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value="desc">Date Descending</option></select></div><div class="o-input__droplist1 c-sort__page-input"><label for="c-sort2">Show:</label><select name="rows" id="c-sort2" form="facetForm"><option selected="" value="10">10</option><option value="20">20</option><option value="30">30</option><option value="40">40</option><option value="50">50</option><option value="100">100</option></select></div></div><input type="hidden" name="start" form="facetForm" value="0"/><nav class="c-pagination--next"><ul><li><a href="" aria-label="you are on result set 1" class="c-pagination__item--current">1</a></li><li><a href="" aria-label="go to result set 2" class="c-pagination__item">2</a></li><li><a href="" aria-label="go to result set 3" class="c-pagination__item">3</a></li><li><a href="" aria-label="go to result set 4" class="c-pagination__item">4</a></li><li><a href="" aria-label="go to result set 19" class="c-pagination__item">19</a></li><li class="c-pagination__next"><a href="" aria-label="go to Next result set">Next</a></li></ul></nav></div><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-thesis">Thesis</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/91s9c4rh"><div class="c-clientmarkup">Neural Connectivity during Multisensory Episodic Memory in Schizophrenia</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AMoran%2C%20Zachary">Moran, Zachary</a> </li><li class="c-authorlist__begin"><span class="c-authorlist__heading">Advisor(s):</span> <a href="/search/?q=author%3ACannon%2C%20Tyrone%20D">Cannon, Tyrone D</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_etd">UCLA Electronic Theses and Dissertations</a> (2013)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><p>Evidence suggests that the core cognitive features of schizophrenia (SZ) include impairments in auditory and visual memory systems and that each of these deficits individually correlates with functional impairment. However, recent basic research suggests that numerous levels of cognitive processing, from perception to learning, optimally function under multisensory conditions, i.e., with multiple sensory modalities engaged at the same time by the same stimulus. Growing evidence points to the possibility that multisensory learning facilitates neuroplasticity beyond what is possible in unisensory modalities, and, what is more, multisensory information has increasingly been found to rely upon neural communication both within specific cortical modules and also across broad neural networks. In the area of SZ research, recent formulations of the disorder suggest that it is precisely in the domain of neural communication, or connectivity and plasticity, that patients are characteristically impaired. Yet, in the extant literature, one finds very few investigations of memory or other processes in which the more ecologically valid, multisensory stimuli were employed. Furthermore, while the dysconnection model of SZ is promising theoretically and supported by neurological data, very few studies seek instantiations of these effects behaviorally or the emergent properties of their biomarkers. The current study examined SZ patients' capacity to benefit from multisensory encoding of auditory memoranda relative to healthy controls. It further sought to delineate the electrophysiological substrates predictive of behavioral performance within the framework of a neuroconnectivity-based model of episodic memory function. In addition to replicating pilot data findings of benefits to auditory recognition from multisensory encoding in controls, the data also demonstrated a capacity for SZ patients to capitalize upon this same process for improvement of auditory memory deficits. In keeping with the theoretical model, results revealed that recognition of unisensory-encoded sounds were predicted by low frequency connectivity across a broad, hippocampally-centered network. Auditory memory deficits in patients were statistically mediated by impairments in the operation of this system and several measures of SZ symptomatology were associated with those same biomarkers. Increases in memory for multisensory-encoded sounds appeared to be predicted by both low- and high-frequency posterior connectivity for which no group differences were found.