Neurotransmitter changes in dementia with Lewy bodies and Parkinson disease dementia in vivo
Neurotransmitter changes in dementia with Lewy bodies and Parkinson disease dementia in vivo
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DOI：
10.1212/wnl.0b013e3181d55f61
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发表时间：
2010-03-16
期刊：
影响因子：
9.9
通讯作者：
Hilker, R.
中科院分区：
文献类型：
--
作者：
Klein, J. C.;Eggers, C.;Hilker, R.
目的：尽管帕金森病伴痴呆（PDD）和路易体痴呆（DLB）显示出广泛的临床和神经病理学重叠，但它们根据认知和运动症状出现的顺序和潜伏期进行区分。两者是否是不同的疾病实体是一个持续的争议。方法：对8例PDD患者、6例DLB患者和9例无痴呆的PD患者进行18氟多巴（FDOPA）、N-C-11-甲基-4-哌啶乙酸酯（MP 4A）和18氟脱氧葡萄糖（FDG）PET检查，并与年龄匹配的对照组进行比较。数据进行了分析，以体素为基础的统计参数映射和区域的利益为基础statistics.Results：我们发现了减少FDOPA摄取在纹状体和边缘系统和关联的前额叶区在所有患者组。PDD患者和DLB患者的新皮层中MP 4A和FDG结合严重减少，从额叶到枕叶区域的信号衰减增加。PDD和DLB之间的显着差异没有发现在任何使用的放射性配体。没有痴呆的PD患者有一个轻微的胆碱能赤字，没有FDG减少vs controls.Conclusions：患者与路易体痴呆和帕金森病痴呆共享相同的dopaminergicand胆碱能赤字配置文件在大脑中，似乎代表了同一枚硬币的两面在一个连续的路易体疾病。除了运动症状外，胆碱能缺陷似乎对痴呆症的发展至关重要。胆碱能缺陷和能量代谢低下的空间一致性认为，皮质传入阻滞是由于基底前脑投射纤维的退化。神经病学（R）2010; 74：885-892
Objective: Although Parkinson disease with dementia (PDD) and dementia with Lewy bodies (DLB) show a wide clinical and neuropathologic overlap, they are differentiated according to the order and latency of cognitive and motor symptom appearance. Whether both are distinct disease entities is an ongoing controversy. Therefore, we directly compared patients with DLB and PDD with multitracer PET.Methods: PET with (18)fluorodopa (FDOPA), N-C-11-methyl-4-piperidyl acetate (MP4A), and 18-fluorodeoxyglucose (FDG) was performed in 8 patients with PDD, 6 patients with DLB, and 9 patients with PD without dementia vs age-matched controls. Data were analyzed with voxel-based statistical parametric mapping and region of interest-based statistics.Results: We found a reduced FDOPA uptake in the striatum and in limbic and associative prefrontal areas in all patient groups. Patients with PDD and patients with DLB showed a severe MP4A and FDG binding reduction in the neocortex with increasing signal diminution from frontal to occipital regions. Significant differences between PDD and DLB were not found in any of the radioligands used. Patients with PD without dementia had a mild cholinergic deficit and no FDG reductions vs controls.Conclusions: Patients with dementia with Lewy bodies and Parkinson disease dementia share the same dopaminergicand cholinergic deficit profile in the brain and seem to represent 2 sides of the same coin in a continuum of Lewy body diseases. Cholinergic deficits seem to be crucial for the development of dementia in addition to motor symptoms. The spatial congruence of cholinergic deficits and energy hypometabolism argues for cortical deafferentation due to the degeneration of projection fibers from the basal forebrain. Neurology (R) 2010; 74: 885-892