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Biomedical subjects

J Ulrich

Publications and source records attributed to J Ulrich.

At least 109 records · Page 6Linked to original sources
PubMed1987

Neurofibrillary tangles and the neuronal cytoskeleton.

Antibodies to neurofilaments and the microtubule-associated protein, tau, have been used with anti-paired helical filament (PHF) serum to study Alzheimer neurofibrillary tangles. Tangles and their constituent PHF contain epitopes derived from or cross-reactive with both neurofilaments and tau proteins. These same structures are labelled with anti-PHF antibodies. A component of the anti-PHF serum is against tau proteins. We conclude that PHF are at least in part derived from an abnormal neuronal cytoskeleton.

Alzheimer Disease↗
PubMed1987

Cytoskeletal immunohistochemistry of Alzheimer's disease.

The first half of this paper is devoted to a review on the cytoskeletal immunocytochemistry of the various morphological changes in Alzheimer's disease (AD), i.e. neurofibrillary tangles (NFT), senile plaques (SP), granulovacuolar degeneration (GV) and Hirano bodies (HB). In the second half it is demonstrated that sera raised against the paired helical filaments (PHF) in NFT, and monoclonal antibodies to phosphorylated epitopes on neurofilament proteins, also stain structures within neuronal perikarya without PHFs in some diseases. These include Pick bodies and swollen cells in Pick's disease, neurons in old dogs without NFTs, and occasional neurons without NFT in AD. We conclude that PHF constituent proteins can be accumulated in neuronal perikarya of cases with these diseases without being actually assembled to PHFs. In AD and in the old dogs, such accumulations occurring without the formation of PHFs might represent a precursor state of the latter.

Alzheimer Disease↗
PubMed1986

Dementia of Alzheimer type (DAT)--a review of its morbid anatomy.

The most important morphological findings in dementia of Alzheimer type (DAT) are Alzheimer neurofibrillary tangles, senile plaques, amyloid angiopathy, granulovacuolar degeneration and Hirano bodies. The morphological and immunocytochemical findings in these changes are described, in particular those related to the pathological cytoskeleton. Their possible relationship to the disturbed synthesis of neurotransmitters recently demonstrated is considered, and their relevance for the clinical syndrome of dementia is discussed. Hypothetical etiologies (ageing per se, genetics, infection and chronic intoxication) are briefly mentioned.

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PubMed1986

The brain diseases causing senile dementia. A morphological study on 54 consecutive autopsy cases.

Brains from 54 patients with organic dementia were examined systematically. As in previous investigations a predominance of Alzheimer type changes was observed. Seventeen patients showed Lewy bodies in the nucleus basalis, the substantia nigra and the locus coeruleus as well as other lesions of parkinsonian type. In 5 cases these changes were thought to be responsible for dementia. In 8 patients no convincing morphological substrate of dementia was found. These patients were older than average; therefore age per se might have been responsible for dementia. It is emphasized that subjective judgements are almost unavoidable in assessing the cause of organic dementia.

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PubMed1986

Alzheimer neurofibrillary tangles contain phosphorylated and hidden neurofilament epitopes.

Three monoclonal antibodies to neurofilaments (RT97, BF10 and 147), two of which also recognised neurofibrillary tangles (RT97 and BF10), have all been shown to be specific for phosphorylated epitopes. Treatment of histological sections with alkaline phosphatase prior to immunostaining resulted in reduction of axonal neurofilament staining with all three whilst the neurofibrillary tangles staining with BF10 was unaffected. Antibody 147 was found to recognise weakly some neurofibrillary tangles following alkaline phosphatase treatment. The results presented confirm the presence of structurally abnormal but phosphorylated neurofilaments in neurofibrillary tangles.

Alkaline Phosphatase↗
PubMed1985

Adrenergic neurons in human brain demonstrated by immunohistochemistry with antibodies to phenylethanolamine-N-methyltransferase (PNMT): discovery of a new group in the nucleus tractus solitarius.

Adrenaline neurons in human brain were demonstrated by immunohistochemistry using antibody to phenylethanolamine-N-methyltransferase (PNMT), the final enzyme in the pathway of adrenaline synthesis, using fixed frozen sections and a highly sensitive free floating technique which utilizes metallization. Small densely packed PNMT-immunoreactive neurons were observed to form a nucleus lying just ventrolateral to the area postrema and in the dorsal part of the nucleus tractus solitarius. Larger adrenergic neurons were also present in and around the lateral reticular nucleus and in relationship with the dorsal motor nucleus of the vagus in regions equivalent to the C1 and C2 groups in rats. Longitudinally oriented PNMT-positive axons constitute a subset of tyrosine hydroxylase-immunoreactive axons in the dorsomedial reticular formation.

Adrenergic Fibers↗
PubMed1985

Alzheimer changes in nondemented patients younger than sixty-five: possible early stages of Alzheimer's disease and senile dementia of Alzheimer type.

