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Biomedical subjects

J Ulrich

Publications and source records attributed to J Ulrich.

At least 127 records · Page 7Linked to original sources
PubMed1984

The effect of age on the microheterogeneous pattern of human myelin basic protein.

Dry weight, total basic protein and myelin basic protein (MBP) in human corpus callosum tissue were found to be significantly reduced with age, confirming other reports. The heterogeneous patterns of the MBP samples were investigated and could be classified into three groups: a normal one with peak 1 larger than peak 3; an old-age pattern with peak 1 smaller than peak 3; and a pathological pattern with peak 1 greatly reduced. Because peak 1 is the only one which is significantly reduced with age, it is suggested that future investigations could be simplified. The physiological and pathophysiological role of MBP heterogeneity is discussed.

Adult↗
PubMed1984

Studies on neurotransmitter binding in senile dementia. Comparison of Alzheimer's and mixed vascular-Alzheimer's dementias.

Binding of 3H-labeled agonists and antagonists to muscarinic-cholinergic, alpha- and beta-adrenergic, dopaminergic, serotoninergic, and opiate receptors was studied in four regions of the neocortex and in hippocampus, thalamus, putamen, and caudatus in autoptic material from patients with senile dementia of Alzheimer type and of mixed vascular-Alzheimer pathogenesis. Different patterns of changes in ligand binding were found for the two groups. Some of these changes were quantitatively correlated with the histological scores of plaques and neurofibrillary tangles.

Aged↗
PubMed1983

Neuritic plaques in senile dementia of Alzheimer type: a Golgi analysis in the hippocampal region.

Tissue sections from the hippocampal region of patients with senile dementia of Alzheimer type were examined in 75-100 microns thick vibratome sections impregnated by the Golgi-Cox method and counterstained with cresyl violet. The morphology of dendrites and axons with neuritic plaques was frequently abnormal. Abnormalities included pleomorphic outpouchings of terminal and preterminal dendritic and axonal segments, many of which contained filiform processes occurring singly and in tufts. The axon collaterals of some hippocampal neurons appeared to branch richly as they entered plaques. Impregnated neurites could occasionally be traced from a neuritic plaque to adjacent pyramidal and local circuit neurons. The findings confirm that local neurons of different types contribute dendrites and axons to plaques and that these processes may proliferate within the confines of the plaques.

Aged↗
PubMed1983

Immunocytochemical investigations of murine leukodystrophies. A study of the mutants 'jimpy' (jp) and 'myelin deficient' (mld).

Sections of the central nervous system of the leukodystrophic mouse mutants 'jimpy' (jp) and 'myelin deficient' (mld), as well as of healthy littermates, were immunostained for glial fibrillary acidic protein (GFA), myelin basic protein (MBP) and myelin-associated glycoprotein (MAG). Adjacent sections were stained conventionally for myelin. In jp, GFA-stained astrocytes were abnormally prominent already at the age of 12 days. A considerable amount of MBP and MAG was present in the vicinity of axons, although no myelin was visible in the conventional stains for myelin. In mld, GFA-staining astrocytes were present in normal numbers. MAG could be demonstrated in its normal localization along axons, but MBP was visible only in the comparatively old animal (85 days). Here, it was demonstrated in an abnormal site--the perikarya and the proximal parts of the processes of oligodendrocytes. Thin myelin sheaths present in this animal could not be stained for MBP.

Animals↗
PubMed1983

Neurologic complications induced by gold treatment.

Two patients developed a Guillain-Barre-like syndrome and a third suffered neuropathy and myokymia during therapy with sodium aurothiomalate. The cumulative dose at the time of development of neuropathy was different in all 3 cases. Evidence for gold toxicity was suggested by clinical, electromyographic, and histologic findings, as well as the disappearance of symptoms and signs on cessation of gold injections.

Aged↗
PubMed1983

Pick's disease: an immunocytochemical study of neuronal changes. Monoclonal antibodies show that Pick bodies share antigenic determinants with neurofibrillary tangles and neurofilaments.

We used rabbit antisera to the 210,000; 155,000; and 70,000 mol. wt. neurofilament - polypeptides and monoclonal antibodies (BF 10; RT97) known to react with human neurofilaments in an immunohistochemical study of neuronal changes in Pick's disease and in senile dementia of the Alzheimer type. Pick bodies as well as neurofibrillary tangles and neurites showed strong reactivity with the monoclonal antibodies but remained unlabeled when treated with the rabbit polyclonal antisera. Our results indicate that the stained material in Pick bodies share antigenic determinants with neurofibrillary tangles and neurofilaments.

