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Biomedical subjects

J Kálmán

Publications and source records attributed to J Kálmán.

At least 19 recordsLinked to original sources
PubMed2006

Unchanged rat brain amyloid precursor protein levels after exposure to benzodiazepines in vivo.

BACKGROUND AND OBJECTIVE: Recent studies emphasize a positive correlation between (cardiac) surgical interventions and increased risk for developing Alzheimer's disease in the late postoperative period. Since amyloid precursor protein and its neurotoxic derivatives play key roles in the development of Alzheimer's dementia, the impact of several agents used in the intra- and perioperative period is examined. METHOD: Amyloid precursor protein concentrations were assessed by semi-quantitative Western-immunoblot in brains of rats following intraperitoneal treatment with diazepam and midazolam. RESULTS: There were no significant changes in the amyloid precursor protein concentrations. CONCLUSION: Both diazepam and midazolam are considered to be relatively safe with respect to amyloid precursor protein metabolism.

Alzheimer Disease↗
PubMed2005

Gene expression profile analysis of lymphocytes from Alzheimer's patients.

Since the function and metabolism of peripheral lymphocytes is known to be altered in Alzheimer's disease (AD), a pilot study was carried out to examine differences in gene expression profiles of these cells in 16 AD patients and aged control probands. Using a cDNA microarray representing 3200 distinct human genes, we identified 20 candidate genes whose expression is altered in AD lymphocytes compared with the control probands. Among these were the alpha2C-adrenoreceptor gene, known to regulate blood pressure and learning, the defensin, histocompability complex enhancer-binding protein, carboxypeptidase M, and the Fc fragment of IgE known to be involved in cellular and humoral immune responses. Others, like human cell death protein, TRAIL, and galectin-4 participate in the regulation of apoptosis. Real-time quantitative reverse transcription-polymerase chain reaction analysis was performed in order to confirm the expression changes in AD lymphocytes, and it could detect down-regulation of defensin and alpha2c-adrenoceptor genes, while other genes seemed unaltered in their expression, including heat-shock protein (hsp90), cholesteryl ester transfer protein, and apolipoprotein B100 (apoB). The altered expression profile of these genes might be connected with the previously reported AD-specific lymphocyte abnormalities. It remains to be elucidated, however, how these genes are related to the pathomechanism of dementia and whether the gene expression differences of AD lymphocytes reflect disease traits or stage processes.

Aged↗
PubMed2002

Codon 311 (Cys --> Ser) polymorphism of paraoxonase-2 gene is associated with apolipoprotein E4 allele in both Alzheimer's and vascular dementias.

The gene of an esterase enzyme, called paraoxonase (PON, EC.3.1.8.1.) is a member of a multigene family that comprises three related genes PON1, PON2, and PON3 with structural homology clustering on the chromosome 7.(1,2) The PON1 activity and the polymorphism of the PON1 and PON2 genes have been found to be associated with risk of cardiovascular diseases such as hypercholesterolaemia, non-insulin-dependent diabetes, coronary heart disease (CHD) and myocardial infaction.(3-8) The importance of cardiovascular risk factors in the pathomechanism of Alzheimer's disease (AD) and vascular dementia (VD)(9-13) prompted us to examine the genetic effect of PON2 gene codon 311 (Cys-->Ser; PON2*S) polymorphism and the relationship between the PON2*S allele and the other dementia risk factor, the apoE polymorphism in these dementias. The PON2*C and PON2*S allele frequencies were similar in both AD (25% and 75%) and VD groups (23% and 77%), respectively, compared with the controls (27% and 73%). The ratio of the PON2*S carriers was significantly higher among the apoE4 allele carrier AD (27%) and VD (25%) groups than in the control (12%). Our results indicate that the PON2*S and apoE4 alleles have interactive effect on the development of the two most common forms of dementias AD and VD, and further support the hypothesis that cardiovascular factors contribute to the development of AD.

Aged↗
PubMed2001

UVB irradiation-induced apoptosis increased in lymphocytes of Huntington's disease patients.

Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by CAG repeat expansion in the IT-15 gene coding for huntingtin. The mechanism of neuronal degeneration induced by the mutant huntingtin is not known. Apoptosis may play a role in it. Huntingtin is widely expressed in the cells, so abnormalities can be expected also in non-neural tissue. We examined the susceptibility of lymphocytes from HD patients, asymptomatic carriers and normal individuals to UVB irradiation-induced apoptosis. Lymphocytes from eight HD patients and two asymptomatic carriers showed increased apoptotic cell death compared to controls. Our results suggests that sensitivity of HD cells to induced apoptosis is not restricted to neurons.

Adult↗
PubMed2001

[Severe necrotic processes of the penis and scrotum].

Authors summarise the two-decade experience of their department in severe tissue necrosis of penis and scrotum. Presented cases represent a shared field of urology with dermatology, infectology, nephrology and andrology. Tissue necrosis extended to different depth of the penis, from superficial skin and subcutaneous tissues, fascias to the entire organ. Underlying diseases are acute and chronic inflammations, metabolic diseases, vascular lesions. Diagnostic difficulties and therapeutic choices, both conservative and operative, are discussed.

Abscess↗
PubMed2001

High cholesterol diet down regulates the activity of activator protein-1 but not nuclear factor-kappa B in rabbit brain.

Cardiovascular risk factors and alterations in cholesterol metabolism are implicated in the pathogenesis of Alzheimer's dementia (AD). The hypercholesterolemic rabbit model of atheroslerosis and AD was utilized in this study to examine oxidative stress related changes in the brain. The high cholesterol diet induced dramatic increases in plasma and liver cholesterol concentrations, but brain cholesterol levels remained constant. Similar effects have been found regarding lipid oxidation products. The amounts of conjugated dienes, trienes and thiobarbituric acid reactive substances (TBARS) significantly increased in the plasma of cholesterol treated animals while the brain cortex showed no signs of increased lipid peroxidation. The oxidative damage sensitive nuclear transcription factor kappa B (NF-kappaB) and activator protein-1 (AP-1) diverged in their responses. Accordingly, the AP-1 DNA binding activity decreased by more than 50% in brain nuclear protein extracts while the NF-kappaB binding activity remained unaltered by the hypercholesterol diet. These results indicate that despite the relative resistance of the central nervous system to dietary manipulation of its lipid composition and lipid peroxidation products, chronic dietary intake of cholesterol can alter the function of certain proteins involved in regulation of gene expression in the brain.

Animals↗
PubMed2001

Are Alzheimer's disease patients able to learn visual prototypes?

Recently, controversial results emerged regarding visual prototype learning in Alzheimer's disease (AD). The aim of this study was to elucidate this issue in a larger population of AD patients. The AD patients (N=72) and age-matched healthy control subjects (N=25) learned to recognize and to categorize visual dot patterns. In comparison with the control subjects, the AD patients as a group showed dysfunctions in the recognition task, whereas categorization was relatively spared in their case. Recognition was impaired in patients with mild AD (Mini-Mental score: 18-23) and moderate AD (Mini-Mental score<18), whereas categorization was impaired only in patients with moderate AD. These results suggest that while the medio-temporal/diencephalic explicit memory system is markedly affected even in early AD, the sensory neocortical areas mediating implicit category learning display a sufficient degree of functional capacity until later stages of the disease.

Aged↗
PubMed2001

Comparative studies on [Ca2+]i-level of fibroblasts from Alzheimer patients and control individuals.

The accumulation of the beta-amyloid peptide (betaAP) in the brain, produced from the ubiquitously expressed amyloid precursor protein (APP) is a defining feature of Alzheimer's disease (AD). Consistent with studies demonstrating the importance of skin biopsy in the diagnosis of neurodegenerative disorders, we investigated whether differences in intracellular free calcium levels ([Ca2+]i) of cultured cutaneous fibroblasts derived from sporadic AD patients and from age-matched control individuals might be present. [Ca2+]i was measured in Fura-2AM-loaded human fibroblasts by dual wavelength spectrofluorimetry. AD cells exhibited lower [Ca2+]i as compared to the control cultures. Exposure of fibroblasts to betaAP resulted in increased [Ca2+]i of the control cells, but not of AD fibroblasts. Our test could prove useful in supporting the diagnosis of (sporadic) AD in patients suspected of suffering from the disease.

