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Biomedical subjects

M Barcikowska

Publications and source records attributed to M Barcikowska.

At least 37 records · Page 2Linked to original sources
PubMed1998

ApoE polymorphism in Polish patients with Alzheimer's disease.

Alzheimer's disease is a genetically heterogeneous disorder of CNS. The presence of APOE-epsilon 4 allele is known to increase the risk of early and late onset sporadic and late onset familial forms of AD. In various Western European countries, USA, Canada, Japan and Australia the allelic frequency ranges between 0.1-0.18 in controls, and between 0.24-0.52 in AD patients. In the present study on Polish population, we analyzed the frequency of APOE-epsilon 4 allele in persons with Alzheimer's disease (AD). APOE genotypes were determined in 30 mild to moderate AD (83%) and mixed dementia (MIX, 17%), as well as in 11 nondemented first-degree relatives of AD (NDR), recruited from AD patient registry in Warsaw. Among the AD and MIX patients the APOE-epsilon 4, epsilon 3, epsilon 2 allele frequency was 0.333, 0.65 and 0.017 respectively.

Alzheimer Disease↗
PubMed1997

Transport of human beta-amyloid peptide through the rat blood-brain barrier after global cerebral ischemia.

In an attempt to produce an animal model of the Alzheimer's disease (AD), beta-amyloid-(1-42)-peptide (beta A1-42) was injected into the femoral vein in rats after single and repeated cardiac arrest (CA). After survival of 3.5 months, the brains immunoreactivity was evaluated using light microscopic immunocytochemistry of monoclonal beta-amyloid peptide (beta A) antibody 4G8 (mAb 4G8). Rats receiving beta A1-42 after CA demonstrated multifocal and widespread extravasation of beta A1-42 in extra- and intracellular space. The permeability to beta A1-42 was significantly higher in rats after repeated cerebral ischemia. As in AD, there were irregular diffuse amyloid plaque-like deposits and neuronal loss with reactive gliosis. Our data in ischemic rats with beta A1-42 represent a novel animal model of Alzheimer's pathology.

Amyloid beta-Peptides↗
PubMed1997

Krabbe disease: an ultrastructural study of globoid cells and reactive astrocytes at the brain and optic nerves.

We report here a detailed ultrastructural study of a brain biopsy along with post-mortem brain and optic nerve specimens from a case of Krabbe disease, a relatively rare leukodystrophy caused by a mutation in the gene for galactocerebrosidase (GALC) mapped to the 14q31 region of chromosome 14. GALC is responsible for lysosomal hydrolysis of several galactolipids including galactosylceramide, a major sphingolipids of the white matter of the central nervous system, galactosylsphingosine (psychosine) and galactosyldigluceride. The main neuropathological features such as accumulation of globoid cells, loss of myelin and marked gliosis were observed in the white matter. The monocytic origin of globoid cells was confirmed by CD-68 and ferritin-positivity and periodic acid Schiff (PAS) positivity. Ultrastructural study of the globoid cells showed the accumulation of tubular crystalloids, which are highly specific for this disease. The differences with Gaucher's disease and the pathomechanism of neuropathological damage are discussed.

Astrocytes↗
PubMed1996

Evidence of blood-brain barrier permeability/leakage for circulating human Alzheimer's beta-amyloid-(1-42)-peptide.

Brains from patients with Alzheimer's disease contain amyloid plaques which are composed of beta-amyloid peptide and are considered to play a causal role in the neuropathology of this disease. The origin of beta-amyloid peptide in brain parenchyma and vessels of Alzheimer's disease patients is not known. This study examined the permeability of the blood-brain barrier to beta-amyloid peptide in rats subjected to single or repeated episodes of global cerebral ischaemia followed by i.v. injections of human synthetic beta-amyloid-(1-42)-peptide. Rats receiving beta-amyloid peptide after ischaemia demonstrated multifocal and widespread accumulation of beta-amyloid peptide in hippocampus, cerebral cortex and occasionally in white matter. beta-Amyloid peptide penetration involved arterioles, veins and venules. Neuronal, glial and pericyte bodies were observed filled with beta-amyloid peptide. Direct evidence that soluble human beta-amyloid-(1-42)-peptide crosses the blood-brain barrier and enters the brain from the circulation is thus provided for the first time.