</p></div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/91s9c4rh"><img src="/cms-assets/a7ea10a7b3786aa73637fd4983f84910101e02e9d5271ab17e33c50c10a1c888" alt="Cover page: Neural Connectivity during Multisensory Episodic Memory in Schizophrenia"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-thesis">Thesis</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/41n0x4rm"><div class="c-clientmarkup">Amygdala-Prefrontal Function and Clinical Course among Adolescents and Young Adults at Clinical High Risk for Psychosis</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AGee%2C%20Dylan">Gee, Dylan</a> </li><li class="c-authorlist__begin"><span class="c-authorlist__heading">Advisor(s):</span> <a href="/search/?q=author%3ACannon%2C%20Tyrone%20D">Cannon, Tyrone D</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ATottenham%2C%20Nim">Tottenham, Nim</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_etd">UCLA Electronic Theses and Dissertations</a> (2015)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><p>Emotion processing deficits are core features of schizophrenia, and patients display abnormalities in emotion processing at the neural level. However, the extent to which these deficits are present prior to the onset of psychosis and the role that they might play in its development are not well understood. Given the severity of psychotic illness and limitations of extant treatments, research has increasingly focused on the early detection of risk for psychosis to elucidate mechanisms underlying risk progression and facilitate early intervention. Integrating biological markers derived through neuroimaging into predictive algorithms represents a promising avenue to improve risk detection. Based on prior findings of amygdala-prefrontal abnormalities in schizophrenia, the present study investigated whether alterations in amygdala-prefrontal circuitry predate the onset of psychosis and predict clinical outcomes. Participants were adolescents and young adults at clinical high risk (CHR) for psychosis and healthy controls who completed an emotional faces fMRI task at baseline and received follow-up clinical assessments through the North American Longitudinal Prodrome Study. Findings revealed differential activation and functional connectivity at baseline among CHR participants who recovered symptomatically within six months or who converted to psychosis. Compared with non-converting CHR participants and healthy controls, converters exhibited reduced activation in the amygdala and prefrontal cortex (PFC) during emotion processing. Converters showed positive amygdala-PFC connectivity, compared with the expected pattern of negative connectivity in this regulatory circuit. In contrast, the recovery group resembled controls and showed increased amygdala and PFC activation, as well as stronger negative amygdala-prefrontal functional connectivity. Behaviorally, CHR participants who converted to psychosis also performed with lower accuracy during the emotional faces task at baseline, compared with CHR participants who recovered from the at-risk state. The present findings suggest that the extent to which amygdala-prefrontal circuitry is abnormal or typical among individuals at risk for psychosis may relate to the severity of clinical course. Taken together, these results provide novel insight into the nature of emotion processing deficits in the development of psychosis and may enhance early identification of risk for psychosis.</p></div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/41n0x4rm"><img src="/cms-assets/35b205fb6996ad0c88869261eb2aabf6e75463aa691319ecb7c563e3f858297a" alt="Cover page: Amygdala-Prefrontal Function and Clinical Course among Adolescents and Young Adults at Clinical High Risk for Psychosis"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-thesis">Thesis</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/8944z06b"><div class="c-clientmarkup">Disruption in peripheral expression of genes related to cognition among patients with schizophrenia and bipolar disorder and their co-twins</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AViehman%2C%20Rachael%20W.">Viehman, Rachael W.</a> </li><li class="c-authorlist__begin"><span class="c-authorlist__heading">Advisor(s):</span> <a href="/search/?q=author%3ACannon%2C%20Tyrone%20D">Cannon, Tyrone D</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_etd">UCLA Electronic Theses and Dissertations</a> (2012)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><p>Schizophrenia and bipolar disorder are substantially heritable psychiatric illnesses. This study examined peripheral gene expression in an initial sample recruited in Sweden consisting of 35 individuals with schizophrenia and their unaffected co-twins, 24 individuals with bipolar disorder and their unaffected co-twins, and 60 control twins without a history of significant