Understanding the Neurocognitive Heterogeneity in Bipolar Disorder
Understanding the Neurocognitive Heterogeneity in Bipolar Disorder
批准号:
9065620
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 2017-03-31
关键词:
Activities of Daily LivingAcuteAddressAffectiveAffective SymptomsAlcohol or Other Drugs useAnxiety DisordersArchitectureAreaAttentionBiologicalBiological AssayBiological MarkersBipolar DisorderBlood specimenBrain-Derived Neurotrophic FactorChild AbuseCircadian RhythmsClinicalClinical MarkersCluster AnalysisCognitiveCommunitiesComorbidityDataData AnalyticsDevelopmental CourseDiagnosticDiseaseDisease remissionEtiologyEvaluationFrequenciesFutureHealthHeterogeneityImpaired cognitionImpairmentIndependent LivingIndividualInterleukin-12Interleukin-2MeasuresMediator of activation proteinMedicalModelingNeurocognitionNeurocognitiveNeurocognitive DeficitOccupationalOutcomePatientsPatternPeripheralPhenotypePsychotic DisordersQuality of lifeRecording of previous eventsRecoveryResearchRiskRoleSamplingSchizophreniaSeveritiesSleepStructureSubgroupTNF geneTestingVerbal Learningabuse neglectbasecognitive performancecohortcytokinedesigndisabling symptomeffective therapyexecutive functionfunctional disabilityfunctional outcomesinflammatory markerinsightneurotrophic factornovelnovel strategiespediatric traumaperformance testssocialtrait
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,即使在情感缓解期,BPD患者也存在持续的、特征样的神经认知障碍模式。在群体水平上,这些缺陷的严重程度比平均水平低3/4到1个标准差,明显低于精神分裂症的严重程度(SZ)。然而,最近的证据表明,在心境良好的BPD患者中,认知功能障碍的发生率约为40-60%,其中相当大比例的患者表现为认知功能完好。这与SZ中这种表型的相对均匀性形成对比,SZ中bbb90 %的患者表现出明显的损伤。更好地了解BPD的认知异质性,为什么有些患者会出现明显的认知困难,而另一些患者则没有,对于优化患者的生活质量至关重要。目前的建议旨在使用一种新方法确定350名BPD患者认知功能障碍的临床和生物学预测因素。我们将在基于神经认知表现的样本中对同质亚组进行经验测试,并测试一系列临床特征和生物标志物作为损伤的潜在预测因素。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。数据将为BPD的神经认知基础结构及其病因提供重要信息,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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