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Biomedical subjects

T J Crow

Publications and source records attributed to T J Crow.

At least 253 records · Page 14Linked to original sources
PubMed1985

A comparison of the effects of cytotoxic cerebrospinal fluid on cell cultures with other cytopathogenic agents.

Protein synthesis, antigen synthesis, and cell membrane permeability were analyzed after inoculating human diploid fibroblasts with control or cytotoxic CSF, herpes simplex virus type 1 (HSV 1), poliovirus 3, or Clostridium difficile toxin. Whereas protein synthesis and membrane permeability were affected by the viruses, and virus antigens detectable by pooled human serum were synthesized, the bacterial toxin and cytotoxic CSF did not induce any new proteins or antigens, although the cytotoxic CSF reduced cellular protein synthesis levels and caused an increase in the permeability of the cell membranes. The effect of the cytotoxic CSF in cell culture resembles that of a toxin rather than a replicating virus.

Animals↗
PubMed1985

Loss of endoplasmic reticulum-associated enzymes in affected brain regions in Huntington's disease and Alzheimer-type dementia.

Post-mortem brain samples from patients with either Huntington's disease, Alzheimer-type dementia or appropriate controls were assayed for endoplasmic reticulum enzymes, NADPH-cytochrome c reductase, neutral alpha-glucosidase, inosine diphosphatase, alpha-mannosidase and glucose-6-phosphatase and for Golgi enzymes, fucosyl- and galactosyl-transferases. In Alzheimer-type dementia there was a selective decrease in alpha-glucosidase activity in the temporal cortex. In Huntington's disease there was a selective decrease of putamen alpha-glucosidase and fucosyl-transferase activities. It is suggested that these changes reflect highly specific alterations in glycoprotein synthesis and processing and may contribute to the underlying pathology of these disorders.

Adult↗
PubMed1985

Herpes simplex virus encephalitis. Neuroanatomical and neurochemical selectivity.

Intracerebral infection of mice with HSV-1 was found to produce a 2-3-fold increase in dopamine and serotonin metabolism in cortex, striatum, diencephalon and brain stem. Neurochemical markers of GABA and acetylcholine neurones, and neurotransmitter receptor binding sites were unchanged. The immunohistochemical distribution of virus antigen revealed high levels of immunoreactivity in s. nigra, ventral tegmental area, locus coeruleus and dorsal raphe nucleus, whilst other areas of brain stem were clear of virus antigen. The changes in monoamine metabolism observed in experimental HSV encephalitis may be related to the concentration of virus in monoamine neurones.

Acetylcholine↗
PubMed1985

Neurotransmitter metabolites, enzymes and receptors in experimental scrapie.

A comprehensive study has been made of metabolites, enzymes and receptors for a variety of neurotransmitter systems in different parts of the CNS from mice affected with 139A scrapie. Studies were made at the early clinical stage so as to minimise secondary alterations in terminally sick mice. Even though histological lesions (vacuolation) are widespread in the CNS in this model of scrapie, no consistent neurochemical changes were found in mid- or anterior brain. In the cerebellum, the activity of glutamic acid decarboxylase was reduced and the binding of [3H]muscimol to gamma-aminobutyric acid receptors was increased. In the brain stem, the concentration of 5-hydroxyindoleacetic acid (5-HIAA) was increased and there was a reduced binding of appropriate ligands to serotonin and to muscarinic cholinergic receptors. In the spinal cord, the activity of choline acetyl transferase was reduced and the concentration of 5-HIAA was increased. The extent of these alterations was about 20-40% of control values. The specificity of these changes for a few neurotransmitter systems in hind brain and spinal cord raised the possibility of their being a primary cause of clinical disease and led us to study a different scrapie model. Present and published findings show that an increased concentration of 5-HIAA, some alterations in the binding properties of serotonin receptors and a decreased number of muscarinic receptor sites are common to both 139A scrapie in CW mice and 263K scrapie in hamsters.

Animals↗
PubMed1985

Lateral ventricular size in schizophrenia: relationship to the disease process and its clinical manifestations.

