Linkage between Glucose-6-Phosphate Dehydrogenase Deficiency and Manic-Depressive Psychosis

1980 ◽  
Vol 137 (4) ◽  
pp. 337-342 ◽  
Author(s):  
J. Mendlewicz ◽  
P. Linkowski ◽  
J. Wilmotte
Keyword(s):  
Dehydrogenase Deficiency ◽  
Dominant Gene ◽  
Linkage Studies ◽  
Positive Evidence ◽  
Manic Depressive Psychosis ◽  
Affective Illness ◽  
X Linkage ◽  
Manic Depressive ◽  
Informative Family ◽  
Glucose 6 Phosphate Dehydrogenase

SummaryHeredity has been shown to be an important factor in the aetiology of manic-depressive psychosis. Recent linkage studies with colour blindness have suggested the presence of an X-linked dominant gene in the transmission of manic-depressive psychosis. We report here positive evidence of a linkage between manic-depressive psychosis and glucose-6-phosphate dehydrogenase deficiency in an informative family assorting for both traits. These results strengthen previous linkage studies in affective illness and support the hypothesis of X-linkage in a subgroup of manic-depressive psychosis.

A Genetic Study of Affective Illness in Patients over 50

1964 ◽  
Vol 110 (465) ◽  
pp. 244-254 ◽  
Author(s):  
G. Hopkinson
Keyword(s):  
General Population ◽  
Later Life ◽  
Manic Depressive Psychosis ◽  
Affective Illness ◽  
Manic Depressive ◽  
Increased Risk ◽  
Involutional Melancholia ◽  
Relationship Of ◽  
The Relationship ◽  
Depressive Patients

The genetic evidence concerning affective illness of later life is still conflicting and the relationship of such conditions to the manic-depressive psychosis unclear. Kallman (1955) believed that, genetically, involutional melancholia bore a closer relationship to schizophrenia than to the manic-depressive psychosis. An increased risk for schizophrenia amongst the relatives of such patients was not observed by Kay (1959) and Stenstedt (1952). Both these writers do however describe a lower loading for manic-depressive psychosis than would be found amongst the relations of manic-depressive patients, though a much higher incidence than in the general population. Both Stenstedt and Kay assumed that they were dealing with a heterogeneous group of patients containing both psychotic and neurotic depressions.

Ancestral Secondary Cases on Paternal and Maternal Sides in Bipolar Affective Illness

1978 ◽  
Vol 133 (1) ◽  
pp. 68-72 ◽  
Author(s):  
G. F. S. Johnson ◽  
M. M. Leeman
Keyword(s):  
Family History ◽  
Depressive Disorder ◽  
Dominant Gene ◽  
Single Dominant Gene ◽  
Polygenic Inheritance ◽  
Positive Group ◽  
Affective Illness ◽  
Manic Depressive ◽  
Second Degree

SummaryAn analysis of the distribution of ancestral secondary cases of affective illness in families of patients with bipolar manic-depressive disorder was undertaken. Twenty probands with at least two affectively ill second degree relatives were available for study. Probands with both parents affected were excluded. The distribution of unilateral to bilateral pairs of all affected relatives, both excluding and including parents, of probands showed no significant differences from that expected in polygenic inheritance. However, separation into bipolar family history, positive or negative, showed significant differences from the expected ratio of unilateral to bilateral pairs in a bipolar family history positive group consistent with a single dominant gene inheritance.

X-Linkage and Manic-Depressive Illness

1975 ◽  
Vol 127 (5) ◽  
pp. 482-488 ◽  
Author(s):  
Armand W. Loranger
Keyword(s):  
Genetic Markers ◽  
Depressive Illness ◽  
Linkage Studies ◽  
Review Of The Literature ◽  
Manic Depressive Illness ◽  
X Linkage ◽  
Manic Depressive ◽  
Affected Parent ◽  
Additional Support ◽  
General Explanation

SummaryThirty years ago it was suggested that the apparently higher incidence of manic-depressive illness in women might be due to X-linked heredity. The hypothesis was undermined by subsequent reports of the frequent occurrence of father to son transmission. Winokur and his associates recently revived it, providing data which indicated that such transmission is absent or rare in the bipolar form of the illness. Additional support has come from linkage studies with known genetic markers located on the X chromosome. The present study, based on the 400 parents of 100 male and 100 female bipolar manic-depressive probands, failed to discover a lack of father-son compared to other affected parent-child pairs. This finding, together with a review of the literature, would indicate that it is premature to invoke X-linked heredity as a general explanation for bipolar manic-depressive illness, though there is mounting evidence that it may account for the illness in some family pedigrees.

Glucose-6-Phosphate Dehydrogenase Deficiency in an Old Woman

2020 ◽  
Vol 6 (3) ◽  
Author(s):  
Briantais Antoine ◽  
Froidefond Margaux ◽  
Seguier Julie ◽  
Swiader Laure ◽  
Durand Jean Marc
Keyword(s):  
Dehydrogenase Deficiency ◽  
Glucose 6 Phosphate Dehydrogenase

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.

Sign in / Sign up

Export Citation Format

Share Document