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. 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. 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). 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.

中文翻译：

---

路易体痴呆患者的神经精神症状概况和阿尔茨海默病型病理学标志物

旨在确定可能具有阿尔茨海默病 (AD) 共病理的路易体痴呆 (LBD) 患者与不具有 AD 型共病理的患者相比，是否表现出更严重的神经精神症状 (NPS)。我们招募了 69 名被诊断患有路易体痴呆 (LBD) 的个体，其中包括路易体痴呆 (DLB) (n = 36) 和帕金森病痴呆 (PDD) (n = 33)。这些参与者可以获得与阿尔茨海默病 (AD) 相关的脑脊液 (CSF) 标记物和认知数据。我们评估了脑脊液中 β-淀粉样蛋白 42 (Aβ42)、磷酸化 tau (p-tau) 和总 tau (t-tau) 的水平。采用尸检验证的 CSF 阈值（t-tau/Aβ42 比率 > 0.3，n = 69），我们将个体分为具有 AD 病理学的 LBD（LBD + AD，n = 31）和无明显 AD 共同病理学的 LBD（LBD - AD） ，n = 38）。此外，汉密尔顿抑郁量表（HAMD24）、汉密尔顿焦虑量表（HAMA14）和神经精神问卷调查表（NPI-Q）用于评估NPS。 Spearman 相关性用于探索 NPS 和 CSF 标记物谱之间的联系。在神经精神症状方面，与 LBD - AD 患者相比，LBD + AD 患者的抑郁症状 (HAMD24) 水平显着升高 (P < 0.001)。但PDD组和DLB组的神经精神症状无显着差异（P＞0.05）。此外，CSF 衍生的 Aβ42 和 t-tau/Aβ42 生物标志物也与 LBD + AD 子样本中的 HAMD24 总分相关（P < 0.05）。 AD 病理标志物与 LBD 的 NPS 之间存在关联。基于生物学的 LBD 分类可能比临床定义的综合征更有利于阐明临床异质性。