Amyloid beta-Peptides↗
PubMed1996

Iron in parkinsonian and control substantia nigra--a Mössbauer spectroscopy study.

We used Mössbauer spectroscopy to study the iron content, the redox state, and the binding site of iron in substantia nigra (SN) from parkinsonian (PD) and control brains. Measurements performed on fresh-frozen, formalin-fixed, and lyophilized samples demonstrated the presence of ferric (Fe3+) iron only, both in PD and control SN. Ferrous iron, if present at all, may represent at most 5% of the total iron. We found no difference in the total amount of iron in SN between PD and control brains. The Mössbauer spectra observed at 4.1 K in fresh (frozen or lyophilized) samples were different from those obtained in formalin-fixed (frozen or lyophilized) samples. In the fresh samples, only ferritin-like iron was observed, whereas in the samples frozen or lyophilized from formalin, non-ferritin iron was detected.

Aged↗
PubMed1996

Pattern of tau-1 and ubiquitin immunoreactivity in the white matter of temporal lobe in senile and with Alzheimer's disease brains.

Immunostaining pattern of the temporal white matter with anti-tau-1 and anti-ubiquitin was different in examined cases of Alzheimer's disease (AD) and normal aging. Tau-1 immunoreactivity was observed in the white matter of all AD brains, in loosely dispersed neuropil threads (NT), a few neurofibrillary tangles (NFT) and scattered glial cells, whereas in majority of senile brains the white matter was immunonegative. Ubiquitin immunoreactivity characterized by dot-like structures, evenly distributed throughout the white matter, was observed in all cases examined being more prominent in AD than in senile brains. The dot-like structures were unrelated to tau-1 immunostaining pattern, as neither NT and NFT nor glial cells were ubiquitin labeled. It was concluded, that different immunostaining with both antibodies used reflects variable pathological changes identified mostly in nerve fibers. There are neurofibrillary changes manifested by tau-1 labeled NT. However, they differed from cortical NT by lack of ubiquitin immunostaining. Non-filamentous ubiquitin-positive depots represent presumably nonspecific nerve fiber changes related to various pathological events, including AD and aging process.

Aged↗
PubMed1996

[A case of multiple intracranial meningiomas].

A case of a 91-years old woman is presented. She had multiple intracranial meningiomas, and the only symptom was the chronic headache. The diagnosis was made on the base of CT scan. The patient finally died. Postmortem examination confirmed the diagnosis.

Aged↗
PubMed1995

A new familial congenital myopathy in children with desmin and dystrophin reacting plaques.

In 5 children with a progressive congenital myopathy representing 3 different families, unusual histological, immunohistochemical and ultrastructural changes in skeletal muscle have been found. Histologically, this myopathy was characterized by the presence of fine hyaline plaques devoid of oxidative as well as ATPase enzyme activities. At the ultrastructural level plaques were composed of helical filaments and amorphous dense material. Helical filament storage corresponded to strong desmin as well as ubiquitin immunoreactivity. In addition they were also dystrophin positive. The exclusive appearance of desmin, ubiquitin and dystrophin positive plaques in muscle specimens from 5 children emphasize the uniqueness of these plaques as well as this special form of a congenital myopathy.

Adolescent↗
PubMed1995

Creutzfeldt-Jakob disease with Alzheimer-type A beta-reactive amyloid plaques.

