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Biomedical subjects

K Jellinger

Publications and source records attributed to K Jellinger.

At least 91 records · Page 5Linked to original sources
PubMed1994

Amygdala pathology in Parkinson's disease.

The amygdala undergoes severe pathological changes during the course of Parkinson's disease (PD). Lewy bodies and Lewy neurites are distributed in a specific manner throughout the nuclear complex. The lesional pattern displays only minor interindividual variation. The most prominent changes occur in the accessory cortical and central nuclei. The cortical, accessory basal and granular nuclei show less severe alterations, while the basal and lateral nuclei, as well as the intercalated cell masses, generally remain uninvolved. The amygdala receives a broad range of afferents, allowing integration of exteroceptive information with interoceptive data. It generates major projections to the isocortex (the prefrontal cortex in particular), limbic system (hippocampus and entorhinal region) and centers regulating endocrine and autonomic functions. The specific lesional pattern seen in PD destroys part of the nuclear gray matter and its connections and, thus, may likely contribute to the development of behavioral changes and autonomic dysfunctions.

Aged↗
PubMed1994

Patterns of oligodendroglia pathology in multiple sclerosis.

Patterns of inflammation, demyelination and oligodendrocyte pathology were studied in acute multiple sclerosis and during early and late exacerbations of chronic multiple sclerosis. Cells within lesions were identified by immunocytochemistry with markers for T lymphocytes, macrophages, oligodendrocytes and astrocytes. In addition, in situ hybridization for proteolipid protein mRNA was used to identify myelinating and myelin supporting oligodendrocytes. Degenerating cells in the lesions were detected by DNA fragmentation in cell nuclei. The inflammatory reaction in all three types of multiple sclerosis lesions was shown to be dominated by T lymphocytes and macrophages. In late chronic multiple sclerosis lesions, a significant increase in the number of immunoglobulin producing plasma cells was found in infiltrates as compared with acute and early multiple sclerosis lesions. In all three types of multiple sclerosis, confluent plaques of demyelination were found to be present. In acute multiple sclerosis, demyelination was found to be associated with extensive destruction of other tissue elements, including oligodendrocytes, astrocytes and axons, but even in these destructive lesions a considerable number of oligodendrocytes was preserved and at disposal therefore, for rapid remyelination. During early exacerbations of chronic multiple sclerosis, selective demyelination was associated with almost complete preservation of oligodendrocytes in the majority of cases. Correspondingly, a high number of remyelinating lesions was present at that stage of disease. In lesions developing late after onset of multiple sclerosis, demyelination generally accompanied extensive destruction and loss of oligodendrocytes. In these lesions, remyelination was sparse and restricted to lesional borders. The observed patterns of cell death suggest that in some cases oligodendrocytes, in others myelin sheaths are the primary target of the destructive process. Our data indicate that the type and amount of inflammation, de- and remyelination, and of tissue damage vary between different forms of multiple sclerosis and between different stages of the disease, possibly reflecting different pathogenic mechanisms in a disease spectrum.

Adult↗
PubMed1994

Preliminary NINDS neuropathologic criteria for Steele-Richardson-Olszewski syndrome (progressive supranuclear palsy).

We present the preliminary neuropathologic criteria for progressive supranuclear palsy (PSP) as proposed at a workshop held at the National Institutes of Health, Bethesda, MD, April 24 and 25, 1993. The criteria distinguish typical, atypical, and combined PSP. A semiquantitative distribution of neurofibrillary tangles is the basis for the diagnosis of PSP. A high density of neurofibrillary tangles and neuropil threads in the basal ganglia and brain-stem is crucial for the diagnosis of typical PSP. Tau-positive astrocytes or their processes in areas of involvement help to confirm the diagnosis. Atypical cases of PSP are variants in which the severity or distribution of abnormalities deviates from the typical pattern. Criteria excluding the diagnosis of typical and atypical PSP are large or numerous infarcts, marked diffuse or focal atrophy, Lewy bodies, changes diagnostic of Alzheimer's disease, oligodendroglial argyrophilic inclusions, Pick bodies, diffuse spongiosis, and prion protein-positive amyloid plaques. The diagnosis of combined PSP is proposed when other neurologic disorders exist concomitantly with PSP.

Brain↗
PubMed1993

Microglial reaction in Pick's disease.

Number and morphology of microglial cells (MC) were compared in 6 cases each of Pick's disease (PD), Alzheimer's disease (AD) and controls using immunohistochemistry with the monoclonal antibody Ki-M1P. The severely involved neocortex of both PD and AD, and in particular the white matter subjacent to spongy PD lesions showed a marked increase of MC density, whereas non-affected PD areas and AD white matter showed no MC changes. The PD hippocampus, particularly the dentate gyrus, showed reduction of MC density and processes. We conclude that (1) MC reaction represents a major element of PD histopathology, and (2) density, morphology and distribution of MC are different in AD and PD.

Aged↗
PubMed1993

Synaptic pathology of Alzheimer's disease.

