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Biomedical subjects

K Jellinger

Publications and source records attributed to K Jellinger.

At least 109 records · Page 6Linked to original sources
PubMed1993

How to run a brain bank. A report from the Austro-German brain bank.

The sophisticated analysis of and growing information on the human brain requires that acquisition, dissection, storage and distribution of rare material are managed in a professional way. In this publication we present the concept and practice of our brain bank. Both brain tissue and information are handled by standardized procedures and flow in parallel from pathology to neuropathology and neurochemistry. Data concerning brain material are updated with clinical information gained by standardized procedures.

Austria↗
PubMed1993

[Necrotizing myopathy with antilipemic agents. Case report and review of the literature].

A 73 year old male who had been prescribed fenofibrate for years developed a slightly asymmetric paraparesis of both lower extremities. CPK values rose to 9800 U/l, EMG of the quadriceps femoris muscle was myopathic. Muscle biopsy revealed a necrotic myopathy. Discontinuation of fenofibrate induced a rapid decline of CPK values, followed by a slower remission of muscular symptoms and persisting pseudo-myotonic discharges in EMG. The spectrum of neuromuscular side effects of cholesterol lowering agents, consisting of myalgia, cramps and reversible CPK elevation, is discussed. Only rarely necrotic myopathies have been described.

Aged↗
PubMed1992

Reduced and oxidized glutathione in the substantia nigra of patients with Parkinson's disease.

Reduced and oxidized glutathione concentrations in post-mortem brain tissue from the substantia nigra of control subjects and patients with neuropathologically confirmed Parkinson's disease were measured by a coulometric method using high-pressure liquid chromatography and electrochemical detection. Reduced glutathione concentrations were decreased in the substantia nigra of parkinsonian patients compared with controls. Differences in the concentration of oxidized glutathione and in the percentage of oxidized glutathione of the total glutathione were not observed between parkinsonian and control subjects. The finding that oxidized glutathione is not decreased in Parkinson's disease suggests that the decrease in reduced glutathione is not exclusively the consequence of neuronal loss in the substantia nigra but may indicate a state of oxidative stress.

Aged↗
PubMed1992

Allocortical neurofibrillary changes in progressive supranuclear palsy.

Silver techniques for intraneuronal cytoskeleton abnormalities (neurofibrillary tangles and neuropil threads) and extracellular A4-amyloid deposits were used to examine lesions of the cerebral cortex in six cases of progressive supranuclear palsy (three were mentally unimpaired and three showed moderate degrees of dementia). Deposits of A4-amyloid protein occurred in small numbers or were absent. Neurofibrillary tangles and neuropil threads were present in all cases and were largely confined to the allocortex. A characteristic pattern of changes was found in the entorhinal cortex. The three mentally unimpaired individuals had mild cortical changes virtually confined to the transentorhinal region while all of the demented patients showed severe destruction of the superficial cellular layer in both the transentorhinal and entorhinal region. This pattern of allocortical destruction closely resembles that seen in clinically incipient Alzheimer's disease or in mentally impaired cases of Parkinson's disease. The entorhinal region receives dense input from isocortical association areas and projects via the perforant path to the hippocampal formation. The cells of origin of major portions of the perforant path are located within the superficial entorhinal cellular layer. Destruction of this layer partially or totally disconnects the hippocampus from the isocortex. The specific pattern of entorhinal destruction is considered to contribute to cognitive impairment and personality changes, frequently seen in patients with progressive supranuclear palsy.

Aged↗
PubMed1992

Circulating antineuronal antibodies reach neurons in vivo: an autopsy study.

In serum and cerebrospinal fluid of 6 out of 15 patients with small cell lung cancer circulating antineuronal antibodies could be detected by indirect immunofluorescence. None of the patients showed signs of a neurological paraneoplastic syndrome, usually associated with the presence of these antibodies. On sections of frontal brain, cerebellum, dorsal root ganglia and peripheral nerve, obtained at autopsy, a direct immunofluorescence test was performed. Only in antibody-positive individuals were membrane-bound immunoglobulin deposits detected on neurons of dorsal root ganglia and Purkinje cells. The present study showed that circulating antineuronal antibodies reach the central and peripheral nervous system in vivo. These findings support the theory that these antibodies might be directly involved in the pathogenesis of neurological paraneoplastic syndromes.

