Abstract：
BACKGROUND: To determine whether Lewy body dementia (LBD) patients with likely copathology of Alzheimer\'s disease (AD) exhibit greater neuropsychiatric symptom (NPS) compared to those without likely AD-type copathology.
METHODS: We enrolled 69 individuals diagnosed with Lewy body dementia (LBD), comprising both dementia with Lewy bodies (DLB) (n = 36) and Parkinson\'s disease dementia (PDD) (n = 33). These participants had accessible cerebrospinal fluid (CSF) markers related to Alzheimer\'s disease (AD) and cognitive data. We assessed CSF levels of β-amyloid 42 (Aβ42), phosphorylated tau (p-tau), and total tau (t-tau). Employing autopsy-validated CSF thresholds (t-tau/Aβ42 ratio > 0.3, n = 69), we categorized individuals into LBD with AD pathology (LBD + AD, n = 31) and LBD without apparent AD co-pathology (LBD - AD, n = 38). Moreover, the Hamilton Depression Scale (HAMD24), Hamilton Anxiety Scale (HAMA14), and Neuropsychiatric Inventory Questionnaire (NPI-Q) was used to assess the NPS. Spearman correlations were utilized to explore links between NPS and CSF marker profiles.
RESULTS: In terms of neuropsychiatric symptoms, LBD + AD patients demonstrated notably elevated levels of depressive symptoms (HAMD24) in comparison to LBD - AD patients (P < 0.001). However, based on PDD and DLB groups, no significant variations were noted in the neuropsychiatric symptoms(P＞0.05). Moreover, CSF-derived biomarkers of Aβ42, and t-tau/Aβ42 were also associated with HAMD24 total scores in the LBD + AD subsample (P < 0.05).
CONCLUSIONS: There is an association between AD pathological markers and the NPS of LBD. The biologically based classification of LBD may be more advantageous in elucidating clinical heterogeneity than clinically defined syndromes.
METHODS: We enrolled 69 individuals diagnosed with Lewy body dementia (LBD), comprising both dementia with Lewy bodies (DLB) (n = 36) and Parkinson\'s disease dementia (PDD) (n = 33). These participants had accessible cerebrospinal fluid (CSF) markers related to Alzheimer\'s disease (AD) and cognitive data. We assessed CSF levels of β-amyloid 42 (Aβ42), phosphorylated tau (p-tau), and total tau (t-tau). Employing autopsy-validated CSF thresholds (t-tau/Aβ42 ratio > 0.3, n = 69), we categorized individuals into LBD with AD pathology (LBD + AD, n = 31) and LBD without apparent AD co-pathology (LBD - AD, n = 38). Moreover, the Hamilton Depression Scale (HAMD24), Hamilton Anxiety Scale (HAMA14), and Neuropsychiatric Inventory Questionnaire (NPI-Q) was used to assess the NPS. Spearman correlations were utilized to explore links between NPS and CSF marker profiles.
RESULTS: In terms of neuropsychiatric symptoms, LBD + AD patients demonstrated notably elevated levels of depressive symptoms (HAMD24) in comparison to LBD - AD patients (P < 0.001). However, based on PDD and DLB groups, no significant variations were noted in the neuropsychiatric symptoms(P＞0.05). Moreover, CSF-derived biomarkers of Aβ42, and t-tau/Aβ42 were also associated with HAMD24 total scores in the LBD + AD subsample (P < 0.05).
CONCLUSIONS: There is an association between AD pathological markers and the NPS of LBD. The biologically based classification of LBD may be more advantageous in elucidating clinical heterogeneity than clinically defined syndromes.
摘要：
背景：为了确定路易体痴呆（LBD）患者是否有可能的阿尔茨海默病（AD）的副病理学表现出更大的神经精神症状（NPS）相比，没有可能的AD型副病理学。
方法：我们招募了69名诊断为路易体痴呆（LBD）的个体，包括路易体痴呆（DLB）（n=36）和帕金森病痴呆（PDD）（n=33）。这些参与者获得了与阿尔茨海默病（AD）和认知数据相关的脑脊液（CSF）标记。我们评估了β-淀粉样蛋白42（Aβ42）的CSF水平，磷酸化tau（p-tau），和总tau（t-tau）。采用尸检验证的脑脊液阈值（t-tau/Aβ42比值>0.3，n=69），我们将个体分类为患有AD病理的LBD(LBD+AD，n=31）和LBD无明显AD共病（LBD-AD，n=38）。此外，汉密尔顿抑郁量表（HAMD24），汉密尔顿焦虑量表（HAMA14），神经精神量表（NPI-Q）用于评估NPS。利用Spearman相关性来探索NPS和CSF标志物谱之间的联系。
结果：就神经精神症状而言，与LBD-AD患者相比，LBD+AD患者的抑郁症状（HAMD24）水平明显升高（P<0.001）。然而,基于PDD和DLB组，神经精神症状无明显变化(P＞0.05).此外，CSF衍生的Aβ42和t-tau/Aβ42的生物标志物也与LBD+AD子样本中的HAMD24总分相关(P<0.05)。
结论：AD病理标志物与LBD的NPS之间存在关联。LBD的生物学分类可能比临床定义的综合征更有利于阐明临床异质性。
方法：我们招募了69名诊断为路易体痴呆（LBD）的个体，包括路易体痴呆（DLB）（n=36）和帕金森病痴呆（PDD）（n=33）。这些参与者获得了与阿尔茨海默病（AD）和认知数据相关的脑脊液（CSF）标记。我们评估了β-淀粉样蛋白42（Aβ42）的CSF水平，磷酸化tau（p-tau），和总tau（t-tau）。采用尸检验证的脑脊液阈值（t-tau/Aβ42比值>0.3，n=69），我们将个体分类为患有AD病理的LBD(LBD+AD，n=31）和LBD无明显AD共病（LBD-AD，n=38）。此外，汉密尔顿抑郁量表（HAMD24），汉密尔顿焦虑量表（HAMA14），神经精神量表（NPI-Q）用于评估NPS。利用Spearman相关性来探索NPS和CSF标志物谱之间的联系。
结果：就神经精神症状而言，与LBD-AD患者相比，LBD+AD患者的抑郁症状（HAMD24）水平明显升高（P<0.001）。然而,基于PDD和DLB组，神经精神症状无明显变化(P＞0.05).此外，CSF衍生的Aβ42和t-tau/Aβ42的生物标志物也与LBD+AD子样本中的HAMD24总分相关(P<0.05)。
结论：AD病理标志物与LBD的NPS之间存在关联。LBD的生物学分类可能比临床定义的综合征更有利于阐明临床异质性。
