Grammas P, Moore P, Botchlet T, Hanson-Painton O, Cooper D R, Ball M J, Roher A
Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City 73190, USA.
Neurobiol Aging. 1995 Jul-Aug;16(4):563-9. doi: 10.1016/0197-4580(95)00048-j.
Protein kinase C (PKC) is an important intracellular signalling enzyme. Numerous studies have suggested that alterations in this enzyme occur in aging and dementia. The objective of this study was to examine PKC in the cerebral microcirculation in aging and Alzheimer's disease. PKC activity, amount, and isoform distribution were analyzed in microvessels from adult and aged rodents as well as from Alzheimer patients and nondemented elderly controls. PKC activity was lower in Alzheimer vessels than in vessels from control brains, despite the presence of similar levels of PKC enzyme. In contrast, both activity and enzyme levels in young and aged rats were comparable. The beta-isoform was present in both rat and human microvessels and there were no age- or disease-related alterations. The loss in activity in cerebromicrovascular PKC in Alzheimer's suggest that perturbations in phosphorylation signalling cascades may exist at the Alzheimer blood-brain barrier.
蛋白激酶C（PKC）是一种重要的细胞内信号酶。大量研究表明，这种酶的改变发生在衰老和痴呆过程中。本研究的目的是检测衰老和阿尔茨海默病患者脑微循环中的PKC。分析了成年和老年啮齿动物以及阿尔茨海默病患者和非痴呆老年对照者微血管中的PKC活性、含量和同工型分布。尽管PKC酶水平相似，但阿尔茨海默病患者血管中的PKC活性低于对照脑的血管。相比之下，年轻和老年大鼠的活性和酶水平相当。β同工型存在于大鼠和人类微血管中，且没有与年龄或疾病相关的改变。阿尔茨海默病患者脑微血管PKC活性的丧失表明，阿尔茨海默病血脑屏障处可能存在磷酸化信号级联的紊乱。