psychiatric illness. Results were confirmed with a secondary sample of 18 individuals with schizophrenia and their unaffected co-twins and 37 non-psychiatric control twins recruited in Finland. Expression in peripheral blood lymphocytes was measured using the Illumina Human WG6 v3.0 gene chip. A cognitive endophenotype was used to screen for genes that varied in relation to cognition out of the genome-wide panel. Results of the mixed-model ANOVA revealed 28 genes showed a significant association with cognitive performance at a corrected 伪 = 0.05 and 47 at a corrected 伪 = 0.10. Twelve of these genes showed significantly decreased expression in patients with schizophrenia and five showed decreased expression in patients with bipolar disorder compared to controls. Nine genes also showed decreased expression in the unaffected co-twins of patients with schizophrenia compared to controls. All twelve genes also showed decreased expression in the secondary sample of patients with schizophrenia. Further research is necessary to determine the relationship between decreased peripheral expression of these genes and expression levels in the central nervous system and relationships with other factors such as duration of illness and psychotropic medication use.</p></div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/8944z06b"><img src="/cms-assets/a81b76d6cbfb4866b1fac3d07096a49559edecbed138e89908b693d43f41c821" alt="Cover page: Disruption in peripheral expression of genes related to cognition among patients with schizophrenia and bipolar disorder and their co-twins"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/8mt4m6nd"><div class="c-clientmarkup">Depression, family interaction and family intervention in adolescents at clinical-high risk for psychosis.</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ARinne%2C%20Gabrielle">Rinne, Gabrielle</a>; </li><li><a href="/search/?q=author%3AOBrien%2C%20Mary">OBrien, Mary</a>; </li><li><a href="/search/?q=author%3AMiklowitz%2C%20David">Miklowitz, David</a>; </li><li><a href="/search/?q=author%3AAddington%2C%20Jean">Addington, Jean</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ACannon%2C%20Tyrone">Cannon, Tyrone</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_postprints">UCLA Previously Published Works</a> (2021)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">AIM: The relationship between family behaviour and depression in adolescents at clinical high risk (CHR) for psychosis remains understudied despite high rates of depression in this population. This study examines the relationship between family problem-solving behaviours and depression in CHR adolescents and the impact of family interventions targeting subthreshold symptoms of psychosis on reducing symptoms of depression over 2-years. METHODS: Participants were a subset of the North American Prodrome Longitudinal Study who were randomized to 6-months of family focused therapy for individuals at CHR or family psychoeducational treatment. We evaluated the relationship between communication during family conflict discussion and adolescents symptoms of depression before treatment. At follow-up assessments the family treatment groups were compared on depression. Finally, we compared those in family treatment with matched controls. RESULTS: Adolescents constructive communication was associated with less severe symptoms of depression before treatment. Symptoms of depression improved for adolescents in both family treatment groups. However, there were no significant group by treatment interactions. When adolescents who participated in either type of family intervention were compared to CHR adolescent controls, symptoms of depression improved for adolescents in treatment and control groups, but there were no significant time by treatment interactions. CONCLUSIONS: The communication skills of CHR adolescents are related to both depression and their parents communication skills pre-treatment. However, reductions in depression over the course of the treatment trial cannot be attributed to family treatment. It is imperative to incorporate interventions that directly target depression into future family treatment studies.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/8mt4m6nd"><img src="/cms-assets/b7ec1383b38e31acd4222ccde84f45b0fdaa7c74c2acb4fb2db07a35c9900652" alt="Cover page: Depression, family interaction and family intervention in adolescents at clinical-high risk for psychosis."/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/733482p5"><div class="c-clientmarkup">Psychosis risk screening in different populations using the Prodromal Questionnaire: A systematic review.