tissue areas with abundant amyloid deposits collected from 32 autopsy cases. The beta/A4-immunoreactive products were found in numerous macrophages, appearing as early as 24 h after the onset of stroke. Immunogold electron microscope studies allowed us to localize the reaction product to the secondary lysosomes. Our study clearly demonstrates the differences between macrophages engaged in amyloid removal and microglial cells associated with amyloid deposits, which according to previous observations contain beta/A4 material within endoplasmic reticular channels.

Aged↗
PubMed1990

Alzheimer neuropathology in non-Down's syndrome mentally retarded adults.

We examined the brains of 385 mentally retarded adults aged 23-90 years without Down's syndrome (DS), metabolic disorder, or hydrocephalus to extend our knowledge about the occurrence of Alzheimer-type neuropathology in this population. Relevant measures of neuropathology also were related to selected information available from clinical records. The presence of one or more neurofibrillary tangles (NFT) and/or neuritic plaques (NP) was observed in 63.4% of all cases and varied with age. The prevalence of positive cases was higher when mental retardation was due to head trauma, congenital malformation, or familial factors and when a history of seizures was reported. Comprehensive morphometric analyses of neocortical, hippocampal and parahippocampal areas indicated that recommended age-specific quantitative criteria for the diagnosis of Alzheimer disease [Khachaturian ZS (1985) Arch Neurol 42:1097-1105] were met in 9.5% of cases less than 50 years of age, 54.2% between 50 and 65, 70% between 66 and 75, and 87% of the cases greater than 75 years of age. However, a limited immunohistochemical study revealed that in most cases the NP did not have a neuritic component containing paired helical filaments and in this respect most of the plaques observed in this population may differ from those most strongly associated with Alzheimer disease. In addition, substantial numbers of NFT were seen in frontal cortex, contrasting with results reported in the literature for nonretarded populations. The number of NP per mm2 consistently increased with age for all areas examined, while the relationship between NFT density and age varied across areas, and was clearly not monotonic.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

About the presence of paired helical filaments in dystrophic neurites participating in the plaque formation.

Immunocytochemistry with monoclonal antibodies to the beta-protein and to antigens associated with paired helical filaments (PHF) allows us to selectively stain two major components of neuritic (senile) plaques (NP): PHF and amyloid deposits. Using this method, the structure of NP in the brains of Alzheimer disease victims was compared to their structure in the brains of non-demented aged individuals selected for high numbers of NP. It is demonstrated that the dystrophic neurites participating in the plaque formation contain PHF only when cortical nerve cells in the same brain area form neurofibrillary tangles (NFT). People with many NP and many NFT were always demented, whereas people with many NP but few, if any NFT were not. It is speculated that there is individual susceptibility to the formation of PHF and that their appearance may represent a nonspecific response of the neuronal network to different kinds of injuries, like the deposition of amyloid in Alzheimer disease, or other pathogenic factors associated with various dementive neurodegenerative diseases. It is hypothesized that the deposition of brain amyloid in people resistant to neurofibrillary pathology may induce too little dysfunction for the development of dementia.

Aged↗
PubMed1989

Spectrum of morphological appearance of amyloid deposits in Alzheimer's disease.

Immunocytochemical staining with monoclonal antibodies to the beta-protein on tissue sections which have been pretreated with formic acid is not only a very specific but also a highly sensitive method for the detection of amyloid deposits in the brains of Alzheimer's disease victims. We report here a spectrum of morphological appearance of the brain amyloid deposits which are one of the main histopathological correlates of this disorder. Deposits of the beta-protein are not only found in the well-known lesions [congophilic angiopathy and senile (neuritic) plaques] but are also seen under various morphological forms for which the word "plaques" does not appear an appropriate term: amyloid fibrils are found as large areas of diffuse infiltration of the neuropil, as ribbon-like infiltration in the subpial layer of the cerebral cortex, as granular deposits in the white matter, as diffuse deposits in the molecular layer of the cerebellum and the basal ganglia and as star-shaped deposits in the cerebellar Purkinje cell layer. The morphology of these deposits seems to depend on the cyto- and fibroarchitectonics of the brain region in which they are found, on the amount of amyloid deposited, and also on the type of staining technique used. It is only under specific circumstances that the deposition of amyloid in the neuropil is accompanied by the formation of paired helical filaments in nerve cell processes and their parent perikarya. In conclusion, our studies suggest that the extent of brain amyloidosis in Alzheimer's disease is much wider than so far appreciated.

Aged↗