Autoantibodies↗
PubMed1992

Human brain phenolsulfotransferase. Regional distribution in Parkinson's disease.

Brain phenolsulfotransferase (PST) in 105.000 x g supernatant fractions prepared from post mortem human brain catalyzes the sulfate conjugation of dopamine (DA). Using 50 microM DA, the PST activity was linear up to one hour. The KM value for DA was 3.1 microM. Higher concentrations of DA from 25 b microM up caused inhibition of PST activity. Assessment of regional distribution in normal brain using 20 microM DA concentration revealed the highest PST activities in temporal and frontal cortex. About ten times lower activities were measured in parietal and occipital lobe, amygdala, hypothalamus, and hippocampus, whereas the nucleus accumbens, nucleus basalis of Meynert, caudate nucleus, and substantia nigra showed the lowest activities (about 1% of those in frontal and parietal cortex). In the brains of subjects with Parkinson's disease (PD) treated with levodopa, a significant reduction of PST activities was observed in hypothalamus, frontal and temporal cortex, amygdaloid nucleus, occipital and parietal cortex (between 20 and 38.8% of controls). Depletion of PST activity was less severe in hippocampus (46% of controls), nucleus accumbens, putamen, and substantia nigra (67 and 72% of controls, respectively). No changes were observed in the nucleus basalis of Meynert, while PST activity was increased in the caudate nucleus (174 to 203% of controls). The presented data indicate that on PD brain the PST activity is reduced in areas of the cerebral isocortex and limbic system, while in the basal ganglia it is either mildly reduced (putamen) or increased (caudate nucleus). Selective changes of PST activity in PD brain may indicate an important function of this enzyme in the metabolism and/or storage of DA under pathological conditions.

Aged↗
PubMed1992

Synaptic pathology in Alzheimer's disease: immunological data for markers of synaptic and large dense-core vesicles.

We have analysed several markers for small synaptic vesicles (synaptin-synaptophysin, p65 and SV2) and large dense-core vesicles (chromogranin A, secretogranin II/chromogranin C) in the brains of patients with Alzheimer's disease, and normal controls by immunoblotting and immunohistochemistry. In comparison to age-matched controls the levels of all three synaptic vesicle markers were decreased in temporal cortex of Alzheimer patients. On the other hand, the levels of chromogranin A were increased, and those of secretogranin II lowered. This resulted in a significant increase of the ratios of chromogranin A to synaptophysin, p65 or SV2 and of that for chromogranin A to secretogranin II. These increases were significantly correlated to clinical severity of dementia and extent of neuropathological changes. By immunohistochemistry a high percentage of senile plaques was found to contain chromogranin A-reactive dystrophic neurites, whereas synaptophysin reactivity within plaques was rare. These results indicate that the number of synaptic vesicles is lowered in Alzheimer's disease, and that one component of large dense-core vesicles, i.e. chromogranin A, is elevated. We, thus, suggest that in Alzheimer's brain distinct changes occur for both types of synaptic organelles.

Aged↗
PubMed1992

Iron-melanin complex in substantia nigra of parkinsonian brains: an x-ray microanalysis.

Using energy-dispersive x-ray analysis on an electron microscope working in the scanning transmission electron microscopy mode equipped with a microanalysis system, we studied the subcellular distribution of trace elements in neuromelanin-containing neurons of the substantia nigra zona compacta (SNZC) of three cases of idiopathic Parkinson's disease (PD) [one with Alzheimer's disease (AD)] and of three controls, in Lewy bodies of SNZC, and in synthetic dopamine-melanin chemically charged or uncharged with Fe. Weak but significant Fe peaks similar to those of a synthetic melanin-Fe3+ complex were seen only in intraneuronal highly electron-dense neuromelanin granules of SNZC cells of PD brains, with the highest levels in a case of PD plus AD, whereas a synthetic melanin-Fe2+ complex showed much lower iron peaks, indicating that neuromelanin has higher affinity for Fe3+ than for Fe2+. No detectable Fe was seen in nonmelanized cytoplasm of SNZC neurons and in the adjacent neuropil in both PD and controls, in Lewy bodies in SNZC neurons in PD, and in synthetic dopamine-melanin uncharged with iron. These findings, demonstrating for the first time a neuromelanin-iron complex in dopaminergic SNZC neurons in PD, support the assumption that an iron-melanin interaction contributes significantly to dopaminergic neurodegeneration in PD and PD plus AD.

