Gonatas N K, Moss A
Hum Pathol. 1975 Sep;6(5):571-82. doi: 10.1016/s0046-8177(75)80042-6.
Ultrastructural studies of cerebral biopsy specimens from patients with various forms of psychomotor retardation and dementia have disclosed pathologic changes in axons and presynaptic or postsynaptic processes. The clinical disorders with lesions in axons and presynaptic terminals are reviewed. Three basic abnormalities have been detected: proliferation of tubulovesicular structures which probably originate from the smooth endoplasmic reticulum, "abnormal" mitochondria, and proliferation of 80 to 100 A filaments. Understanding of the pathogenesis of human disorders associated with axonic or "synaptic" lesions will probably depend on progress in areas of basic biomedical research concerned with the synthesis and turnover of biological membranes and the packaging and secretion of neurotransmitters, elucidation of mechanisms of cytoplasmic streaming and axoplasmic flow, and biophysical and biochemical characteristics and functions of "fibrous" proteins (neurotubules, neurofilaments, pathologic fibrous proteins). In several cases of mental retardation of unknown etiology, abnormal dendritic spines of cortical neurons have been observed with the use of the Golgi method. These dendritic (postsynaptic) disorders have been attributed to defective development ("dysgenesis"). The knowledge provided by ultrastructural analysis of brain tissue from the human disorders of mental retardation or dementia is "still formless, incomplete, lacking the essential threads of connection," and only future developments in lacking neurobiology will make possible the dissection of the primary phenomena from the secretory and probably irrelevant findings.
对患有各种形式精神运动迟缓及痴呆症患者的脑活检标本进行的超微结构研究,已揭示出轴突以及突触前或突触后结构的病理变化。本文对伴有轴突及突触前终末病变的临床病症进行了综述。已检测到三种基本异常情况:可能源自滑面内质网的管状囊泡结构增殖、“异常”线粒体以及80至100埃细丝的增殖。对与轴突或“突触”病变相关的人类疾病发病机制的理解,可能取决于基础生物医学研究领域的进展,这些领域涉及生物膜的合成与更新、神经递质的包装与分泌、细胞质流动和轴浆运输机制的阐明,以及“纤维状”蛋白质(神经微管、神经丝、病理性纤维蛋白)的生物物理和生化特性及功能。在几例病因不明的智力发育迟缓病例中,运用高尔基方法观察到了皮质神经元的树突棘异常。这些树突(突触后)紊乱被归因于发育缺陷(“发育异常”)。通过对人类智力发育迟缓或痴呆症患者脑组织的超微结构分析所提供的知识“仍然不成形、不完整,缺乏基本的联系线索”,只有神经生物学未来的发展才有可能从分泌性且可能无关的发现中剖析出主要现象。