Department of Neurology, College of Medicine, Hanyang University Medical Center, Seongdong-gu, Seoul, Republic of Korea.
J Alzheimers Dis. 2013;35(1):129-36. doi: 10.3233/JAD-122320.
This study aimed to evaluate the relationship between loss of white matter cholinergic pathways, atrophy of the nucleus basalis of Meynert (NBM), and cognitive function in patients with subcortical ischemic vascular dementia (SIVD) or Alzheimer's disease (AD).
The participants included 26 SIVD, 17 probable AD with or without white-matter changes, and 20 age-matched healthy controls. Thin-section coronal T2-weighted images were acquired using 3.0 T MR. The extent of white matter hyperintensities within cholinergic pathways were assessed using the cholinergic pathways hyperintensities scale (CHIPS). NBM atrophy was assessed from the thickness of the substantia innominata (SI) at the level of the crossing of the anterior commissure. Cognitive impairment was measured using the Mini-Mental State Examination (MMSE) and Clinical Dementia Rating (CDR). Correlations between CHIPSs, SI thickness, and cognitive impairment were evaluated using the Spearman ranked correlation test.
In AD, MMSE scores and CDR were correlated with SI thickness (ρ = 0.450, p = 0.006 and ρ = -0.520, p = 0.030, respectively) but not with CHIPS scores (ρ = -0.160, p = 0.530 and ρ = 0.270, p = 0.292, respectively). By contrast, aggravated MMSE score and CDR in SIVD had a tendency to correlate with elevated CHIPS scores (ρ = -0.344, p = 0.127 and ρ = 0.521, p = 0.021, respectively) but not with SI thickness (ρ = -0.210, p = 0.480 and ρ = 0.080, p = 0.736, respectively).
Loss of cholinergic pathways correlates with cognitive dysfunction in both AD and SIVD. The mechanisms appear to differ: NBM atrophy is likely to be the predominant contributor to cognitive impairments in AD, whereas, the cognitive dysfunction of SIVD was associated with compromised subcortical cholinergic fibers not with nucleus itself.
本研究旨在评估皮质下缺血性血管性痴呆（SIVD）或阿尔茨海默病（AD）患者的白质胆碱能通路丧失、基底核梅内尔特核（NBM）萎缩与认知功能之间的关系。
参与者包括 26 例 SIVD、17 例可能的 AD（伴或不伴白质改变）和 20 名年龄匹配的健康对照者。使用 3.0 T MR 采集冠状薄层 T2 加权图像。使用胆碱能通路高信号量表（CHIPS）评估胆碱能通路内的白质高信号程度。从前交叉点水平的无名质厚度评估 NBM 萎缩。使用简易精神状态检查（MMSE）和临床痴呆评定量表（CDR）评估认知障碍。使用 Spearman 等级相关检验评估 CHIPSs、SI 厚度与认知障碍之间的相关性。
在 AD 中，MMSE 评分和 CDR 与 SI 厚度相关（ρ=0.450，p=0.006 和 ρ=-0.520，p=0.030），但与 CHIPS 评分无关（ρ=-0.160，p=0.530 和 ρ=0.270，p=0.292）。相比之下，SIVD 中 MMSE 评分和 CDR 的恶化与 CHIPS 评分的升高呈正相关趋势（ρ=-0.344，p=0.127 和 ρ=0.521，p=0.021），但与 SI 厚度无关（ρ=-0.210，p=0.480 和 ρ=0.080，p=0.736）。
胆碱能通路的丧失与 AD 和 SIVD 中的认知功能障碍相关。其机制似乎不同：NBM 萎缩可能是 AD 认知障碍的主要原因，而 SIVD 的认知功能障碍与皮质下胆碱能纤维受损有关，而不是与核本身有关。