Creutzfeldt-Jakob disease and Gerstmann-Sträussler-Scheinker syndrome are classified as transmissible cerebral amyloidoses, in contrast to the non-transmissible amyloidoses of Alzheimer's disease type. While the aetiologies of Creutzfeldt-Jakob disease and Alzheimer's disease and the molecular composition of their amyloids are different, similar basic pathogenetic mechanisms operate in both diseases through synthesis and processing of amyloid precursor proteins, to produce an accumulation of amyloid deposits. We report here a case of Creutzfeldt-Jakob disease exhibiting numerous diffuse A beta immunoreactive plaques, thus presenting features of both Creutzfeldt-Jakob disease and Alzheimer's disease. The existence of such cases underlines the existence of a 'grey' area between the two types of amyloidoses.

Adult↗
PubMed1995

A case of radionecrosis mimicking metastatic tumor of the cerebral hemisphere.

A case of delayed radiation necrosis of the cerebral hemisphere in a patient with irradiation after orbital adenocarcinoma surgery is presented in order to warn of a possible misdiagnosis with a metastatic CNS tumor. In the case surgical treatment of orbital adenocarcinoma was followed by X-ray therapy. Focal necrotic changes appearing two years later were the cause of neurological symptoms.

Adenocarcinoma↗
PubMed1995

Pathology of the vessels in cerebral amyloid angiopathy.

We review here current data on congophilic amyloid angiopathy (congophilic angiopathy) or cerebral amyloid angiopathy in both transmissible and non-transmissible cerebral amyloidoses. A beta peptide is the amyloid in congophilic angiopathy of Alzheimer's disease, and in majority of cases of Creutzfeld-Jakob disease and Gerstmann-Sträussler-Scheinker disease. A variant of Cystatin C is the amyloid in hereditary cerebral hemorrhage with amyloidosis-Icelandic type. The only exception is a curious GSS-like family from Japan characterized by 145 stop codon at the PRNP gene. Both molecular pathology and neuropathology are covered by this review.

Amyloid↗
PubMed1995

Reactive and degenerative changes of tissues surrounding a brain tumor.

We report here immunohistochemical and ultrastructural studies of the pattern of brain degeneration being a consequence of the presence of brain tumors. Robust microglial reaction with upregulation of MHC II type antigens within and around the brain tumor were seen along with the purely degenerative phenomena like neuroaxonal dystrophy (NAD) and myelin dilatation ("ballooning"). The reaction was monotonous and independent of the histological type of the brain tumor.

Atrophy↗
PubMed1995

A case of progressive supranuclear palsy with widespread appearance of neurofibrillary changes and associated senile and vascular brain lesions.

A case of progressive supranuclear palsy in association with vascular and senile brain changes in a 70-year-old woman is described. Neuropathological study with immunocytochemistry anti-tau-1 revealed widely distributed neurofibrillary tangles (NFT) and neuropil threads (NT) in several subcortical nuclei, including pallidum, subthalamic nucleus, substantia nigra, brain stem tegmentum and, to a lesser extent, in cerebral cortex. Moreover, the tau-1 positive NT were observed in many fiber bundles of the subcortical white matter. All NFT and NT were immunonegative against ubiquitin. Electron microscopic study disclosed straight filaments of about 15 nm diameter in the axoplasm of large myelinated fibers. Ultrastructural findings and appearance of abnormal tau in the white matter indicate an extension of characteristic cytoskeletal pathology with subcortical projection fibers involvement in the presented case.

Aged↗
PubMed1994

[Level of vitamin B12 and folic acid in blood serum of patients with senile dementia].

85 cases over 65 were examined to establish concentration of B12 and folate acid in the serum. 25 cases of Alzheimer's Disease (AD), 33 patients with Multi Infarct Dementia (MID) and 27 non demented persons were collected. Folstein's Mini Mental State and Hachinski scales were chosen for the purpose of the study 2 AD case (8%) patients demonstrated lower concentration of B12. No improvement after treatment was observed, although normalization of vitamin B12 level was reached. In elderly control group as well as in MID patients B12 and folic acid level in serum was in normal range. Statistically significant negative correlation between B12 serum concentration and dementia in woman population with MID was noted.

Aged↗