Using computed tomography, lateral ventricular size was studied in a sample of 112 institutionalized chronic schizophrenic patients (selected from 510 cases to investigate the correlates of the defect state and intellectual decline and the effects of insulin, electroconvulsive and neuroleptic treatment), and compared with matched groups of non-institutionalized schizophrenics, patients with first schizophrenic episodes, institutionalized and non-institutionalized patients with primary affective disorder, and neurotic out-patients. Age was significantly correlated (P less than 0.0002) with lateral ventricular size, but the institutionalized schizophrenic patients had significantly larger (P less than 0.025) lateral ventricles than the neurotics when age was taken into account. Ventricular enlargement was unrelated to past physical treatment (neuroleptics, insulin coma and electroconvulsive therapy). Within the group of institutionalized schizophrenic patients few correlates of ventricular enlargement were identified; thus in this population increased ventricular size was not clearly associated with the features of the defect state (negative symptoms and intellectual impairment). However, there was a curvilinear (inverted-U) relationship between intellectual function and ventricular size. Increased ventricular size was significantly related to absence of hallucinations, impairment of social behaviour, inactivity and the presence of abnormal involuntary movements. The findings confirm that structural brain changes do occur in chronic schizophrenia, but illustrate some of the difficulties in elucidating the clinical significance of ventricular enlargement. Lateral ventricular size is strongly age-related and the distribution in chronic schizophrenia is skewed and not bimodal; the relationship to particular features of the disease is complex and likely to emerge only in studies with a large sample size.

Adult↗
PubMed1985

The two-syndrome concept: origins and current status.

The two-syndrome concept postulates two "dimensions of pathology" underlying schizophrenia--a reversible (and potentially neuroleptic-responsive) component and a sometimes progressive and relatively irreversible component associated with the deficit state and poor long-term outcome. Negative symptoms (narrowly defined) appear to be more closely associated with the latter component (the type II syndrome), as also are cognitive impairments, abnormal involuntary movements, and behavioral deterioration. This syndrome is assumed to be more closely related than the type I syndrome of positive symptoms to the structural brain changes inferred from pneumoencephalograms, computed tomography scans, and recent post-mortem studies. However, since both syndromes often occur in the same patient--sometimes at the same point in time--they presumably have the same etiology.

Antipsychotic Agents↗
PubMed1985

Search for cytomegalovirus in postmortem brain tissue from patients with Huntington's chorea and other psychiatric disease by molecular hybridization using cloned DNA.

Postmortem human brain extracts were examined for the presence of human cytomegalovirus (CMV) DNA by molecular hybridization using a dot blot technique. The method was able to detect picogram quantities of homologous DNA, but CMV specific hybridization was detected in only one of 83 brains examined. The positive case came from a patient who had received immunosuppressive therapy. We were not able to confirm the report that CMV is present in the brains of patients with Huntington's chorea, nor was CMV detected in the temporal cortex of brains from schizophrenic patients. Our findings are discussed in relation to the methodology for investigating a possible viral etiology of some neuropsychiatric diseases.

Adult↗
PubMed1985

Tritiated etorphine and naloxone binding to opioid receptors in caudate nucleus in schizophrenia.

Opioid receptor binding sites were assessed in membrane preparations of caudate nucleus from post-mortem brains of controls and of patients with schizophrenia. There was no difference between the two groups in the total specific binding of 3H-etorphine or in its 'mu' and ('delta + kappa') components. Similarly, the binding of 3H-naloxone did not differ between patients and controls. It is concluded that a previous report of reduced opioid receptors in caudate of schizophrenics is unlikely to prove a consistent finding and that the results of the present study offer no support to the claim that there is a general disturbance in opiate mechanisms in schizophrenia.

Aged↗
PubMed1984

Striatal dopamine receptors in Alzheimer-type dementia.

Dopamine D1 and D2 receptors were studied in putamen of post-mortem brains from controls and patients with Alzheimer-type dementia (ATD). A significant reduction in dopamine D2 receptors was observed in ATD, whereas dopamine D1 receptors were unchanged. Neurochemical markers of striatal acetylcholine and GABA-containing neurones were also within the normal range. The results are consistent with a loss of D2 receptors located on cortico-striatal neurones in putamen of some ATD patients. In contrast, markers of intrinsic neurones may remain unchanged.

Aged↗
PubMed1984

Neuropeptide Y in the stria terminalis: evidence for an amygdalofugal projection.