</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ASavill%2C%20Mark">Savill, Mark</a>; </li><li><a href="/search/?q=author%3ADAmbrosio%2C%20Jennifer">DAmbrosio, Jennifer</a>; </li><li><a href="/search/?q=author%3ACannon%2C%20Tyrone">Cannon, Tyrone</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ALoewy%2C%20Rachel">Loewy, Rachel</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsf_postprints">UC San Francisco Previously Published Works</a> (2018)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">AIM: Diagnosing individuals at ultra high risk (UHR) for psychosis can improve early access to treatment, and a two-stage model utilizing self-report screening followed by a clinical interview can be accurate and efficient. However, it is currently unclear which screening cut-offs to adopt with different populations. METHODS: A systematic review of diagnostic accuracy studies evaluating the Prodromal Questionnaire (PQ) as a preliminary screener for UHR and psychosis was conducted to examine screening effectiveness in different contexts. MedLine, PsycInfo, SCOPUS and ProQuest Dissertations and Abstracts databases were electronically searched, along with a review screen and citation search of key papers. Findings were summarized in a narrative synthesis. RESULTS: In total, 14 diagnostic accuracy studies and 45 studies using the PQ as a screening tool for UHR and psychosis were included. In all settings, the 3 different versions of the PQ were all found to accurately identify UHR and full psychosis. Higher cut-off points were required in non-help-seeking samples, relative to general help-seeking populations, which in turn were higher than those needed in samples highly enriched with UHR participants. CONCLUSION: The findings support the use of the PQ as a preliminary screening tool for UHR in different settings; however, higher thresholds in lower UHR-prevalence populations are necessary to minimize false positives. Including the distress criteria, rather than just number of symptoms, may improve screening effectiveness. Different thresholds may be appropriate in different contexts depending on the importance of sensitivity vs specificity. Protocol registration: CRD42016033004.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/733482p5"><img src="/cms-assets/809dad02cf37dbe7336ce28bfa5bd12d0770777e2b09500011ce83e47781981c" alt="Cover page: Psychosis risk screening in different populations using the Prodromal Questionnaire: A systematic review."/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/2fd6h2rx"><div class="c-clientmarkup">Decreases in Perceived Maternal Criticism Predict Improvement in Subthreshold Psychotic Symptoms in a Randomized Trial of Family-Focused Therapy for Individuals at Clinical High Risk for Psychosis</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AO%E2%80%99Brien%2C%20Mary%20P">O鈥橞rien, Mary P</a>; </li><li><a href="/search/?q=author%3AMiklowitz%2C%20David%20J">Miklowitz, David J</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ACannon%2C%20Tyrone%20D">Cannon, Tyrone D</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_postprints">UCLA Previously Published Works</a> (2015)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">Perceived criticism (PC) is a measure of how much criticism from 1 family member "gets through" to another. PC ratings have been found to predict the course of psychotic disorders, but questions remain regarding whether psychosocial treatment can effectively decrease PC, and whether reductions in PC predict symptom improvement. In a sample of individuals at high risk for psychosis, we examined a) whether Family Focused Therapy for Clinical High-Risk (FFT-CHR), an 18-session intervention that consists of psychoeducation and training in communication and problem solving, brought about greater reductions in perceived maternal criticism, compared to a 3-session family psychoeducational intervention; and b) whether reductions in PC from baseline to 6-month reassessment predicted decreases in subthreshold positive symptoms of psychosis at 12-month follow-up. This study was conducted within a randomized controlled trial across 8 sites. The perceived criticism scale was completed by 90 families prior to treatment and by 41 families at 6-month reassessment. Evaluators, blind to treatment condition, rated subthreshold symptoms of psychosis at baseline, 6- and 12-month assessments. Perceived maternal criticism decreased from pre- to posttreatment for both treatment groups, and this change in criticism predicted decreases in subthreshold positive symptoms at 12-month follow-up. This study offers evidence that participation in structured family treatment is associated with improvement in perceptions of the family environment. Further, a brief measure of perceived criticism may be useful in predicting the future course of attenuated symptoms of psychosis for CHR youth.