Experimental studies of sedative self-administration by humans.
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Biomedical subjects
Publications and source records attributed to L L Heston.
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In both human Alzheimer's disease and aluminum encephalopathy of animals, changes are observed in neurofibrillary structures. We have found that brains from Alzheimer patients contain approximately 1.4 times the aluminum level found in a control series. Some possible methodological problems are discussed. We have proposed a plausible chemical mechanism for the changes of aluminum encephalopathy.
Relatives of probands with histologically confirmed Alzheimer's disease had excessive morbidity from Alzheimer's disease, Down's syndrome, and hematologic malignancies. These associations coupled with two previously reported ones, the indistinguishable histopathological changes in brain in Alzheimer's disease and Down's syndrome, and the 20-fold increased incidence of leukemia among persons with Down's syndrome, are evidence that some instances of those disorders are associated with a unitary genetic etiology. The genetic defect may be expressed through disorganization of microtubules. Other evidence suggests that the same process may be involved in aging and in other chromosomal aberrations.
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In the first of three articles on schizophrenia, evidence for a genetic component is reviewed, including the high concordance in monozygotic twins, even when reared apart, and in children born to a schizophrenic parent or parents. The myth of the "schizophrenogenic mother" is rejected, though it does appear that as yet undefined environmental factors, by bringing about biochemical changes, may play an important role.
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Controlled pore glass (CPG) chromatography was employed to simply (one pass through column) and rapidly (60 minutes) purify a human brain specific protein having a high molecular weight (approximately 250,000 mol. wt.) from a crude brain extract containing proteins of varying molecular weights. This method, either exactly as described herein or by adjusting the pore size of the CPG, should be adaptable to other purification problems.
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Prospective developmental data on 33 children of consensus diagnosed schizophrenic parents were compared to control samples of children of other psychiatric patients and children of normal parents. Contrary to several reports the children of schizophrenics, observed from birth to age seven, were remarkably normal on a host of pregnancy and delivery variables, neurological examinations, physical growth measures, and psychological tests. However, a combination of three indicators characterized five of the 116 children, and all five were offspring of schizophrenics (17 per cent of the high risk sample), thus matching the expected lifetime risk for schizophrenia previously observed in such samples. Case histories show that all five children have enduring patterns of maladjustment and exhibit behaviours often reported in the premorbid histories of schizophrenics. Most have family histories heavily loaded with schizophrenia. In terms of a diathesis-stress model, these five children appear especially vulnerable to future schizophrenia in the absence of rational methods of prevention.
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Diagnosis is a central problem in Alzheimer's research, including linkage studies in particular. The magnitude of expected diagnostic error, its likely effect on research, and way to minimize it, provides the focus of this commentary.