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1

Amyloid protein - cause or effect of Alzheimer's disease ?

100%
Leszek J.
Postępy Higieny i Medycyny Doświadczalnej
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1994
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vol. 48
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issue 1
1-18
2
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The transmissible brain amyloidoses: a comparison with the non transmissible brain amyloidoses of Alzheimer type

100%
Liberski P. P.
Acta Neurobiologiae Experimentalis
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1993
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vol. 53
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issue 1
337-349
EN
I report here the basic concepts of the transmissible and non-transmissible cerebral amyloidoses. The pathogenesis of both types of brain amyloidoses consist of a synthesis of amyloid precursor followed by its processing to yield a final postranslationally modified deposit. PrPc and APP serve as precursor proteins while modified PrP (PrPsc and PrP 27-30) and beta-A4 as final deposits in transmissible and non-transmissible brain amyloidoses, respectively. The hallmark of both types of brain amyloidoses is amyloid deposits immunureactive to appropriate amyloids. Other, mostly unspecific, neuropathological phenomena as neurofibrillary tangles, dystrophic neurites and granulovacuolar degeneration are also discussed. The only disease-specific structure for transmissible cerebral amyloidoses are tubulovesicular structures of unknown biological significance. They may even be the infectious virus.
3

Molecular genetics of Alzheimer?s disease: Presenilin 1 gene analysis in a cohort of patients from the Pozna? region

80%
Kowalska A., Wender M., Florczak J., Pruchnik-Wolinska D., Modestowicz R., Szczech J., Rossa G., Kozubski W.
Journal of Applied Genetics
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2003
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vol. 44
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issue 2
231-234
EN
Alzheimer?s disease (AD) is a progressive neurodegenerative disorder characterized by memory loss and personality changes. Pathological hallmarks of AD are: deposition of amyloid plaques and neurofibrillary tangles in the brain, accompanied by neuronal and synaptic loss. The genetic background of AD is heterogeneous and strongly depends on the form of the disease. In most of the families with early-onset AD (EOAD) (10% of the total population of patients), the disease segregates as an autosomal dominant fully penetrant trait. To date, some missense mutations in three genes encoding the amyloid precursor protein, presenilin 1 (PS1) and 2 (PS2) have been found to cause familial EOAD. We screened for mutations in the presenilin genes in a sample of 55 patients with familial or sporadic form of EOAD from the Poznan region. We found 4 missense mutations in the PS1 gene: A246E in exon 7, P267L in exon 8, E318G in exon 9, and L424R in exon 12 among 5 unrelated patients. The frequency of PS1 mutations was 11% (5 of 55) in the whole sample of the patients with EOAD or 50% (3 of 6) if the analysis was restricted to familial cases with a positive history of dementia in the patient?s family.
4
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ApoE polymorphism in Polish patients with Alzheimer's disease

80%
Lalowski M., Czyzewski K., Pfeffer A., Barcikowska M., Kwiecinski H. l.
Acta Neurobiologiae Experimentalis
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1998
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vol. 58
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issue 1
65-68
EN
Alzheimer's disease is a genetically heterogeneous disorder of CNS. The presence of APOE-epsilon4 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-epsilon4 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 APOEepsilon4, epsilon3,epsilon2 allele frequency was 0.333, 0.65 and 0.017 respectively.
5
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Alzheimer's disease - immunological aspects

80%
Leszek J., Dobrzanska I., Gasiorowski K.
Acta Neurobiologiae Experimentalis
|
1993
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vol. 53
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issue 1
351-355
EN
Alzheimer's Disease (A.D.) is a multifarious, complex syndrome, which probably comprises different etiopathogenic subunits. Work by several authors has shown immunological disturbances in A.D. underlining the importance of immunological imbalance in the explanation of the etiopathogenesis and progress of some forms of A.D. An early diagnosis of A.D. is important because changes in central nervous system respond well to immunomodulatory treatment in the early course of disease. This justifies a search for diagnostic methods permitting an early diagnosis of the disease and establishment of immunological disturbances and consequently an early start of treatment. In the present paper, the literature regarding immunological disturbances observed in A.D. patients is reviewed.
6
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Expression of astroglial nerve growth factor in damaged brain

80%
Oderfeld-Nowak B., Bacia A.
Acta Neurobiologiae Experimentalis
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1994
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vol. 54
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issue 2
73-80
7
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Dilatation of the lateral part of the transverse fissure of the brain in Alzheimer's disease