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/2fd6h2rx"><img src="/cms-assets/e37c39d4683c4c0a564e2bdfd9316c13cb1200d11c0a1749d9e68d603d3db55a" alt="Cover page: Decreases in Perceived Maternal Criticism Predict Improvement in Subthreshold Psychotic Symptoms in a Randomized Trial of Family-Focused Therapy for Individuals at Clinical High Risk for Psychosis"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-thesis">Thesis</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/3xb4m2m4"><div class="c-clientmarkup">Spatial Working Memory in Twins Discordant for Schizophrenia and Bipolar Disorder</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AHigier%2C%20Rachel%20Gloria">Higier, Rachel Gloria</a> </li><li class="c-authorlist__begin"><span class="c-authorlist__heading">Advisor(s):</span> <a href="/search/?q=author%3ACannon%2C%20Tyrone%20D">Cannon, Tyrone D</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ARissman%2C%20Jesse%20A">Rissman, Jesse A</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_etd">UCLA Electronic Theses and Dissertations</a> (2014)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><p>Emerging evidence indicates substantial genetic overlap between schizophrenia and bipolar disorder, but the neurobiological mechanisms underlying these shared susceptibility factors remain unclear. Examining the specific neural disruptions associated with susceptibility to these illnesses, and clarifying the nature of overlap between them, is critical to understanding the etiological bases of these disorders. In view of prior reports supporting working memory dysfunction as a candidate endophenotype of schizophrenia and bipolar disorder, we examined the neural mechanisms subserving working memory function in individuals carrying liability for both syndromes. To our knowledge, no prior neuroimaging study has simultaneously examined twin pairs discordant for schizophrenia and bipolar disorder to determine whether liability-related disruptions of working memory in the disorders overlap. We employed a trial-based spatial working memory task paradigm designed to separate activation in encoding and retrieval phases. As predicted, schizophrenia and bipolar probands as well as their non-affected co-twins </p><p>exhibited hypoactivation as well as hypoconnectivity in fronto-parietal working memory circuitry compared with controls, indicating significant endophenotypic overlap in aberrant task-related functional and network activation. These cortical alterations were significantly more pronounced during encoding phases of working memory compared with retrieval phases. Additionally, both proband groups showed hyperactivation in key nodes of the default network during retrieval phases of working memory, suggesting that failure to disengage this network during memory-guided response may represent an area of phenotypic overlap. These findings are consistent with previous evidence indicating overlapping functional alterations in schizophrenia and bipolar disorder and may inform models of mechanisms underpinning the apparent biological overlap between disorders, particularly in regards to encoding processes. Findings from this study help to characterize the nature of overlap and are consistent with a model of shared inheritance of working memory dysfunction in schizophrenia and bipolar disorder.</p></div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/3xb4m2m4"><img src="/cms-assets/93bee55fe3851a66e9ad119d26d744e41303972a2773855e4dac8c0fc1c6fd79" alt="Cover page: Spatial Working Memory in Twins Discordant for Schizophrenia and Bipolar Disorder"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/58h8q7wr"><div class="c-clientmarkup">Family Communication With Teens at Clinical High-Risk for Psychosis or Bipolar Disorder</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ASalinger%2C%20Julia%20M">Salinger, Julia M</a>; </li><li><a href="/search/?q=author%3AO%E2%80%99Brien%2C%20Mary%20P">O鈥橞rien, Mary P</a>; </li><li><a href="/search/?q=author%3AMiklowitz%2C%20David%20J">Miklowitz, David J</a>; </li><li><a href="/search/?q=author%3AMarvin%2C%20Sarah%20E">Marvin, Sarah E</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ACannon%2C%20Tyrone%20D">Cannon, Tyrone