Lesions of the stria terminalis in the rat brain indicate that neuropeptide Y, a recently isolated peptide of the pancreatic polypeptide family, projects rostrally in an efferent pathway from the amygdaloid complex. Marked depletions of NPY-immunoreactivity observed by immunocytochemistry were apparent in the laterobasal septum and suprachiasmatic nucleus of the hypothalamus, but most markedly in rostrolateral regions of the bed nucleus of the strial terminalis.

Amygdala↗
PubMed1984

Dopamine D2 receptors in substantia nigra in schizophrenia.

Dopamine D2 receptors were assessed in samples of substantia nigra from controls and schizophrenics. Specific [3H]spiperone binding was significantly increased in both neuroleptic-free and neuroleptic-treated schizophrenics. This supports our previous suggestion that the increase in D2 receptors observed in striatum of schizophrenics is not wholly due to neuroleptic medication.

Aged↗
PubMed1984

Studies on neurotransmitter receptor systems in neocortex and hippocampus in senile dementia of the Alzheimer-type.

Ligand binding to alpha 1-, alpha 2- and beta-adrenergic, serotonin, benzodiazepine and GABA receptors was studied in neocortex and hippocampus of controls and patients with senile dementia of the Alzheimer-type. A selective loss of serotonergic binding sites characterised as a loss of both S1 and S2 sites was observed. The reduction in serotonin receptors did not correlate with a clinical assessment of the degree of dementia, or with the extent of Alzheimer-type neuropathological change.

Aged↗
PubMed1984

Elevation of neuropeptide Y (NPY) in substantia innominata in Alzheimer's type dementia.

Concentrations of neuropeptide Y (NPY) have been determined in 12 areas of control brains and compared to those found in brains from patients with Alzheimer's type dementia (ATD). The distribution of NPY in the control brains was compared with those reported previously. Highest concentrations were identified in the subcortical structures, in particular, nucleus accumbens (203 +/- 21.7 pmol/g), amygdala (136.7 +/- 15.8 pmol/g), and substantia innominata (109.0 +/- 12.6 pmol/g). A significant elevation in NPY concentrations was identified in the region of the substantia innominata of Alzheimer brains (controls: 109.0 +/- 12.6 pmol/g, ATD: 206 +/- 28.2 pmol/g, P less than 0.001). This change in NPY concentration was similar to the increase in somatostatin concentration in this region of ATD brain. In contrast, although cortical concentrations of somatostatin were reduced in ATD, no change was found in the concentrations of NPY in the 4 regions of cerebral cortex and the remaining subcortical areas examined.

Aged↗
PubMed1984

Neurotransmitter receptors and monoamine metabolites in the brains of patients with Alzheimer-type dementia and depression, and suicides.

In patients with Alzheimer-type dementia, in addition to the well-known losses of cholinergic neurones, there is evidence of degeneration of the noradrenergic and serotonergic innervation of the cerebral cortex. While noradrenergic and cholinergic receptors are preserved there is a loss of serotonin S1 and S2 receptors, particularly in the temporal lobe. The loss of serotonin S2 receptors may occur at an early stage of the disease and, in temporal and frontal cortex, is correlated with the loss of somatostatin immunoreactivity. In patients dying in hospital with depression, and in individuals committing suicide, there are no consistent changes in monoamine metabolites. Noradrenergic, serotonergic, and other neurotransmitter receptors were found to be unchanged, although there was a moderate decrease in imipramine binding in a small group (n = 6) of subjects with a history of depression, who had committed suicide.

Aged↗
PubMed1984

Characterisation and distribution of vasoactive intestinal polypeptide binding sites in human brain.

The binding of 125I-vasoactive intestinal polypeptide (VIP) to human brain membranes has been studied. The binding was saturable with a dissociation constant (KD) of 4.4 +/- 2.0 nM and maximum binding value (Bmax) of 8.6 +/- 6.2 fmoles/mg tissue (mean +/- SD, n = 4), and was displaced by unlabelled VIP with an IC50 of 4 nM; secretin was much less potent with an IC50 of approximately 8 microM. The regional distribution of 125I-VIP binding in human brain revealed highest binding values to be in frontal and temporal cortices with intermediate values in amygdala, caudate and cerebellum, with lowest values in hippocampus, substantia nigra and hypothalamus.

Binding Sites↗