Understanding the Neurocognitive Heterogeneity in Bipolar Disorder
Understanding the Neurocognitive Heterogeneity in Bipolar Disorder
批准号:
8596131
负责人:
Katherine Elizabeth Burdick
金额:
$42.38万
依托单位国家:
美国
项目类别:
财政年份:
2013
资助国家:
美国
项目状态:
已结题
起止时间:
2013-08-05 至 2018-04-30
关键词:
Activities of Daily LivingAcuteAddressAffectiveAffective SymptomsAlcohol or Other Drugs useAnxiety DisordersArchitectureAreaAttentionBiologicalBiological AssayBiological MarkersBipolar DisorderBlood specimenBrain-Derived Neurotrophic FactorChild AbuseCircadian RhythmsClinicalClinical MarkersCluster AnalysisCognitiveCommunitiesComorbidityDataDevelopmentDiagnosticDiseaseDisease remissionEtiologyEvaluationFrequenciesFutureHeterogeneityImpaired cognitionImpairmentIndependent LivingIndividualInterleukin-12Interleukin-2MeasuresMediator of activation proteinMedicalModelingNeurocognitionNeurocognitiveNeurocognitive DeficitOccupationalOutcomePatientsPatternPerformancePeripheralPhenotypePsychotic DisordersQuality of lifeRecording of previous eventsRecoveryRelative (related person)ResearchRiskRoleSamplingSchizophreniaSeveritiesSleepStructureSubgroupSymptomsTestingTumor Necrosis Factor-alphaVerbal Learningabuse neglectbasecohortcytokinedesigneffective therapyexecutive functionfunctional disabilityfunctional outcomeshuman TNF proteininflammatory markerinsightneurotrophic factornovelnovel strategiespediatric traumaperformance testspublic health relevancesocialtrait
中文摘要
描述(由申请人提供):双相情感障碍(BPD)患者曾被认为可以实现完全的发作间恢复,特别是在认知功能障碍方面。最近的数据表明,BPD患者的神经认知障碍具有持续性、特征样模式,即使在情感缓解期间也是如此。在组水平上,这些缺陷的严重程度是低于平均值的3/4至1个完整的标准差,这明显低于精神分裂症(SZ)中观察到的缺陷。然而,最近的证据表明,心境正常的BPD患者中认知障碍的频率约为40- 60%,其中很大一部分患者的特征是认知功能减退。这与SZ中该表型的相对同质性形成对比,在SZ中> 90%的患者表现出显著的损伤。更好地理解BPD的认知异质性,为什么有些患者会出现明显的认知困难,而另一些患者则不会,这对优化患者的生活质量至关重要。目前的提案旨在使用一种新的方法确定350例BPD患者认知障碍的临床和生物学预测因素。我们将凭经验检验样本中基于神经认知表现的同质亚组,并检验临床特征和生物标志物的盒作为损伤的潜在预测因子。我们还将研究神经认知功能与职业,社会和独立生活能力领域的日常功能能力之间的关系。这些数据将为BPD及其病因学的神经认知基础结构提供重要信息,指导未来针对这些致残症状进行治疗的努力。
英文摘要
DESCRIPTION (provided by applicant): Patients with bipolar disorder (BPD) were once thought to achieve complete inter-episode recovery, particularly with regard to cognitive dysfunction. More recent data suggest a persistent, trait-like pattern of neurocognitive impairments in BPD, even during periods of affective remission. At the group level, the severity of these deficits is 3/4 to 1 full standard deviation below average, which is significantly less severe than deficits noted in schizophrenia (SZ). Recent evidence, however, suggests that the frequency of cognitive impairment in euthymic BPD patients is ~40-60%, with a substantial proportion of patients characterized as cognitively- spared. This contrasts with the relative homogeneity of this phenotype in SZ where > 90% of patients demonstrates significant impairment. A better understanding of the cognitive heterogeneity in BPD, why some patients develop significant cognitive difficulties while others do not, is critical toward optimizing patiets' quality of life. The current proposal aims to determine the clinical and biological predictors of cognitive impairment in 350 patients with BPD using a novel approach. We will empirically test for homogeneous subgroups within the sample based neurocognitive performance and test a cassette of clinical features and biomarkers as potential predictors of impairment. We will also investigate the relationship between neurocognitive functioning and everyday functional capacity in the areas of occupational, social and independent living ability. Data will provide important information on the underlying structure of neurocognition in BPD and its etiology, guiding future efforts to target these disabling symptoms with treatment.
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