D</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_postprints">UCLA Previously Published Works</a> (2018)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">Previous research has found that family problem-solving interactions are more constructive and less contentious when there is a family member with bipolar disorder compared with schizophrenia. The present study extended this research by examining whether family problem-solving interactions differ between clinical high-risk (CHR) stages of each illness. Trained coders applied a behavioral coding system (O'Brien et al., 2014) to problem-solving interactions of parents and their adolescent child, conducted just prior to beginning a randomized trial of family-focused therapy. The CHR for psychosis sample included 58 families with an adolescent with attenuated positive symptoms, brief intermittent psychosis, or genetic risk and functional deterioration; the CHR for bipolar disorder sample included 44 families with an adolescent with "unspecified" bipolar disorder or major depressive disorder and at least one first or second degree relative with bipolar I or II disorder. When controlling for adolescent gender, age, functioning, and parent education, mothers of youth at CHR for psychosis displayed significantly more conflictual and less constructive communication than did mothers of youth at CHR for bipolar disorder. Youth risk classification did not have a significant relationship with youths' or fathers' communication behavior. The family environment among help-seeking adolescents may be more challenging for families with an adolescent at CHR for psychosis compared with bipolar illness. Accordingly, families of adolescents at clinical high-risk for psychosis may benefit from more intensive or focused communication training than is required by families of adolescents at clinical high-risk for bipolar disorder or other mood disorders. (PsycINFO Database Record</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/58h8q7wr"><img src="/cms-assets/8007701b1bf268cd729a24f30d41bd5e253770f6270789a314c3a0aa4c283137" alt="Cover page: Family Communication With Teens at Clinical High-Risk for Psychosis or Bipolar Disorder"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/1st5b8zp"><div class="c-clientmarkup">Dysbindin Modulates Prefrontal Cortical Glutamatergic Circuits and Working Memory Function in Mice</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AJentsch%2C%20James%20David">Jentsch, James David</a>; </li><li><a href="/search/?q=author%3ATrantham-Davidson%2C%20Heather">Trantham-Davidson, Heather</a>; </li><li><a href="/search/?q=author%3AJairl%2C%20Corey">Jairl, Corey</a>; </li><li><a href="/search/?q=author%3ATinsley%2C%20Matthew">Tinsley, Matthew</a>; </li><li><a href="/search/?q=author%3ACannon%2C%20Tyrone%20D">Cannon, Tyrone D</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ALavin%2C%20Antonieta">Lavin, Antonieta</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_postprints">UCLA Previously Published Works</a> (2009)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">Behavioral genetic studies of humans have associated variation in the DTNBP1 gene with schizophrenia and its cognitive deficit phenotypes. The protein coded for by DTNBP1, dysbindin, is expressed within forebrain glutamatergic neurons, in which it interacts with proteins involved in vesicular trafficking and exocytosis. In order to further delineate the cellular, physiological, and behavioral phenotypes associated with reduced dysbindin expression, we conducted studies in mice carrying a null mutation within the dtnbp1 gene. Dysbindin mutants showed impairments of spatial working memory compared with wild-type controls; heterozygous mice showed intermediate levels of cognitive dysfunction. Deep-layer pyramidal neurons recorded in the prefrontal cortex of mutant mice showed reductions in paired-pulse facilitation, and evoked and miniature excitatory post-synaptic currents, indicating a difference in the function of pre-synaptic glutamatergic terminals as well as elevated spike thresholds. Taken together, these data indicate that dysbindin potently regulates excitatory transmission in the prefrontal cortex, potentially through a pre-synaptic mechanism, and consequently modulates cognitive functions depending on this brain region, providing new insights into the molecular mechanisms underlying cortical dysfunction in schizophrenia.