An overview of bipolar disorder-related content on Genes to Cognition Online.
There are two main forms of bipolar disorder. Type I is characterized by one or more manic/mixed episodes. Type II is characterized by hypomania and one or more major depressive episodes. It can be difficult to differentiate bipolar disorder from schizophrenia, both symptomatically and genetically. Candidate genes bipolar disorder shares with schizophrenia include NRG1, DAOA, and DISC1. It has been known for some time that bipolar disorder is a highly genetic disorder and new techniques such as genome scans that search for copy number variants have become increasingly important to identifying relevant genetic mechanisms. Dopamine may be important to understanding the biochemistry of bipolar, and is associated with extreme highs and lows. At the cellular level, glial cells are decreased in individuals with depression and bipolar disorder. The amygdala, hippocampus, and cingulate regions of the brain have been identified as potentially relevant brain structures to bipolar disorder, but there is no clear consensus among researchers. The diathesis-stress model helps us understand gene-environment interactions that can cause or give rise to bipolar-type episodes.
Selected items on the Genes to Cognition Online “subway line” explore key areas in bipolar disorder research.
Family and twin studies have long identified bipolar disorder as a genetic condition, with heritable factors estimated to be in the region of 70%. While many genes and loci have subsequently been found to associate with bipolar disorder, none have been unambiguously identified as causal. One explanation for the difficulty in finding genes for bipolar is that it is a highly complex disorder. Genes with the strongest association are also candidate genes for schizophrenia and major depression. This is not surprising given that the disorders share some common symptoms. For example, psychosis is a feature of both bipolar and schizophrenia (although the delusions and hallucination in schizophrenia seem to be related to self-awareness as opposed to mood-incongruence). Candidate genes for bipolar disorder include G72/DAOA, DISC1, NRG1, TPH2, BDNF, 5-HTT, and DAT1. Use the chromosome Map of Disorders and Processes to explore some of the more prominent genes associated with bipolar disorder. New techniques such as genome scans for Copy Number Variants are providing new ways of understanding these complex genetic processes.
A number of biochemicals have been associated with bipolar disorder, including dopamine, norepinephrine, and serotonin. Dopamine is particularly interesting because when it is decreased, in illnesses such as Parkinson’s disease, is associated with low mood and loss of ability to enjoy things. Conversely, when high dopamine increases motivational drive and can produce feelings of euphoria. The dopamine system, therefore, has the capability for producing low and high emotions, the range of symptoms that you see in the depression versus the mania phase of bipolar disorder. Professor Wayne Drevets discusses this in the Biochemistry and Neuropathology of Bipolar Disorder and Depression.
Post-mortem studies allow researchers to physically examine the brains of individuals with bipolar disorder. These studies highlight a loss of glial cells, which are a support network across brain systems (and which also participate in transmission of biochemicals). The type of glial cell that has been most implicated in bipolar disorder is called the oligodendrocyte, which makes the myelin. Myelin is that sheath that surrounds neurons and supports the connections between brain regions. It might be the case that the decreased oligodendrocyte may give rise to impaired communication and balance between different structures. You can read about this in Brain Cells for Depression/Bipolar Disorder.
In bipolar disorder, neuroimaging studies have not shown any particular region to be consistently abnormal in size or in volume. There are some studies showing abnormal activity in certain regions, including the anterior cingulate gyrus. In The Neuropathology of Depression and Bipolar, Professor James Potash discusses these correlates. The amygdala, hippocampus, and prefrontal cortex may also be important to bipolar disorder.
Bipolar Disorder is an illness that was once referred to as manic depressive illness. Bipolar refers to the two different poles of mood, the high pole and the low pole; the low pole being depression, and the high pole being at its extreme mania, and then a milder version of that is called hypomania. Mania is symptomatic of bipolar type I disorder, and hypomania of bipolar type II disorder. Bipolar disorder differs from schizophrenia in that typically it’s what we refer to as an episodic illness; meaning that people get ill, then they get well again and then the illness may come back again at a later date. G2C Online features an illuminating series of video clips with researcher Kay Redfield Jamison, who discusses her personal experience as an individual with bipolar disorder.
The diathesis-stress model provides a useful template for understanding how genes and the environment may contribute to bipolar disorder, both as causes and factors in initiating a bipolar episode. FKBP5 is a gene involved in mood disorders and the stress response. It is a co-chaperone of the glucocorticoid receptor, which is the receptor for the stress hormone cortisol, and seems to be involved in bipolar disorder and depression risk. Professors Wayne Drevets and James Potash discuss the model with additional reference to major depression.
Students reveal their preconceptions about depression, then use G2C Online to learn about symptoms of the disorder, genes, and neurotransmitters associated with it, and challenges involved in diagnosis and treatment.