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用于研究路易体痴呆的研究模型。

Research models to study lewy body dementia.

作者信息

Boschen Suelen Lucio, A Mukerjee Aarushi, H Faroqi Ayman, E Rabichow Ben, Fryer John

机构信息

Department of Neuroscience, Mayo Clinic Jacksonville, 4500 San Pablo Rd, Jacksonville, FL, 32224, USA.

Department of Neurosurgery, Mayo Clinic Jacksonville, 4500 San Pablo Rd, Jacksonville, FL, 32224, USA.

出版信息

Mol Neurodegener. 2025 Apr 23;20(1):46. doi: 10.1186/s13024-025-00837-w.

Abstract

Lewy body dementia (LBD) encompasses neurodegenerative dementias characterized by cognitive fluctuations, visual hallucinations, and parkinsonism. Clinical differentiation of LBD from Alzheimer's disease (AD) remains complex due to symptom overlap, yet approximately 25% of dementia cases are diagnosed as LBD postmortem, primarily identified by the presence of α-synuclein aggregates, tau tangles, and amyloid plaques. These pathological features position LBD as a comorbid condition of both Parkinson's disease (PD) and AD, with over 50% of LBD cases exhibiting co-pathologies. LBD's mixed pathology complicates the development of comprehensive models that reflect the full spectrum of LBD's etiological, clinical, and pathological features. While existing animal and cellular models have facilitated significant discoveries in PD and AD research, they lack specificity in capturing LBD's unique pathogenic mechanisms, limiting the exploration of therapeutic avenues for LBD specifically. This review assesses widely used PD and AD models in terms of their relevance to LBD, particularly focusing on their ability to replicate human disease pathology and assess treatment efficacy. Furthermore, we discuss potential modifications to these models to advance the understanding of LBD mechanisms and propose innovative research directions aimed at developing models with enhanced etiological, face, predictive, and construct validity.

摘要

路易体痴呆(LBD)包括以认知波动、视幻觉和帕金森综合征为特征的神经退行性痴呆。由于症状重叠,LBD与阿尔茨海默病(AD)的临床鉴别仍然很复杂,但约25%的痴呆病例在死后被诊断为LBD,主要通过α-突触核蛋白聚集体、tau缠结和淀粉样斑块的存在来确定。这些病理特征将LBD定位为帕金森病(PD)和AD的共病,超过50%的LBD病例表现出共同病理。LBD的混合病理使反映LBD病因、临床和病理特征全貌的综合模型的开发变得复杂。虽然现有的动物和细胞模型在PD和AD研究中促成了重大发现,但它们在捕捉LBD独特的致病机制方面缺乏特异性,限制了针对LBD的治疗途径的探索。本综述根据其与LBD的相关性评估了广泛使用的PD和AD模型,特别关注它们复制人类疾病病理和评估治疗效果的能力。此外,我们讨论了对这些模型的潜在修改,以推进对LBD机制的理解,并提出创新的研究方向,旨在开发具有更高病因、表面、预测和结构效度的模型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b9/12020038/eac0c1b55801/13024_2025_837_Fig1_HTML.jpg

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