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Biomedical subjects

E D Bird

Publications and source records attributed to E D Bird.

At least 127 records · Page 7Linked to original sources
PubMed1980

Chemical pathology of Huntington's disease.

Huntington's disease (HD), a dominantly inherited disorder of the nervous system, is usually manifest about middle age by dance-like movements. The disorder may occur in children, when epilepsy and rigidity may be the predominant signs. Degeneration of neurons occurs throughout the whole brain, but this is most marked in the basal ganglia. Neurochemical examination of postmortem brain frozen at the time of autopsy has been collected from patients dying with HD and compared with postmortem brain from psychotic patients and cases without neuropsychiatric disease. A number of alterations in neurotransmitters and their biosynthetic enzymes have been found. There are decreased concentrations of the neuroinhibitory transmitter gamma aminobutyric acid and this is associated with increased concentrations of dopamine and serotonin in the basal ganglia. In addition, there is decreased activity of glutamic acid decarboxylase, choline acetyltransferase, angiotensin-converting enzyme, as well as a decreased concentration of the neuropeptide substance P. Various pharmacologic agents have been tried based on the neurochemical alterations, but nothing has been found to be superior to the various neuroleptics in common use.

Acetylcholine↗
PubMed1979

Antipsychotic drug action in schizophrenic patients: effect on cortical dopamine metabolism after long-term treatment.

In the brains of deceased schizophrenics who underwent long-term treatment with antipsychotic drugs, the concentration of homovanillic acid (a dopamine metabolite) was significantly increased in the orbital frontal, cingulate, and temporal tip areas of the cortex, but not in the putamen or the nucleus accumbens. The concentration of homovanillic acid was normal in the brains of schizophrenics who were not treated with drugs.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1979

Abnormalities of neurotransmitter enzymes in Huntington's chorea.

The activities of L-glutamate decarboxylase (GAD), GABA-transaminase (GABA-T), choline acetyltransferase (CAT), and cysteic and cysteinesulfinic acids decarboxylase (CAD/CSAD) in putamen and frontal cortex in both Huntington's chorea and normal tissues were measured. The greatest difference between Huntington's and normal tissues occurred in putamen, in which the apparent CSAD activity was reduced by 85%, while no difference was observed in frontal cortex. GAD, CAD, and CAT activities were also reduced in putamen by 65%, 63%, and 42%, respectively (P less than 0.05). Slight reduction in the enzyme activities was also observed in frontal cortex. However, these reductions appeared to be statistically insignificant (P greater than 0.05 in all cases). GABA-T showed little difference in both putamen and frontal cortex in Huntington's chorea and normal tissues. GAD and GABA-T from Huntington's tissues were indistinguishable from those obtained from normal tissues by double diffusion test and by microcomplement fixation test, which is capable of distinguishing proteins with a single amino acid substitution. Furthermore, the similarity of the complement fixation curves for GAD from Huntington's and normal tissues suggests that the decrease in GAD activity is probably due to the reduction in the number of GAD molecules, presumably through the loss of neurons, and not due to the inhibition or inactivation of GAD activity by toxic substances which might be present in Huntington's chorea.

4-Aminobutyrate Transaminase↗
PubMed1979

Increased dopamine concentration in limbic areas of brain from patients dying with schizophrenia.

Dopamine, noradrenaline, glutamate decarboxylase (GAD) and choline acetyl-transferase (CAT) were measured in post-mortem brain samples from more than 50 patients dying with a hospital diagnosis of schizophrenia and an equal number of controls. GAD was measured in 14 different brain regions, and was significantly lower in both control and schizophrenia patients who died following a protracted illness. If GAD values from patients who died suddenly were compared, no significant differences were observed between the control and schizophrenia groups. There was also no differences between the CAT values measured in 13 different brain regions in the two groups. Noradrenaline values were not different in the two groups in most limbic areas or in the caudate nucleus, but were elevated in the schizophrenic group in nucleus accumbens and in anterior perforated substance. These differences were not, however, statistically significant. On the other hand dopamine concentrations in nucleus accumbens and in anterior perforated substance were significantly elevated (by 34 and 95 per cent, respectively) in the schizophrenia group as compared with controls, although dopamine values were not different in caudate nucleus, putamen, septal nuclei or amygdala. The finding of elevated concentrations of dopamine in certain areas of the limbic forebrain in schizophrenia is discussed in relation to current hypotheses of the involvement of dopamine in this illness, and the difficulties of determining whether the observed changes are related to chronic treatment with antischizophrenic drugs.

Brain Chemistry↗
PubMed1979

Distribution of beta-endorphin in normal and schizophrenic human brains.

beta-Endorphin was measured by radioimmunoassay in post-mortem human brains. Samples of brain were taken from five discrete areas, both from control brains and brains of schizophrenic patients. No difference in beta-endorphin levels was found in these two groups of brains. beta-Endorphin was confirmed to be widely distributed in the brain, but there were considerable differences in the concentrations in different areas.

Brain Chemistry↗