Aged↗
PubMed1983

Immunocytochemical investigations of some human leukodystrophies.

One case of each of the following human leukodystrophies was examined immunocytochemically with antisera against myelin basic protein (MBP), myelin associated glycoprotein (MAG) and gliofibrillary acidic protein (GFA): Metachromatic leukodystrophy (MLD), connatal adrenoleukodystrophy (ALD), sudanophilic leukodystrophy of the adult (SLD) and connatal Pelizaeus-Merzbacher disease (PMD). A case of canine globoid cell leukodystrophy (GLD) was also included under the assumption that this disease was the same in the dog as in man. It was shown that the storage process in MLD and GLD did not involve MBP or MAG and that the breakdown of myelin with the formation of fat granule cells containing droplets of neutral fat in ALD and SLS proceeds in a similar way as in experimental Wallerian degeneration. In PMD, MBP is present in the vicinity of axons not surrounded by a myelin sheath demonstrable with conventional means. The globoid cells of GLD could be demonstrated to be of non-astrocytic origin.

Adolescent↗
PubMed1982

Evidence for a chronic axonal atrophy in oculopharyngeal "muscular dystrophy".

We report on morphometric investigations of peripheral nerves in a woman, who died at the age of 69, presenting the classical symptoms of oculopharyngeal muscular dystrophy (OPMD) and a typical family history with several members (males and females) affected over three generations. Evidence for chronic axonal atrophy was found in peripheral nerves and especially in oculomotor nerves with severe axon loss in endomysial nerve twigs of extraocular, laryngeal, and tongue muscles. Whereas limb muscles presented features of neurogenic atrophy, severe changes of "myopathic" type were evident in extrinsic eye muscles, laryngeal constrictor, tongue, and diaphragma. However, we interpreted these changes as neurogenic in origin in view of the severe denervation found in those muscles. Our findings suggest that OPMD is a disease of primary neurogenic origin rather than a primary myopathic disorder.

Aged↗
PubMed1982

Senile dementia of Alzheimer type: astroglial reaction to extracellular neurofibrillary tangles in the hippocampus. An immunocytochemical and electron-microscopic study.

Two types of Alzheimer neurofibrillary tangles may be found in the hippocampus in senile dementia of the Alzheimer type. Besides classical flame-shaped intraneuronal tangles, there are less compact tangles representing extracellular remnants of destroyed neurons with neurofibrillary change. Strong immunoreactivity for glial fibrillary acidic protein (GFA) was found in the second type of tangles, which was due to penetration of fine processes of fibrous astrocytes into bundles of paired helical filaments (PHF). PHF appear to be a strong stimulus for astrocytic reaction when they are not segregated from the neuropil by the neuronal cell membrane.

Aged↗
PubMed1982

Senile plaques and neurofibrillary tangles of the Alzheimer type in nondemented individuals at presenile age.

100 unselected brains of patients dying at the ages of 55--64 years were examined for the presence of Alzheimer type changes. These changes were found in 25 brains. This number is lower than that in a comparable investigation from Japan, but it is clearly above the number found in selected nondemented patients from England. Although none of the patients had suffered from an easily recognizable presenile dementia, an important proportion of them had been noted for unusual psychology. The occurrence of Alzheimer type changes was not dependent on the diseases the patients had suffered from.

Alcoholism↗
PubMed1982

Focal necrotizing brain stem encephalopathy and cranial radiculopathy in a kidney transplant recipient.

A 48-year-old female patient developed sensory and motor palsy of the V-Xth cranial nerves immediately after kidney transplantation due to terminal uremia. A second exacerbation followed about 4 weeks later. After 46 days post transplantation she died from bronchopneumonia. Autopsy showed multiple acute and subacute necrotic foci in proximal portions of the cranial nerves as well as a discontinuous necrotizing encephalopathy localized mainly in the subpial zone of the brain stem. The mechanism by which lesions of the nervous system were produced remains speculative. A possible neurotoxic role was attributed to the drugs administered after transplantation. Herpes virus hominis antigen could be demonstrated in the cells of the pons and of the trigeminal ganglion, but its presence was thought to be coincidental and probably not causally related to the described lesions.

Brain↗