Prospective clinico-pathological studies on dementia in Alzheimer's disease (AD), performed during the past decades, revealed a relatively poor correlation between the degree of clinical deficit and the severity of the typical neuropathological lesions of AD, the amyloid plaques and the neurofibrillary tangles. More recent data, obtained by electron microscopy, immunocytochemical as well as immunochemical techniques indicate that synaptic loss may be a better structural correlate of dementia than other brain lesions. Synaptic pathology is reflected by a loss of all major components of small synaptic vesicles and most peptides, stored in large dense cored vesicles. The significant increase of chromogranin A proprotein, a major component of large dense cored vesicles, may rather represent a defect of protein processing than preservation of a specific synaptic subpopulation. Within the brain of AD patients, the degree of synaptic loss is uneven. Most prominent reduction of synapses is found in the outer parts of the dentate gyrus molecular layer, possibly reflecting the destruction of neurons, located in the layer 2 of the entorhinal cortex. However, within the neocortex, no preferential loss of synapses in any of the cortical layers has been found. Cerebral amyloid deposition in diffuse plaques has little effect on synapse density and structure. However, within the dense amyloid core of a classical plaque, synapses are completely lost. In the surrounding neuritic portion of the plaques, synaptophysin reactivity is frequently increased, due to enlargement of synaptic boutons and to accumulation of synaptophysin in dystrophic axons. Although the reason for synapse loss in AD is yet unknown, most results suggest that it may reflect degeneration of neurons, projecting into the respective cortical areas.

Alzheimer Disease↗
PubMed1993

Comparison of integrin adhesion molecules expressed by primary brain lymphomas and nodal lymphomas.

The expression of 17 adhesion molecules was immunohistochemically examined in 5 primary cerebral lymphomas (PCL) and in 5 histologically similar nodal lymphomas (NL) to evaluate their possible involvement in selective targeting of lymphoma cells to the brain. PCL and NL tumor cells showed very similar expression patterns: they were consistently positive for alpha 3, alpha 4 and beta 1 integrin chains; negative for alpha 1, alpha 2, alpha 6, beta 3 and beta 4 integrin chains; and heterogeneous for alpha 5, alpha L, alpha M, alpha X, beta 2 and beta 7 integrin chains, as well as for intercellular adhesion molecule-1 (ICAM-1) and the selectin LECAM-1. Loosely infiltrating PCL showed lower levels of the alpha L beta 2 integrin than compact cell clusters. Vessels stained for ICAM-1 and vascular cell adhesion molecule-1 (VCAM-1). We conclude that the adhesion molecules implicated in the extravasation of non-neoplastic leukocytes (alpha 4 beta 1/VCAM-1 and alpha L beta 2/ICAM-1) are also expressed by both PCL and NL. The adhesion molecules examined are apparently not selective mediators of lymphoma cell homing to the brain, but at least alpha L beta 2 integrin might be related to the infiltration pattern of PCL within the brain parenchyma.

Antibodies, Monoclonal↗
PubMed1993

Schizophrenia: normal sequence in the dopamine D2 receptor region that couples to G-proteins. DNA polymorphisms in D2.

Because dopamine (DA) D2 receptors are a target in neuroleptic therapy and have been found to be elevated in schizophrenia, the human DA D2 receptor gene was examined for possible abnormalities in schizophrenia. Moreover, since D2 receptors in psychosis have a reduced coupling to D1 receptors, the cytoplasmic third loop of D2 was chosen for deoxyribonucleic acid (DNA) sequencing, since this region is essential for coupling to G-proteins. This region also contains exon 5, which is expressed in the long form of D2, but not in the short form of D2. In eight schizophrenia cases, this region had normal exon sequences (exons 4, 5 and 6), and normal sequences at its intron-exon junctions. However, exon 6 contained three DNA polymorphic base changes, and introns 4 and 5 revealed three missing bases and two polymorphic base changes, none of which would be expected to alter the D2 receptor protein in schizophrenia.

Amino Acid Sequence↗
PubMed1993

Human herpesvirus-6 and Epstein-Barr virus genome in primary cerebral lymphomas.

Using dot blotting, we found Epstein-Barr virus genome in three AIDS-related primary cerebral lymphomas (PCLs), but in none of 39 sporadic PCLs. Human herpesvirus-6 sequences were present only in one sporadic PCL, as revealed by polymerase chain reaction and Southern analysis. We conclude that these viruses do not appear to play a major role in PCL pathogenesis in immunocompetent subjects.

Aged↗
PubMed1993

[Pathology of the central nervous system in AIDS. An overview of 184 patients].

Based on a consecutive autopsy series of 184 patients with AIDS, a critical review of the pathology of the central nervous system (CNS) is given. The lesions can be divided into three groups: 1. opportunistic/non-opportunistic infections, 2. changes due to the human immunodeficiency virus (HIV), and 3. neoplasms. The frequency and morphology of CNS lesions in our cohort are compared with those in other series. Marked lesions of the CNS were found in 111 patients (60%), while mild/nonspecific changes were seen in 52 cases (28%). Toxoplasmosis (23%) was the most frequent CNS infection, followed by cytomegalovirus (17%), and papovirus (5%). HIV giant cell encephalitis, HIV leukoencephalopathy, vacuolar myelopathy and leukoencephalopathy were observed in 11%. Primary CNS lymphomas were present in 6%, while secondary involvement of the CNS in systemic lymphomas was seen in only two cases (1%). Lesions due to CNS infections in patients with AIDS often show atypical patterns, and frequently, there are multiple infections with simultaneous involvement of the CNS by lesions of different etiology. The present study confirms the frequent involvement of the CNS in AIDS, although there are differences in the incidence and pattern of lesions related to geographic and/or demographic factors.

AIDS Dementia Complex↗
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↗