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/1st5b8zp"><img src="/cms-assets/da12393368fb29940eea3c4d0fdb1461f1a011f57a74bf509da712d825883c15" alt="Cover page: Dysbindin Modulates Prefrontal Cortical Glutamatergic Circuits and Working Memory Function in Mice"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/72s545s2"><div class="c-clientmarkup">Treatment fidelity in FFT鈥怌HR</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AMarvin%2C%20Sarah%20E">Marvin, Sarah E</a>; </li><li><a href="/search/?q=author%3AMiklowitz%2C%20David%20J">Miklowitz, David J</a>; </li><li><a href="/search/?q=author%3AO'Brien%2C%20Mary%20P">O'Brien, Mary P</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ACannon%2C%20Tyrone%20D">Cannon, Tyrone D</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_postprints">UCLA Previously Published Works</a> (2016)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><h3>Aim</h3>Family psychoeducation is an effective adjunct to pharmacotherapy in delaying relapse among patients with schizophrenia and bipolar disorder. This study tested the treatment adherence and competence of newly trained clinicians to an adaptation of family-focused therapy for individuals at clinical high risk for psychosis (FFT-CHR).<h3>Methods</h3>The sample included 103 youth or young adults (ages 12-30 years) who had attenuated positive symptoms of psychosis. Families participated in a randomized trial comparing two psychosocial interventions: FFT-CHR (18 sessions over 6 months) and enhanced care (EC; 3 sessions over 1 month). Following a 1.5-day training seminar, 24 clinicians from eight study sites received teleconference supervision in both treatment protocols for the 2-year study period. Treatment fidelity was rated with the 13-item Therapy Competence and Adherence Scales, Revised.<h3>Results</h3>Supervisors classified 90% of treatment sessions as above acceptable fidelity thresholds (ratings of 5 or better on a 1-7 scale of overall fidelity). As expected, fidelity ratings indicated that FFT-CHR included a greater emphasis on communication and problem-solving skills training than EC, but ratings of non-specific clinician skills, such as maintaining rapport and appropriately pacing sessions, did not differ between conditions. Treatment fidelity was not related to the severity of symptoms or family conflict at study entry.<h3>Conclusions</h3>FFT-CHR can be administered with high levels of fidelity by clinicians who receive training and supervision. Future studies should examine whether there are more cost-effective methods for training, supervising and monitoring the fidelity of FFT-CHR.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/72s545s2"><img src="/cms-assets/c787f7db6d204a5827793e703098b618fe4b92dc1091f4d23313dd61192847bd" alt="Cover page: Treatment fidelity in FFT鈥怌HR"/></a></div></section><nav class="c-pagination--next"><ul><li><a href="" aria-label="you are on result set 1" class="c-pagination__item--current">1</a></li><li><a href="" aria-label="go to result set 2" class="c-pagination__item">2</a></li><li><a href="" aria-label="go to result set 3" class="c-pagination__item">3</a></li><li><a href="" aria-label="go to result set 4" class="c-pagination__item">4</a></li><li><a href="" aria-label="go to result set 19" class="c-pagination__item">19</a></li><li class="c-pagination__next"><a href="" aria-label="go to Next result set">Next</a></li></ul></nav></section></main></form></div><div><div class="c-toplink"><a href="javascript:window.scrollTo(0, 0)">Top</a></div><footer class="c-footer"><nav class="c-footer__nav"><ul><li><a href="/">Home</a></li><li><a href="/aboutEschol">About eScholarship</a></li><li><a href="/campuses">Campus Sites</a></li><li><a href="/ucoapolicies">UC Open Access Policy</a></li><li><a href="/publishing">eScholarship Publishing</a></li><li><a href="https://www.cdlib.org/about/accessibility.html">Accessibility</a></li><li><a href="/privacypolicy">Privacy Statement</a></li><li><a href="/policies">Site Policies</a></li><li><a href="/terms">Terms of Use</a></li><li><a href="/login"><strong>Admin Login</strong></a></li><li><a href="https://help.escholarship.org"><strong>Help</strong></a></li></ul></nav><div class="c-footer__logo"><a href="/"><img class="c-lazyimage" data-src="/images/logo_footer-eschol.svg" alt="eScholarship, University of California"/></a></div><div class="c-footer__copyright">Powered by the<br/><a href="http://www.cdlib.org">California Digital Library</a><br/>Copyright 漏 2017<br/>The Regents of the University of California</div></footer></div></div></div></div> <script src="/js/vendors~app-bundle-7424603c338d723fd773.js"></script> <script src="/js/app-bundle-63f992b6abba5f8338a3.js"></script> </body> </html>