An investigation in Psychotherapy and Psychosomatics explores how psychoeducation may affect white matter plasticity inbipolar disorder. Bipolar disorder (BD) is a severe mood disorder which is often difficult to treat. Pharmacological treatments are often effective in symptom management, but their effects are generally insufficient on a functional level. Among psychosocial interventions, psychoeducation has recently shown significant and long-lasting effects on treatment adherence, relapse prevention and global functioning. Psychoeducation is now positioned as an essential part of therapeutic strategies in BD, although its mechanistic neural action has not yet been precisely identified. In the present study the Authors tested the hypothesis that psychoeducation would be associated with anatomical changes of the frontolimbic connectivity in patients with BD.
Twenty-four euthymic patients with BD were randomly assigned to a 3-month psychoeducation (PED) or support (SUP) group program. Twelve HS were included to form a control (CTL) group for an initial between-group comparison. Ten patients and 10 HS had participated in a previous fMRI study with different aims. Both PED and SUP group programs were conducted in a parallel design, i.e., 12 sessions, 1 session per week, within the same period to exclude potential seasonality-induced variability.
Results showed that BD patients experienced a significant decrease in depressive symptom severity and a significant increase in global functioning after the psychoeducation but not after the SUP group. Patients of the PED group presented significantly reduced MD along the left uncinate fasciculus after the psychoeducation program compared to before whereas patients of the SUP group did not. In both patient groups, we observed no change in GFA of right and left uncinate fasciculus. There were no significant differences between BD and CTL at t1 either on GFA or on MD within both right and left uncinate fasciculus. As the Authors explain, the decrease of the MD within the left uncinate fasciculus after the psychoeducation suggests beneficial effects of psychoeducation on frontolimbic tracts. Since higher levels of MD are associated with myelin damage, a possible explanation for the observed MD change in our study is increased myelination after psychoeducation.
Gene associated with schizophrenia, bipolar disorder, autism, ADHD, and depression linked to brain cell death in mice.
A new study shows the death of newborn brain cells may be linked to a genetic risk factor for five major psychiatric diseases, and at the same time shows a compound currently being developed for use in humans may have therapeutic value for these diseases by preventing the cells from dying.
In 2013, the largest genetic study of psychiatric illness to date implicated mutations in the gene called CACNA1C as a risk factor in five major forms of neuropsychiatric disease — schizophrenia, major depression, bipolar disorder, autism, and attention deficit hyperactivity disorder (ADHD). All the conditions also share the common clinical feature of high anxiety. By recognizing an overlap between several lines of research, scientists at the University of Iowa and Weill Cornell Medicine of Cornell University have now discovered a new and unexpected role for CACNA1C that may explain its association with these neuropsychiatric diseases and provide a new therapeutic target.
The new study, recently published in eNeuro, shows that loss of the CACNA1C gene from the forebrain of mice results in decreased survival of newborn neurons in the hippocampus, one of only two regions in the adult brain where new neurons are continually produced – a process known as neurogenesis. Death of these hippocampal neurons has been linked to a number of psychiatric conditions, including schizophrenia, depression, and anxiety.
“We have identified a new function for one of the most important genes in psychiatric illness,” says Andrew Pieper, MD, PhD, co-senior author of the study, professor of psychiatry at the UI Carver College of Medicine and a member of the Pappajohn Biomedical Institute at the UI. “It mediates survival of newborn neurons in the hippocampus, part of the brain that is important in learning and memory, mood and anxiety.”
Moreover, the scientists were able to restore normal neurogenesis in mice lacking the CACNA1C gene using a neuroprotective compound called P7C3-A20, which Pieper’s group discovered and which is currently under development as a potential therapy for neurodegenerative diseases. The finding suggests that the P7C3 compounds may also be of interest as potential therapies for these neuropsychiatric conditions, which affect millions of people worldwide and which often are difficult to treat.
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