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Biomedical subjects

T J Crow

Publications and source records attributed to T J Crow.

At least 217 records · Page 12Linked to original sources
PubMed1986

Postmortem evidence of structural brain changes in schizophrenia. Differences in brain weight, temporal horn area, and parahippocampal gyrus compared with affective disorder.

The brains of 232 patients with a case-note diagnosis of schizophrenia or affective disorder who died in one mental hospital over a period of 22 years were weighed, and were assessed in a coronal section at the level of the interventricular foramina. From this sample were eliminated the brains of patients whose illnesses did not meet the Washington University criteria for a diagnosis of definite schizophrenia or primary affective disorder and those brains that showed significant histopathologic evidence of Alzheimer's-type change or cerebrovascular disease. This left a sample of 41 patients with schizophrenia and 29 patients with affective disorder. With age, sex, and year of birth controlled for, the brains of the patients with schizophrenia were 6% lighter, had lateral ventricles that were larger in the anterior (by 19%), and particularly in the temporal, (by 97%) horn cross section, and had significantly thinner parahippocampal cortices (by 11%). The findings provide postmortem confirmation of reports of ventricular enlargement in radiological studies and suggest that such enlargement is associated with tissue loss in the temporal lobe. The changes in schizophrenia were of a lesser degree than those seen in a sample of brains of patients with Alzheimer's-type dementia and Huntington's chorea.

Aged↗
PubMed1986

The third biannual winter workshop on schizophrenia. Schladming, Austria, Jan 26-31, 1986.

The following general principles seem to summarize the emphasis that was evident from the several days of multiple presentations and discussions. The need exists to continue to develop improvements in the tools applicable to research in psychiatry, both clinical and biological "instruments" that are both sensitive and specific to the questions asked. New molecular genetic technology has already been used to explore genetic susceptibility hypotheses, as well as novel viral associations. Imaging of brain receptor kinetics in vivo is in progress. Improvements in structured clinical rating scales for quantifying changes in biologically important clusters of symptoms (eg, negative vs positive symptoms) or the defining of prodromal symptoms that lead to relapse are critical to progress in etiological and treatment research. A genetic factor or factors for schizophrenia exist, although whether a "familial" type defines only a subgroup of schizophrenia is controversial. The relative importance of genetic vs environmental variables, and whether there is genetic and environmental heterogeneity, continue to be debated. The most important epidemiological data, the seasonality of birth, and the controversial question of geographical variation in prevalence can be clues to the etiology of schizophrenia and are presently being clarified. The pursuit of new treatments and modifications of present conventional treatments to increase the percentage of patients recovering from psychotic illnesses or lead to more complete recovery states is always of prime importance. An emphasis on clarifying the dopamine hypothesis of schizophrenia with PET continues to be at the forefront of psychiatric research. A focus on patients in a first episode of schizophrenia can clarify major issues.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed1986

Neuropeptides in the amygdala of controls, schizophrenics and patients suffering from Huntington's chorea: an immunohistochemical study.

The location of the neuropeptides methionine-enkephalin (ME), neurotensin (NT), neuropeptide Y (NPY) and vasoactive intestinal polypeptide (VIP) within the amygdaloid complex of healthy human individuals, schizophrenics and patients suffering from Huntington's chorea was studied qualitatively by means of immunohistochemistry. VIP-like immunoreactivity (IR) was present predominantly in a dense cluster of fibers and terminals in the central amygdaloid nucleus. ME-IR was observed in fibers, terminals and cell bodies in the same subnucleus, exhibiting a characteristical distribution pattern. NT-positive cell bodies were situated within the center of the central amygdaloid nucleus, fibers and terminals being encountered mainly at the periphery. NPY-IR was found to be evenly distributed throughout the amygdala. Distribution and staining intensity of ME, NPY and NT in the amygdala showed no qualitatively recognizable difference between the normal and schizophrenic specimens, whereas VIP-IR appeared to be slightly increased in the central amygdaloid nucleus of schizophrenics. In the choreic cases, the considerably shrunken amygdala exhibited only very low staining intensity of the four investigated neuropeptides.