Aged↗
PubMed2000

Serum and cerebrospinal fluid cystatin C levels in vascular and Alzheimer's dementia.

INTRODUCTION: Cystatin C, a cysteine protease inhibitor, has been implicated in the neurodegenerative and repair processes of the nervous system, and the deposition of the same protein together with beta amyloid peptide was found as cerebral amyloid angiopathy (CAA) in different types of dementias. OBJECTIVE AND METHODS: Because of the differential diagnostic importance, serum and cerebrospinal fluid (CSF) cystatin C levels of 24 late onset Alzheimer's demented (AD) and 16 ischemic type of vascular demented (VD) probands were compared with 17 aged control (AC) persons. RESULTS: The serum and CSF cystatin levels were found in the normal range in all groups. The ischemic VD probands had the tendency to have higher cystatin C levels than the AD. No correlation has been found with the severity and duration of dementia and with the other measured parameters. CONCLUSION: These results indicate that lower than normal CSF cystatin C level is not a diagnostic marker in ischemic VD and CAA related to AD.

Aged↗
PubMed1999

Early visual impairment is independent of the visuocognitive and memory disturbances in Alzheimer's disease.

Static and dynamic contrast sensitivity (SCS and DCS), semantic object identification, and verbal recall functions were evaluated in 20 Alzheimer's disease (AD) patients and in 20 control subjects. We found general SCS and DCS loss in the 0.48-14.34 c deg-1 spatial frequency range. In relation to the cognitive functions, semantic object identification was intact, whereas explicit memory was markedly impaired in the AD group. There was no significant correlation between the CS and the memory disturbances. The results suggest that early visual impairment and higher-level cognitive disturbances are independent in AD.

Aged↗
PubMed1999

Classification learning in Alzheimer's disease.

Previous research has demonstrated that explicit recognition of dot patterns is impaired in amnesic patients with damage to the limbic-diencephalic memory system, while implicit categorization of the same kind of stimuli is preserved. The aim of the present study was to investigate the relationship between recognition and categorization performances in patients with Alzheimer's disease. Consistent with the findings in amnesic subjects, our results revealed that the explicit recognition of dot patterns was significantly impaired in Alzheimer's disease. However, implicit categorization functions were also disrupted. This was selective for the prototype stimuli; the categorization of non-prototype dot patterns was spared. The impaired category learning is likely to reflect the damage of modality-specific neocortical areas in Alzheimer's disease.

Aged↗
PubMed1998

No mitochondrial haplotype was found to increase risk for Alzheimer's disease.

BACKGROUND: Seventy Alzheimer's disease (AD) patients and 80 age- and sex-matched controls were analyzed for mitochondrial mutations T4336C and A3397G, reported to be associated with AD, and for mutations T4216C/G13708A characteristic for a normal human haplotype associated with increased frequency of occurrence of some hereditary diseases. The distribution of apolipoprotein E (apoE) alleles was also analyzed. METHODS: Mitochondrial DNA was amplified by polymerase chain reaction, and the presence of mutations was detected by digestion with approximately chosen restriction endonucleases (restriction fragment length polymorphism). RESULTS: One patient and 2 controls were found to belong to the T4336C/T1630C haplotype. No A3397G mutant was detected. The T4216C/G13708A haplotype occurred at 5/70 and 5/80 frequency in the two groups. Prevalence of the apoE4 allele was significantly higher in AD patients (25%) than in the control group (8.1%). CONCLUSIONS: The T4336C/T16304C mutations were not found to associated with AD, and no predisposing mitochondrial haplotypes were found.

Aged↗
PubMed1998

Increased apolipoprotein E4 allele frequency is associated with vascular dementia in the Hungarian population.