Senile plaques (SP) and neurofibrillary tangles (NFT) were found in 38 (74.5%) of 51 unselected brains of nondemented patients who died between the ages of 55 and 64 years. A high proportion (22, or 43%) had only NFTs. These were consistently present in the entorhinal cortex and/or the hippocampus; the olfactory bulb, the amygdala, and the nucleus basalis of Meynert were also occasionally involved. Isolated SPs were seen in only 3 brains (6%); SPs and NFTs coexisted in 13 (25.5%). The distribution patterns of NFTs and SPs differed. NFTs were seen in discrete, mostly single neurons of the structure, already noted, whereas SPs occurred in a more generalized distribution over the base and convexity of the cerebrum. The plaques were usually small (30 mu in diameter) and consisted of delicate fibrillary material. Other types of SP were also seen. The incidence of various types of plaques in nondemented patients is considered to indicate a morphological evolution of these structures.

Alzheimer Disease↗
PubMed1985

Morphometric investigation of nerve cells, neuropil and senile plaques in senile dementia of the Alzheimer type.

Eight brains from patients with a mean age of 82 years showing clinical and neuropathological manifestations of senile dementia of the Alzheimer type (SDAT) and 6 control brains from individuals with a mean age of 89 years who were mentally normal or who had minimal senile impairment of memory, were selected by a rigorous elimination procedure for final evaluation from a total of 26 brains. Using an optical electronic image-analysis system, stereological measurements were made of the size and number of senile plaques, and of nerve cell area, capillary diameter, capillary length and intercapillary distance in the medial frontal gyrus, medial temporal gyrus and precentral gyrus. The number and size of senile plaques did not correlate with any of the other parameters measured, whereas Mountjoy et al. (1983) found a correlation between neuronal count and plaque count. In SDAT the cerebral cortex displayed significant atrophy of the neuronal perikarya (mean decrease approximately 50%). The greatest decrease in nerve cell area (55%) was seen in layers III and IV of the medial temporal cortex. Stereological measurements on the capillary network revealed only moderate neuropil shrinkage. Capillary volume was on average 30% greater in SDAT as a result of a decrease in intercapillary distance. These findings indicate that nerve cell shrinkage is a characteristic indicator of senile dementia. Neuropil atrophy may be of secondary importance.

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PubMed1985

Aberrant neurofilament phosphorylation in Alzheimer disease.

Alzheimer tangles, despite their location in neuronal perikarya, react immunocytochemically with monoclonal antibodies to phosphorylated epitopes of neurofilaments. Normal perikarya do not contain phosphorylated neurofilaments. The aberrant phosphorylation in both plaques and tangles seems to be largely restricted to individual phosphorylation sites among the many sites available in neurofilaments. It is suggested that the Alzheimer lesion involves an imbalance within specific kinases responsible for phosphorylation of different sites in neurofilaments.

Alzheimer Disease↗
PubMed1985

Immunohistological study of granulovacuolar degeneration using monoclonal antibodies to neurofilaments.

Neurons undergoing granulovacuolar degeneration have been examined in paraffin sections with three monoclonal antibodies to neurofilaments. Two of these antibodies (BF10, RT97) had been shown previously to react with neurofibrillary tangles. One of these antibodies (RT97) reacted with granular component of granulovacuolar degeneration. BF10 sometimes reacted with the surrounding neuronal cytoplasm. Granulovacuolar degeneration was also detected in a few cells of the anterior olfactory nucleus.

Alzheimer Disease↗
PubMed1984

Cellular receptor levels and glucocorticoid responsiveness of lymphoma cells.

A series of mouse lymphoma cell lines of independent origin was investigated with respect to glucocorticoid sensitivity, cellular receptor levels, and properties of receptors. The concentrations of the glucocorticoid dexamethasone required to produce comparable growth-inhibitory effects varied considerably amongst these cell lines. Also a wide range in the number of receptors per cell was found. When the receptor-steroid complexes were compared with respect to nuclear binding properties and affinities for DNA, no differences were seen. For 7 out of 10 cell lines studied we obtained a direct correlation between hormonal sensitivity and the number of cellular receptor sites divided by the dissociation constants KD for the receptor-dexamethasone complexes. This suggests that the receptor is a major quantitative determinant for steroid responsiveness. The limitations of receptor measurements for glucocorticoid therapy of lymphoid neoplastic disease are discussed.

Animals↗
PubMed1984

Aganglionosis of the colon. Morphologic investigations in 524 patients.

2014 biopsies and surgical specimens of 524 patients with suspected aganglionosis of the colon were analyzed using enzyme histochemical techniques for acetylcholinesterase and lactate dehydrogenase. The diagnosis could be confirmed in 70 patients. Hypoganglionosis was found in 6, neuronal dysplasia (or hyperganglionosis) in 2, and a complete lack of intramural neurons and nerve fibers in 1 patient. The disease was found to occur most often during the first year of life (65.7%) and to be more common in males than females (3.3:1). Enzyme histochemistry is useful for the final diagnosis of aganglionosis provided the biopsy contains mucosa and parts of the submucosa of the colon.

Acetylcholinesterase↗
PubMed1984

The variable topography of Alzheimer type changes in senile dementia and normal old age.

Alzheimer neurofibrillary changes and senile plaques were found in a variety of distribution patterns and intensities in 50 brains of patients older than 73 years who had been carefully examined for signs of organic dementia in a geriatric unit. As noted by earlier observers, the severity of dementia usually corresponded to the intensity of morphologic changes. In 2 patients, clinically identical with other demented subjects, the neocortex was spared and changes were confined to the hippocampus. The same pattern was found in 2 patients with less severe dementia. No patients with isolated temporal lobe changes could be clinically identified as having so-called 'simple senile dementia'.

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