Aged↗
PubMed1992

Interrater reliability in the neuropathologic diagnosis of Alzheimer's disease.

Three neuropathologists evaluated brain sections from 43 aged subjects for the presence of Alzheimer's disease. Moderate-to-substantial agreement was obtained. After discussion of disparate diagnoses, agreement was almost perfect for standardized and substantial for personal criteria. We conclude that reproducibility can be improved if diagnoses based on standardized criteria are discussed by at least two neuropathologists.

Aged↗
PubMed1992

[Classification and virus expression of primary cerebral lymphomas].

Fourty-three primary cerebral lymphomas (PCL) were histologically classified and examined for genome expression of Epstein Barr Virus (EBV) and human herpes virus 6 (HHV6) using dot blotting, polymerase chain reaction, and Southern blotting. Only 20 tumors (16 high grade and 4 low grade lymphomas) could be suitably placed into a category of the Updated Kiel Classification, whereas the non-classified 23 tumors were highly malignant B-lymphomas and referred to as small-cell (SC) or large-cell (LC) blastic PCL. Most of the LC PCL showed a tumor-like infiltration pattern with high cellular density and little remaining parenchyma, whereas the SC PCL more often showed an inflammation-like pattern characterized by loose arrangement of tumor cells and marked astrocytic, microglial and T-lymphocytic reaction. EBV genome was found in 3/3 AIDS cases, but in none of 40 immunocompetent cases, while HHV6 was detected in 2 tumors of immunocompetent patients. We conclude that (1) the Updated Kiel Classification is not applicable to a majority of PCL, and (2) EBV and HHV6 do not appear to play a major role in the pathogenesis of PCL in immunocompetent subjects.

Autopsy↗
PubMed1992

Type VIII collagen in the normal and diseased human brain.

Type VIII collagen has been localized to specialized extracellular matrices in fetal tissues and has been suggested to be associated with cellular proliferation and angiogenesis (Sage and Iruela-Arispe 1990). In view of this hypothesis we studied its distribution in the normal and diseased human brain. Focal immunoreactivity was seen in histologically abnormal vessels of all 10 angiomas and 40 of 52 brain tumors. Staining was very weak in 3 embryonal and fetal brains, and it was absent in 20 normal adult brains and in 15 adult brains showing various cerebrovascular abnormalities. Our results provide additional evidence for the participation of type VIII collagen in some types of angiogenesis.

Adolescent↗
PubMed1991

Morphometry of the corpus callosum in normal aging and Alzheimer's disease.

Changes of the human corpus callosum in normal aging and Alzheimer's disease were analysed by means of morphometry. A standardized computerized evaluation program was implemented allowing objective, quantitative and reproducible data. The various parts of the corpus callosum showed a different pattern of changes in normal aging as compared to Alzheimer's disease. In conclusion, in normal aging affects mostly the front-temporal interhemispheric fiber systems, whereas in Alzheimer's disease the parietotemporal commissural fibers are altered.

Aging↗
PubMed1991

Glutamate receptor antagonism: neurotoxicity, anti-akinetic effects, and psychosis.

There is evidence to suggest that glutamate and other excitatory amino acids play an important role in the regulation of neuronal excitation. Glutamate receptor stimulation leads to a non-physiological increase of intracellular free Ca2+. Disturbed Ca2+ homeostasis and subsequent radical formation may be decisive factors in the pathogenesis of neurodegenerative diseases. Decreased glutamatergic activity appears to contribute to paranoid hallucinatory psychosis in schizophrenia and pharmacotoxic psychosis in Parkinson's disease. It has been suggested that a loss of glutamatergic function causes dopaminergic over-activity. Imbalances of glutamatergic and dopaminergic systems in different brain regions may result in anti-akinetic effects or the occurrence of psychosis. The simplified hypothesis of a glutamatergic-dopaminergic (im)-balance may lead to a better understanding of motor behaviour and psychosis.

Animals↗