A molecular model for bipolar affective disorder.
The biological basis of bipolar disorder is not known. Models for the illness have been proposed that were based on the neurobiological effects of pharmacological agents that affect mood. Although of great interest, these models have not adequately explained the striking clinical pattern of illness in which patients may experience either unipolar episodes or bipolar cycles of mania and depression. We now present a new model suggesting that the unique clinical heterogeneity found in patients with bipolar disorder could be explained by a defect in a 'downstream' portion of a signal transduction pathway that can regulate two or more neurotransmitter systems that have opposite effects on neuronal activity. This model may target specific candidate genes for involvement in bipolar disorder.
Lachman
H M
HM
Department of Psychiatry, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
Papolos
D F
DF
D001714:Bipolar Disorder / Q000188:drug therapy / Q000235:genetics / Q000503:physiopathology*; D001921:Brain / Q000378:metabolism; D004200:Diseases in Twins; D019204:GTP-Binding Proteins / Q000037:antagonists & inhibitors; D005786:Gene Expression Regulation; D018740:Genetic Heterogeneity; D008040:Genetic Linkage; D020022:Genetic Predisposition to Disease; D006801:Humans; D008094:Lithium / Q000494:pharmacology / Q000627:therapeutic use; D008957:Models, Genetic; D008959:Models, Neurological; D008960:Models, Psychological; D009419:Nerve Tissue Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism; D010641:Phenotype; D010744:Phosphoric Monoester Hydrolases / Q000037:antagonists & inhibitors / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology*; D014157:Transcription Factors / Q000502:physiology
D009419:Nerve Tissue Proteins; D014157:Transcription Factors; D008094:Lithium; D010744:Phosphoric Monoester Hydrolases; D019204:GTP-Binding Proteins