Genetic association between monoamine oxidase and manic-depressive illness: Comparison of relative risk and haplotype relative risk data

1997 ◽  
Vol 74 (5) ◽  
pp. 475-479 ◽  
Author(s):  
Abbas Parsian ◽  
Richard D. Todd
Keyword(s):  
Relative Risk ◽  
Monoamine Oxidase ◽  
Genetic Association ◽  
Depressive Illness ◽  
Manic Depressive Illness ◽  
Manic Depressive ◽  
Haplotype Relative Risk

PLATELET-MONOAMINE-OXIDASE ACTIVITY PREDICTS RESPONSE TO LITHIUM IN MANIC-DEPRESSIVE ILLNESS

The Lancet ◽  
1977 ◽  
Vol 310 (8052) ◽  
pp. 1325-1327 ◽  
Author(s):  
JohnL. Sullivan ◽  
Allan Maltbie ◽  
JesseO. Cavenar ◽  
Charles Stanfield
Keyword(s):  
Monoamine Oxidase ◽  
Oxidase Activity ◽  
Depressive Illness ◽  
Monoamine Oxidase Activity ◽  
Manic Depressive Illness ◽  
Manic Depressive ◽  
Platelet Monoamine Oxidase

Trace Metals in Neuropsychiatry

1983 ◽  
Vol 143 (1) ◽  
pp. 85-86 ◽  
Author(s):  
J. L. Crammer
Keyword(s):  
Trace Metals ◽  
Monoamine Oxidase ◽  
Trace Metal ◽  
Depressive Illness ◽  
The Body ◽  
Essential Metals ◽  
Manic Depressive Illness ◽  
Manic Depressive ◽  
Iron And Zinc ◽  
Living Tissues

Naylor's recent hypothesis that vanadium ‘poisoning’ could be a factor in the severity of manic-depressive illness drew attention to the normal and even essential presence of vanadium in the diet, and in human living tissues. The whole brain may contain only about 45 micrograms of vanadium (Underwood, 1977; 1979), as against 500 micrograms of manganese, 130 μgm selenium, and less than 20 μgm molybdenum—others of the 12 or so essential metals required in traces. We might take copper as the principle trace metal—an important component of over 50 enzymes, including monoamine oxidase and dopamine β-hydroxylase—with a total in the whole man of about 100 mg. In contrast, metals like potassium (140 gm), magnesium (35 gm), iron and zinc (3–4 gm) are not present in traces but in gram quantities. Lithium, present naturally in the body in extremely minute amounts, is raised in therapy to occupy a borderline position in the scale, rather more than copper, less than zinc.

Platelet Monoamine Oxidase in Schizophrenia and Manic-Depressive Illness

1976 ◽  
Vol 129 (3) ◽  
pp. 227-232 ◽  
Author(s):  
Robert H. Belmaker ◽  
Kirsten Ebbesen ◽  
Richard Ebstein ◽  
Ranan Rimon
Keyword(s):  
Monoamine Oxidase ◽  
Health Centre ◽  
Depressive Illness ◽  
Manic Depressive Illness ◽  
Manic Depressive ◽  
Platelet Mao ◽  
Schizophrenic Patients ◽  
Mao Activity ◽  
Platelet Mao Activity ◽  
Depressive Patients

SummaryMonoamine oxidase (MAO) is an important enzyme in the catabolism of brain biogenic amines. Platelet MAO has been reported to be moderately reduced in manic-depressive patients and markedly reduced in schizophrenic patients. This enzyme's activity has been shown to be under a large degree of genetic control and has been proposed as a ‘genetic marker’ in schizophrenia. A transcultural replication of the finding of low platelet MAO in schizophrenia and manic-depressive illness was carried out at the Jerusalem Mental Health Centre. Manic-depressive patients were found to have higher platelet MAO activity than schizophrenic patients, as reported previously, but control individuals were as low as the schizophrenic patients. It is unlikely that platelet MAO activity is a transculturally-valid marker for schizophrenia.

Conditioning and Sensitisation in the Longitudinal Course of Affective Illness

1986 ◽  
Vol 149 (2) ◽  
pp. 191-201 ◽  
Author(s):  
Robert M. Post ◽  
David R. Rubinow ◽  
James C. Ballenger
Keyword(s):  
Depressive Illness ◽  
Manic Depressive Illness ◽  
Conceptual Approach ◽  
Longitudinal Course ◽  
Behavioural Sensitisation ◽  
Affective Illness ◽  
Biological Variables ◽  
Manic Depressive ◽  
Progressive Course

Few biological theories of manic-depressive illness have focused on the longitudinal course of affective dysfunction and the mechanisms underlying its often recurrent and progressive course. The authors discuss two models for the development of progressive behavioural dysfunction—behavioural sensitisation and electrophysiological kindling—as they provide clues to important clinical and biological variables relevant to sensitisation in affective illness. The role of environmental context and conditioning in mediating behavioural and biochemical aspects of this sensitisation is emphasised. The sensitisation models provide a conceptual approach to previously inexplicable clinical phenomena in the longitudinal course of affective illness and may provide a bridge between psychoanalytic/psychosocial and neurobiological formulations of manic-depressive illness.

Transmission of Manic-Depressive Illness

JAMA ◽  
1973 ◽  
Vol 224 (8) ◽  
pp. 1187 ◽  
Author(s):  
Julien Mendlewicz
Keyword(s):  
Depressive Illness ◽  
Manic Depressive Illness ◽  
Manic Depressive
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