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Beyond Neuronal Cell Lossin Tissue Atrophy of Alzheimer Type

机译:超越阿尔茨海默病类型的神经元细胞丢失组织萎缩

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Alzheimer disorders of neuritogenesis and of senile plaque formation are progressive in terms of adevelopmental predetermining series of steps in evolution of amyloidogenesis and of neuronal cell depletionand loss. Tissue atrophy of the cerebral cortex and white matter appear both integral aspects of a diseaseprocess that evolves to implicate microcirculatory and vascular wall pathology or impermeability. Theextracellular dimensions of the senile plaque appear exquisitely sensitive to the conditioning and transforminginfluences of pathology of Alzheimer type. Neurofibrillary tangles and congophilic angiopathy and also thevarious other manifestations of Alzheimer brain atrophy include a particular association with neuritic dystrophyand dysfunctionality of synapses and of neuronal circuits. It might be particularly significant to recognize theAlzheimer disease process as one that inherently arises in consequence to a variety of associative factors thatsecondarily determine developmental progression of neuronal cell loss and of tissue atrophy. A central processof apoptosis as transformed dynamics of cell loss and of altered attributes of otherwise active maintenance ofcell metabolic and physiologic pathways might account for a depletion that is genetically programmed butpredominantly associated with acquired associative events of progression.
机译:就淀粉样蛋白生成以及神经元细胞耗竭和丧失的发展中的一系列步骤的发展预先确定而言,神经元形成和老年斑形成的阿尔茨海默氏病是进行性的。大脑皮层和白质的组织萎缩似乎是疾病过程不可或缺的部分,该过程演变为牵涉微循环和血管壁病理或不可渗透性。老年斑的细胞外尺寸似乎对阿尔茨海默病类型的病理状况的调节和转化影响极为敏感。神经原纤维缠结和嗜血性血管病以及阿尔茨海默氏脑萎缩的各种其他表现包括与神经营养不良和突触和神经元回路功能障碍的特定关联。认识到阿尔茨海默氏病过程是由于多种相关因素而固有地产生的疾病过程,这一过程可能特别重要,该过程继而决定了神经元细胞丢失和组织萎缩的发展进程。凋亡的中心过程是细胞丢失的动态变化以及原本主动维持细胞代谢和生理途径的改变的属性,这可能是由遗传程序控制的耗竭,但主要与获得性进展相关。

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