Adult↗
PubMed1986

Gliosis in schizophrenia: a survey.

Increased gliosis has been previously described in schizophrenic brain. In this study, the degree of gliosis in schizophrenic and control brains was assessed quantitatively using an antibody to glial fibrillary acidic protein, immunocytochemical techniques, and a computed image analysis system. Twenty separate brain areas were assessed, and no significant differences were found between the schizophrenic and control groups. It seems unlikely that a specific pattern of pathologically significant gliosis is present in schizophrenic brains. These negative findings are of note because of previously reported structural differences in the temporal lobe in the schizophrenic group in this series.

Adult↗
PubMed1986

Recovery and measurement of specific RNA species from postmortem brain tissue: a general reduction in Alzheimer's disease detected by molecular hybridization.

The recovery of RNA from postmortem (PM) brain tissues was quantified by molecular hybridization. RNA degradation rates postmortem were faster in mice with herpes encephalitis than with uninfected mice, but clear ribosomal peaks could be seen up to 72 hr after death. In a comparison between frontal cortex samples from neurologically normal and Alzheimer's disease cases a reduction in ribosomal, poly A, preproenkephalin, and preprosomatostatin RNA levels was observed in the Alzheimer's disease group. This general reduction may be influenced by the cause of death as well as the pathology.

Alzheimer Disease↗
PubMed1986

Age of onset of schizophrenia in siblings: a test of the contagion hypothesis.

The possibility that schizophrenia is horizontally transmitted has been assessed in an analysis of age of onset in 264 recorded pairs of siblings with the disease. Age of onset was found to be correlated between siblings, and there was a tendency for the disease to occur at an earlier age in the younger sibling. Three explanations for this finding are considered: horizontal transmission, early detection, and ascertainment bias. An analysis by date of birth differences between siblings gives results consistent with horizontal transmission, but analysis by order of onset of illness (which shows that the age shift is not seen in elder-sibling-ill-first pairs) indicates that ascertainment bias (which arises from a tendency to include an excess of early onsets in younger siblings) is a more cogent explanation of the age shift. Although horizontal transmission is not altogether eliminated, the data suggest that age of onset is determined by genetic or prenatal factors rather than environmental precipitants in postnatal life. The retrovirus/transposon hypothesis (Crow, 1984) can accommodate the findings more readily than the gene-virus interaction hypothesis (Crow, 1983).

Adolescent↗
PubMed1986

Transmissible and non-transmissible neurodegenerative disease: similarities in age of onset and genetics in relation to aetiology.

In only a few cases is transmissible dementia known to have been acquired by infection from a source outside the individual; the remaining cases can be classified as sporadic, loosely familial, or autosomal dominant. Each group has a characteristic mean age of onset. A range of neurodegenerative diseases (including Alzheimer-type dementia and amyotrophic lateral sclerosis) can also be classified in this way, with similar characteristic mean ages of onset. The emergence of these diseases in later middle age, and the interdependence of age of onset and the type of familial occurrence suggest that these pathological processes are related to those genetic mechanisms which determine senescence. It is argued that the majority of cases of transmissible dementia arise, not from infection, but from the expression of endogenous virogene sequences as part of the aging processes.

Adult↗
PubMed1986

Viruses in human brains: a search for cytomegalovirus and herpes virus 1 DNA in necropsy tissue from normal and neuropsychiatric cases.

DNA was extracted from the brains of patients with Alzheimer-type dementia, schizophrenia, Huntington's chorea and from patients without neurological disease, and examined for the presence of herpes simplex virus type 1 and human cytomegalovirus sequences. By selecting cloned virus DNA fragments which do not hybridize to normal human DNA we were able to achieve a detection level assessed on reconstruction experiments of 1 virus genome per 50 cells. Screening at such sensitivity did not detect virus sequences in the higher CNS, except in cases of encephalitis or immunosuppression. We conclude that, at this level of sensitivity, these viruses cannot be regarded as normal residents of the higher CNS, and at the time of death they do not appear to be associated with these neuropsychiatric conditions.

