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CCL3 与阿尔茨海默病患者情绪障碍和人格改变的数量相关。

CCL3 correlates with the number of mood disturbances and personality changes in patients with Alzheimer's disease.

机构信息

Department of Neurology, University of Medical Sciences, Poznan, Poland.

出版信息

Psychiatry Res. 2010 Apr 30;176(2-3):261-4. doi: 10.1016/j.psychres.2009.02.007. Epub 2010 Feb 18.

Abstract

Although Alzheimer's disease (AD) is a primary degenerative disorder, a microglial-mediated inflammatory response, provoked by amyloid beta (Abeta), contributes to the neurodegeneration and subsequently to the cell loss. Since such an inflammatory contribution to neurodegeneration may influence disease progression, a basic question arises concerning the mechanisms of possible clinical signs dependent on inflammatory reactions. In the present study we investigated the levels of CCL3 in the peripheral blood of AD patients and correlated findings with the results of clinical tests such as the Mini-Mental State Examination (MMSE) and the Global Deterioration Scale (GDS), as well as with disturbances of behaviour, mood and personality, thereby extending the spectrum of clinical symptoms to ones not assessed by the MMSE or the GDS. CCL3 levels were lower in patients with AD but correlated positively with such noncognitive symptoms as mood disturbances and personality changes.We found that CCL3 did not correlate with the severity of dementia as assessed by the MMSE or with the degree of disease deterioration as assessed by the GDS. The results from our study on CCL3 levels in AD may, in part, explain the mechanisms of some concomitant, noncognitive clinical features of the disease.

摘要

虽然阿尔茨海默病(AD)是一种主要的退行性疾病,但由淀粉样蛋白β(Abeta)引发的小胶质细胞介导的炎症反应导致了神经退行性变,进而导致细胞死亡。由于这种炎症对神经退行性变的贡献可能会影响疾病的进展,因此出现了一个基本问题,即涉及可能依赖于炎症反应的临床症状的机制。在本研究中,我们调查了 AD 患者外周血中 CCL3 的水平,并将发现与临床测试的结果(如 Mini-Mental State Examination (MMSE)和 Global Deterioration Scale (GDS))以及行为、情绪和人格障碍相关联,从而将临床症状的范围扩展到 MMSE 或 GDS 未评估的症状。AD 患者的 CCL3 水平较低,但与情绪障碍和人格改变等非认知症状呈正相关。我们发现 CCL3 与 MMSE 评估的痴呆严重程度或 GDS 评估的疾病恶化程度没有相关性。我们对 AD 患者 CCL3 水平的研究结果可以部分解释该疾病某些伴随的非认知临床特征的机制。

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