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首页> 外文期刊>International Journal of Molecular Medicine and Advance Sciences >Aberrant Neurofilament Trafficking and Membrane-Anchored Proteolytic Events Constituting Transformation Of Senile Brain Atrophy to An Alzheimer Disease Process
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Aberrant Neurofilament Trafficking and Membrane-Anchored Proteolytic Events Constituting Transformation Of Senile Brain Atrophy to An Alzheimer Disease Process

机译：异常的神经丝运输和膜锚定的蛋白水解事件，将老年性脑萎缩转化为阿尔茨海默病过程

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A self-progressive neurodegenerative event of Alzheimer type would involve a distinctive process of increasing membrane proteolysis as the cause of neuronal cell death and of various aberrant attempts at dystrophic recovery. Indeed, a conceptual distinction of the Alzheimer process from senile brain atrophy might arise as a strict phenomenon of evolving protein-protein interactions and of various aberrant patterns of intracellular protein trafficking that mark out the Alzheimer neurodegenerative event as paradoxically both constitutional and possibly also of acquired nature. In terms, indeed, of a progressive phenomenon of atrophy of the brain that is neuronal in specific pathogenesis but also arising inherently as a neurodegenerative series of aberrant pathway attempts at recovery of injured neurons, a single event of degeneration would arise from proteolytic involvement of the neuronal cell body. It is in terms of such a postulated integral event of self-progressive proteolysis arising and evolving within neuronal membranes that there would be implicated not only ApoE isoforms but also Presenilin-1 and ?2 as membrane-anchored molecules of progression in the Alzheimer process. Indeed, an integral neurodegenerative event of neuronal membrane processing would arise and proceed as a series of synaptic and neuritic dystrophic forms of activity specifically distinguishing the disorder from simple senile brain atrophy. It is perhaps in terms of quantitatively significant degrees of increased neuronal cell loss that Alzheimer disease would indeed constitute an active participation of various membrane-based transformations ranging from ubiquination to proteolysis to protein-protein interaction and lipid metabolism to Ca2 + /K + channeling as one constitutive Alzheimer process with added acquired dimensions.
机译：阿尔茨海默病类型的自我进行性神经退行性事件将涉及增加膜蛋白水解作为神经元细胞死亡的原因以及营养不良恢复的各种异常尝试的独特过程。确实，阿尔茨海默氏病与老年性脑萎缩的概念区别可能是蛋白质和蛋白质相互作用不断发展的严格现象，以及细胞内蛋白质运输的各种异常模式的严格现象，这标志着阿尔茨海默氏神经退行性事件既是体质性的，也可能是后天性的。性质。实际上，就特定发病机理而言是神经元的脑萎缩的进行性现象，但也确实是由于神经退行性一系列异常途径试图恢复受损神经元而固有地产生的，单个变性事件将是由蛋白水解所引起的。神经元细胞体。正是根据这种假定的自我进行性蛋白水解在神经元膜内发生和发展的整体事件，才有可能不仅涉及ApoE同工型，还涉及早老蛋白-1和β2作为阿尔茨海默氏病过程中膜锚定的进展性分子。确实，神经元膜加工的整体神经退行性事件将以一系列突触和神经营养不良的活动形式出现，并以特定的方式将疾病与单纯性老年性脑萎缩区分开来。也许从数量上显着程度的增加神经元细胞损失的角度来看，阿尔茨海默氏病确实将构成各种基于膜的转化的积极参与，从泛素化到蛋白水解作用到蛋白质-蛋白质相互作用和脂质代谢再到Ca2 + / K +通道一种本构性的阿尔茨海默方法，增加了获得的尺寸。

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