Aged↗
PubMed1986

Neuropeptides and dopamine in the marmoset. Effect of treatment with 1-methyl-4-phenyl-1, 2, 3, 6 tetrahydropyridine (MPTP): an animal model for Parkinson's disease?

Neurochemical studies of post-mortem human parkinsonian brains have demonstrated specific alterations in neuropeptide concentrations within the substantia nigra and striatal structures. The drug, 1-methyl-4-phenyl-1, 2, 3, 6 tetrahydropyridine (MPTP) has been reported to act as a selective toxin to nigrostriatal dopamine neurons, and induces a parkinsonian-like syndrome in primates. In this study, marmosets developed features typical of Parkinson's disease following treatment with MPTP for four days. The effects of MPTP treatment on the concentrations of dopamine and neuropeptides were determined and changes compared with those reported for Parkinson's disease. It was found that within the substantia nigra, substance P concentrations doubled following treatment with MPTP; in contrast, concentrations of vasoactive intestinal peptide and neuropeptide Y were significantly reduced. No changes were observed in the concentrations of six other neuropeptides measured in this region, notably cholecystokinin. Despite marked depletion of dopamine within the caudate nucleus and putamen, concentrations of all neuropeptides within these structures remained unchanged with the exception of an isolated reduction of neuropeptide Y within the putamen. Somatostatin concentrations within the frontal cortex and hippocampus were significantly elevated in the marmosets treated with MPTP. These neuropeptide changes in the CNS contrast with those reported for Parkinson's disease. In view of the autonomic dysfunction associated with Parkinson's disease, peripheral concentrations of neuropeptides were determined. Significant depletion of neuropeptide Y was identified in the ureter, adrenal and cardiovascular tissue. Thus the neurochemical changes induced by MPTP may not be as selective as previously reported.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1986

Uptake of 77Br-spiperone in the striata of schizophrenic patients and controls.

Twelve patients with a diagnosis of schizophrenia and thirteen control subjects were injected with 77Br-bromospiperone and scanned using single photon emission tomography after 16 h. Although a statistically significant increase in patients by comparison with controls could be demonstrated, wide variations in specific activity of the ligand preclude a firm conclusion. In two patients but no controls an asymmetry in striatal uptake was noted, the uptake on the left being less than that on the right.

Adult↗
PubMed1986

Subclinical infections in mice resulting from the modulation of a lethal dose of Semliki Forest virus with defective interfering viruses: neurochemical abnormalities in the central nervous system.

The lethal encephalitis caused in mice by Semliki Forest virus (SFV) is modulated to a subclinical infection by administration of defective interfering SFV, although virus still multiplies both in the central nervous system (CNS) and systemically. Here we report that such infections result in unique and selective changes in the normal levels of CNS neurotransmitters some of which persist after infectious virus can no longer be detected. This represents a previously undocumented category of infection which may have a bearing on the aetiology of those human neurological and neuropsychiatric diseases to which viruses are believed to contribute.

Animals↗
PubMed1986

Subcellular pathology of human neurodegenerative disorders: Alzheimer-type dementia and Huntington's disease.

Activities of enzyme markers of subcellular organelles have been measured in brain tissue from subjects with Alzheimer-type dementia (ATD) and Huntington's disease (HD). Significant increases in the activity of the lysosomal enzyme beta-glucuronidase were observed in both ATD temporal cortex and HD putamen. It is suggested that beta-glucuronidase activity may be a useful biochemical indicator of cellular damage in the CNS. A significant reduction in neutral alpha-glucosidase activity was observed in ATD temporal cortex and HD putamen. This change may reflect an alteration in glycoconjugate processing and may relate to the susceptibility of neurones to the degenerative processes of ATD and HD.

Aged↗
PubMed1986

A magnetic resonance study of early schizophrenia.

Patients with untreated first schizophrenic episodes and others who had made varying degrees of recovery from such episodes were blindly compared with normal volunteers in terms of the periventricular appearances on spin echo magnetic resonance scans. Significant differences were not found.

Adult↗