80%
Narkiewicz O., Leon M., Convit A., George A. E., Wegiel J., Morys J., Bobinski M., Colomb J., Miller D. C., Wisniewski H. M.
Acta Neurobiologiae Experimentalis
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1993
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vol. 53
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issue 3
457-465
EN
Post-morten MRI (magnetic resonance images) studies followed by histopathological examination were used to study the size and the shape of the of the of the in seven individuals with Alzheimer disease (AD) and five controls. Incontrol brains, the lateral part of the transverse fissure is a narrow cleft protruding laterally as choroid and hippocampal recesses. In AD-affected brains, the lateral part of the transverse fissure becomes a large subarachnoid space as a result of different degrees of atrophy of various hippocampal and parahippocampal structures. Our findings directly indicate the relationship between changes in the hippocampal and parahippocampal structures and the size of the lateral part of the transverse fissure. Sector CA1, the subiculum, the entorhinal cortex, and the parahippocampal isocortex are the most affected, whereas the dentate gyrus is much less affected. Adjacent thalamic structures, which are less vulnerable to the AD pathology, do not appear to contribute to transverse fissure changes. The size and the shape of the lateral part of the transverse fissure of the brain in AD reflect the atrophy of the hippocampus and parahippocampal structures.
8
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Lipid metabolism parameters in patients with Alzheimer disease and their first degree relatives

70%
Czyzewski K., Lalowski M. M., Pfeffer A., Barcikowska M.
Acta Neurobiologiae Experimentalis
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2001
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vol. 61
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issue 1
21-26
EN
Recently, it was suggested that the presence of total cholesterol (TC), age and sex interaction in Alzheimers 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.
9

Biochemical properties and clinical effects of the products formed during the glycation of proteins

70%
Staniszewska M., Gamian A.
Postępy Higieny i Medycyny Doświadczalnej
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2003
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vol. 57
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issue 2
123-147
EN
Advanced glycation end-products (AGEs) are formed during non-enzymatic glycation - the process occurring in vitro and in the organism. The glycation products accumulate in tissues and interact with specific receptors, what induces various cellular responses. Some enzymes important in metabolism can be also glycated. The disturbances of homeostasis, related to the glycation products, are the reason for complications observed in diabetes and aging processes. There are presented in this paper: mechanism of the formation of AGEs, their cellular receptor (RAGE), as well as the effects of glycation in aging, diabetes and Alzheimer disease. Finally, there are described the compounds which could be useful as inhibitors of glycation in clinical practice.
10

Experimental and clinical aspects of neurotoxic effect of aluminium

70%
Nowak P., Brus R.
Postępy Higieny i Medycyny Doświadczalnej
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1996
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vol. 50
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issue 6
621-633
EN
In the paper there were described some problems concerning influence of aluminium on central nervous system mainly. It was shown some aspects of neurotoxic action of aluminium in experimental studies and in some clinical disorders probability connected with intoxication of aluminium.
11

Disturbances in neurotransmission processes in aging and age-related diseases

61%
Ossowska K.
Polish Journal of Pharmacology
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1993
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vol. 45
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issue 2
109-131
EN
This paper reviews the changes in dopaminergic, cholinergic and glutamatergic neurotransmission, which occur in the aging of central nervous system CNS and in age-related diseases: Parkinson's disease (PD) and Alzheimer's disease (AD).
12
Content available remote

Molecular biology of brain aging and neurodegenerative disorders

61%
Wisniewski T., Frangione B.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 1
267-279
EN
A significant component of the aging process is genetically determined. Numerous theories of aging exist, many of which postulate the existence of "longevity genes". Recent advances in molecular biological and other techinques have allowed a significantly greater understanding of aging and age-related disease. This will be illustrated by four genetic and sporadic diseases: Alzheimer's disease (AD) and related disorders, transthyretin dementia, cerebral amyloid angiopathy-Icelandic type and scrapie related diseases. Alzheimer's disease (AD), the most common of this group, is the leading cause of dementia in Western countries. Recent genetic and biochemical studies have shown in involvement of at least four genes in the pathogenesis of AD. In early-onset familial AD mutations in the (beta)PP, S182 (presenilin 1) and STM2 (presenilin 2 or E5-1) genes have been found, while in the more common late-onset AD the presence of the apolipoprotein E4 isotype is a major risk factor. Genetic studies have also helped to elucidate the etiology of rarer cerebral amyloidoses such as the recently described Hungarian amyloidosis that is characterized by meningocerebrovascular amyloid deposition, with resultant dementia. This disease is linked to a mutation in the transthyretin gene. It is hoped that in the near future this increase in knowledge will allow the development of therapeutic approaches to slow the aging process.
13
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The second layer neurones of the entorhinal cortex and the perforant path in physiological agening and Alzheimer's disease

61%
Morys J., Sadowski M., Barcikowska M., Maciejewska B., Narkiewicz O.
Acta Neurobiologiae Experimentalis
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1994
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vol. 54
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issue 1
47-53
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