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Biomedical subjects

M Barcikowska

Publications and source records attributed to M Barcikowska.

At least 19 recordsLinked to original sources
PubMed1999

Ischemic rats as a model in the study of the neurobiological role of human beta-amyloid peptide. Time-dependent disappearing diffuse amyloid plaques in brain.

Brains from patients with Alzheimer's disease contain diffuse and senile amyloid plaques. Using an experimental model, we have addressed the issue whether diffuse plaques of amyloid persist, develop with time, or both, in rats injected with human beta-amyloid-(1-42)-peptide for 3 and 12 mon after brain ischemia. Rats receiving beta-amyloid peptide for 3 months after brain ischemia demonstrated widespread diffuse amyloid plaques in hippocampus and cerebral cortex. Neuronal, glial, ependymal, endothelial and pericyte cell bodies were observed filled with beta-amyloid peptide. No staining was observed in control brains. In the group alive 1 year no deposition of human beta-amyloid peptide was observed, too. Direct evidence that diffuse amyloid plaques can disappear in the brain is thus provided for the first time.

Alzheimer Disease↗
PubMed1999

[Clinical pattern of early phase of Alzheimer's disease].

Modern views are presented on the sequence of neuropathological changes in Alzheimer's disease and their correlation with clinical symptoms in early phase of that process. Attention is called to difficulties in interpretation of the influence of morphotic changes, such as neurofibrillary degeneration and senile plaques, on the progression of clinical symptoms. Data are compared as published by various authors suggesting a diversity of neuropsychological abnormalities manifesting themselves in the early phases of the disease. Genetic studies seem also to confirm the complexity of the Alzheimer process and they may explain the imperfection of clinical diagnostic methods used as yet.

Age Factors↗
PubMed1998

Cerebral accumulation of beta-amyloid following ischemic brain injury with long-term survival.

Deposits that are recognized by antibodies specific for the C-terminal and beta-amyloid peptide (beta A) but not the N-terminal sequences of the amyloid precursor protein (APP) fragments are present in the extra- and intracellular space in ischemic rat brain with 1 year survival. The immunohistochemical profile indicates that the APP in these deposits is truncated between the N-terminal and beta A and terminates at the C-terminal. This process probably is reaching into the extracellular space.

Alzheimer Disease↗
PubMed1998

A case of sporadic Creutzfeldt-Jakob disease with a Gerstmann-Sträussler-Scheinker phenotype but no alterations in the PRNP gene.

We report here an unusual sporadic case of Creutzfeldt-Jakob disease (CJD) characterized by an abundance of prion protein (PrP)-immunopositive kuru and multicentric but not florid plaques. Molecular genetic analysis of the PRNP open reading frame region spanning codons 8-221 was performed. Neither deletion nor insertion mutations were detected in the repeat area of the PRNP. No pathogenic mutation was found in the sequenced region between codon 108-221. Restriction analysis of the amplified fragment using restriction endonucleases DdeI, PvuII and AluI did not show any of the previously described pathogenic mutations at codon 102, 105, and 117 associated with Gerstmann-Sträussler-Scheinker (GSS). The patient was heterozygous for the methionine/valine coding triplet at polymorphic codon 129 of the PRNP gene by sequence, restriction endonuclease analysis and hybridization with allele-specific nucleotides. Furthermore, hybridization with 32P-labeled allele-specific oligonucleotides confirmed the absence of pathogenic mutations at codons 102, 200 and 178. Such a case may present a missing "link" between sporadic CJD and familial GSS.

Amyloid↗
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↗