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M Barcikowska

Publications and source records attributed to M Barcikowska.

At least 19 recordsLinked to original sources
PubMed2002

Behavioural pathology in Alzheimer's disease with special reference to apolipoprotein E genotype.

The aim of this study was to define the co-occurrence of behavioural symptoms and Alzheimer's disease (AD) in relation to apolipoprotein E (APOE) genotype. Probable AD patients from the Alzheimer's Day Clinic (n = 139) were assessed with the 'Behavioural Pathology in Alzheimer's Disease' rating scale, and their APOE genotype was determined. This study demonstrated no relationship between presence of the APOE epsilon4 allele and any of the behavioural symptoms assessed, including delusions, hallucinations, depression, activity disturbances, aggressiveness and anxiety. Activity disturbances, delusions, hallucinations and aggressiveness paralleled the severity of AD, increasing in frequency with the severity of the dementia. The prevalence of delusions, hallucinations, aggressiveness and depression were found to be associated with lower levels of education.

Aged↗
PubMed2001

The diagnostic value of EEG in Alzheimer disease: correlation with the severity of mental impairment.

The aim of our study was to analyze EEG changes in patients with Alzheimer disease (AD) and to determine how closely EEG reflects the progression of mental impairment in people with AD. Ninety-five patients with probable AD according to National Institute of Neurological and Communicative Disorders and Stroke/Alzheimer's Disease and Related Disorders Association criteria treated in our Clinic for Memory Disorders were selected for this study. Patients were divided into three subgroups with mild, marked, and severe dementia according to the results of psychometric scales. The EEG findings were classified using an eight-degree scale according to the background activity, presence and amount of theta and delta waves, focal changes, lateralization of focal changes, synchronization, and presence of sharp and spike waves. A significant correlation between the degree of EEG abnormalities and cognitive impairment was found. We did not observe any correlation between the presence of delta waves and the results of neuropsychological tests. Our study revealed an important diagnostic value of EEG in the estimation of the severity of dementia parallel to psychometric scales.

Adult↗
PubMed2001

Lipid metabolism parameters in patients with Alzheimer's disease and their first degree relatives.

Recently, it was suggested that the presence of total cholesterol (TC), age and sex interaction in Alzheimer's type dementia (AD) is linked with the apolipoprotein E (APOE) genotype. Our objective was to determine whether the serum lipid profile in AD patients and their first degree non-demented relatives of a certain age (NDR) was dependent on APOE genotype. We included 28 mild to moderate AD and 30 NDR according to DSM-III-R and NINCDS-ADRDA criteria. NDR individuals were investigated in an age group similar to the AD group (brother-sister relationship) and in a group including younger individuals (AD patients-children relationship). Our data indicate significant differences between decreased total cholesterol and low density lipoprotein cholesterol ratio in the group of AD patients versus NDR individuals of similar age, independent of APOE genotype, and an increased total cholesterol and low density lipoprotein cholesterol ratio in a group of AD patients versus their children of the same genotype. There was no significant correlation between triglycerides and high density lipoprotein levels with APOE genotype in any of the tested groups. In conclusion, there was a decreased selected lipid serum profile parameters in AD compared to age matched non demented first degree relatives.

Adult↗
PubMed2000

Possible reverse transport of beta-amyloid peptide across the blood-brain barrier.

Our experiments were performed to test the hypothesis that human beta-amyloid peptide 42 (beta A) is able to enter and exit the brain parenchyma through the blood-brain barrier. In an effort to determine the effect of beta A in an animal model, we have injected beta A i.v. into rats following single and repeated brain ischemia. Rats were sacrificed at 3 and 12 months after injection and beta A was localized by monoclonal antibody (mAb) 4G8. The present observations revealed an abundant presence of beta A in the extracellular space of the brain, which appeared to be dilated, and a vigorous uptake of beta A into the cytoplasm of endothelial and ependymal cells, pericytes, astrocytes and neurons. Some of the beta A deposits were associated and/or had migrated to the vessels and to the ventricles, and by 3 months a significant amount of beta A was directly associated with the vessels and was observed inside the ventricular space. Virtually no soluble and aggregating beta A was found in brain tissue 1 year later. This suggests that phagocytic pericytes and astrocytes take up exogenous beta A in an attempt to clear the peptide from the brain extracellular space and deliver it to the circulation. Further, direct removal of beta A from the ventricles by the bloodstream is also possible. These observations suggest that a reverse transport of beta A across endothelial cells of microvessels represents one of the possible mechanisms responsible for removal of extravasated beta A. The findings of the present study indicate that in normal conditions beta A is rapidly cleared from the cerebrospinal fluid and brain parenchyma, suggesting that irreversible changes in the physico-chemical properties of the cerebrovascular endothelial cell surface are involved in beta A deposition in the brain in Alzheimer's disease (AD).

Alzheimer Disease↗
PubMed2000

A new point mutation of the PRNP gene in Gerstmann-Sträussler-Scheinker case in Poland.

We report here a case of Gerstmann-Sträussler-Scheinker (GSS) disease with a new mutation at the codon 232 (Met to Thr) of the PRNP gene. This case was characterized by PrP-immunopositive kuru and multicentric plaques; these plaques were also seen in the cerebral cortex, hippocampus and in the deep subcortical nuclei. Diffuse PrP depositions were also detected. In the temporal cortex, a few plaques were immunopositive for both PrP and Abeta; the latter was expressed at the periphery of the PrP-immunopositive cores. This mutation was absent from 40 healthy Polish controls and from 16 other Polish CJD cases, and we therefore believe that 232Thr is a new pathogenic mutation and not a benign polymorphism.

Amino Acid Substitution↗
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↗