Saldaña M, Aguilar E, Bonastre M, Marin C
Laboratori de Neurologia Experimental, Institut d'Investigacions Biomèdiques August Pi i Sunyer, Barcelona, Spain.
J Neural Transm (Vienna). 2007;114(11):1469-77. doi: 10.1007/s00702-007-0765-x. Epub 2007 Jul 4.
We investigated whether bcl-2 protein family is involved in the pathogenesis of the dopaminergic neurodegeneration that occurs in Dementia with Lewy bodies (DLB). The expression of the proapoptotic protein bax and the antiapoptotic proteins bcl-2 and bcl-xL was investigated by Western blot in the pars compacta of the substantia nigra of pure and common DLB forms. No changes in the nigral expression levels of bax, bcl-2 and bcl-xL proteins were found between control and DLB pure cases. In the common DLB forms, nigral bcl-xL and bcl-2 proteins levels were significantly decreased in the DLB cases associated with a concomitant severe AD pathology (p < 0.05). An increase in nigral bcl-2 protein expression was observed in the DLB cases with a mild AD-associated pathology (p < 0.05). The present results are in agreement with previous observations indicating that DLB cases with severe AD pathology tend to show severe Lewy pathology suggesting that AD pathology might exacerbate Lewy pathology.
我们研究了bcl-2蛋白家族是否参与路易体痴呆（DLB）中发生的多巴胺能神经变性的发病机制。通过蛋白质免疫印迹法，研究了纯合型和常见型DLB患者黑质致密部促凋亡蛋白bax以及抗凋亡蛋白bcl-2和bcl-xL的表达情况。在对照组和纯合型DLB病例之间，未发现黑质中bax、bcl-2和bcl-xL蛋白表达水平有变化。在常见型DLB中，伴有严重阿尔茨海默病（AD）病理改变的DLB病例，其黑质中bcl-xL和bcl-2蛋白水平显著降低（p < 0.05）。在伴有轻度AD相关病理改变的DLB病例中，观察到黑质bcl-2蛋白表达增加（p < 0.05）。目前的结果与先前的观察结果一致，表明伴有严重AD病理改变的DLB病例往往表现出严重的路易小体病理改变，提示AD病理可能会加重路易小体病理改变。
