Department of Neurology & Innovation Center for Neurological Disorders, Xuanwu Hospital, Capital Medical University, National Center for Neurological Disorders, Beijing, China.
Department of Neurology, Zhengzhou University People's Hospital, Henan Provincial People's Hospital, Zhengzhou, China.
Brain Res. 2024 Jun 15;1833:148881. doi: 10.1016/j.brainres.2024.148881. Epub 2024 Mar 21.
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.
为了确定是否路易体痴呆（LBD）患者伴有阿尔茨海默病（AD）的可能共病表现出更大的神经精神症状（NPS），与不伴有可能的 AD 型共病的患者相比。
我们纳入了 69 名被诊断为路易体痴呆（LBD）的个体，包括痴呆伴路易体（DLB）（n=36）和帕金森病痴呆（PDD）（n=33）。这些参与者有可及的与阿尔茨海默病（AD）相关的脑脊液（CSF）标志物和认知数据。我们评估了 CSF 中β-淀粉样蛋白 42（Aβ42）、磷酸化 tau（p-tau）和总 tau（t-tau）的水平。使用经尸检验证的 CSF 阈值（t-tau/Aβ42 比值>0.3，n=69），我们将个体分为伴有 AD 病理学的 LBD（LBD+AD，n=31）和没有明显 AD 共病的 LBD（LBD-AD，n=38）。此外，使用汉密尔顿抑郁量表（HAMD24）、汉密尔顿焦虑量表（HAMA14）和神经精神问卷（NPI-Q）评估 NPS。使用 Spearman 相关分析来探讨 NPS 与 CSF 标志物谱之间的关系。
在神经精神症状方面，LBD+AD 患者的抑郁症状（HAMD24）明显高于 LBD-AD 患者（P<0.001）。然而，根据 PDD 和 DLB 组，神经精神症状没有显著变化（P＞0.05）。此外，在 LBD+AD 亚组中，CSF 来源的 Aβ42 和 t-tau/Aβ42 生物标志物也与 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。