INTRODUCTION: The regulatory role of apolipoprotein E in lipid transport and metabolism was utilized to investigate the allelic association between the apolipoprotein E4 (apoE4) allele and vascular dementia (VD) in a selected sample of Hungarian patients with multiple deep subcortical infarcts and leukoaraiosis. MATERIAL AND METHODS: Thirty-four Caucasian VD cases and 79 healthy control probands were involved in this study according to the criteria of ICD-10 and NINDS-AIREN International Workshop Diagnostic Criteria. The genomic DNA was isolated from whole blood and the apoE alleles were determined by polymerase chain reaction. RESULTS: The E2, E3 and E4 allele frequencies in the VD group were 5%, 76%, and 19%, respectively; and significant (P<0.03) differences were found in comparison with the data on the healthy controls (E2, 6%; E3, 87%; E4, 8%). The apoE4 allele frequency was intermediate between HC and Alzheimer's dementia group (28%). CONCLUSION: These results indicate that the apoE4 allele could be a risk factor not only for certain primary degenerative, but also for vascular dementias.

Aged↗
PubMed1997

Association of the apolipoprotein A-IV codon 360 mutation in patients with Alzheimer's disease.

Specific apolipoprotein E (apoE) alleles determines, in large part, the risk and mean age of onset familial and sporadic Alzheimer disease. The unresolved issues in this relationship support the contribution of other environmental and genetic parts. Among the candidates the apolipoprotein A-IV (apoA-IV) a component of plasma lipid particles similar to apoE has been suggested to play a role in brain metabolism. Since apoA-IV has a common DNA based protein polymorphism with a different function we determined apoA-IV (360:Gln:His) DNA polymorphism in 63 late-onset sporadic Alzheimer's patients. We found that the APOA-IV (360:His) heterozygosity occurs significantly more frequent (20.6% vs. 7.0%, P = 0.021, odds ratio 3.4 (confidence interval 1.1-10.2)) comparing age-matched controls with normal mental score. The significant difference in apoA-IV allelic distribution has been detected dominantly in patients with non-apoE4 genotype. Our data indicate that the apoA-IV-2 allele may confer one of the susceptibility markers for Alzheimer's disease (AD) and strengthen the polygenic risk determination of the variability in expression of AD.

Aged↗
PubMed1997

[Prion dementias: nosology and diagnostic difficulties in the spectrum of Creutzfeld-Jakob encephalopathy].

Creutzfeldt-Jakob disease (CJD) is one form of subacute prion diseases with spongiform encephalopathy. Hereditary, infectious and sporadic types of the disorder can be distinguished. The abnormal transformation of the prion protein, relevant in the normal synaptic transmission is considered as an important factor in the development of this disease. Gerstmann-Sträussler-Scheinker syndrome (GSS) and familial fatal insomnia (FFI) are the other diseases belonging to the same disease spectrum. The common feature of these disorders is that the different mutation of the same prion protein could result in different phenotypes and symptoms. CJD is considered as a neurologic disorder but the clinical symptoms and differential diagnosis of the disease are also relevant problems in psychiatry. Because of the early onset of dementia and the psychotic and delusive symptoms, the patients with CJD are frequently admitted to psychiatric wards. Recently worldwide public interest has been focused on prion dementias because of the possible human transmission of bovine spongiform encephalopathy in the UK. The diagnostic problems of our seven CJD patients diagnosed since 1991 in the catchment area of Szeged city are discussed in the view of recent findings of molecular biology, nosology, diagnostic and therapeutic problems of this devastating disease.

Adult↗
PubMed1997

Experimental immune-mediated damage of septal cholinergic neurons.

Degeneration of cholinergic neurons in the medial septum and the diagonal band of Broca is a frequent neuropathological feature of Alzheimer's disease. To determine whether an immune process can injure these basal forebrain cholinergic neurons, we serially immunized guinea pigs with septal cholinergic hybrid cells (SN-56). Following immunization, a relatively selective damage of septal cholinergic neurons, reduction in septal choline acetyltransferase (ChAT) activity and decrease in acetylcholine release in hippocampus were detected. Serum IgG from guinea pigs immunized with SN-56 cells and stereotactically injected into the medial septal region of rats produced a loss of ChAT activity in the medial septum, frontal cortex and hippocampus, together with impairment of learning and long term spatial memory. These data suggest that relatively selective damage to septal cholinergic neurons can be caused by an immune-mediated process in experimental animals.

Alzheimer Disease↗