共查询到20条相似文献,搜索用时 15 毫秒
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G Miller 《Science (New York, N.Y.)》2012,337(6096):790-792
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Melnick VL 《Science (New York, N.Y.)》1982,215(4535):913-914
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One hundred years ago a small group of psychiatrists described the abnormal protein deposits in the brain that define the most common neurodegenerative diseases. Over the past 25 years, it has become clear that the proteins forming the deposits are central to the disease process. Amyloid-beta and tau make up the plaques and tangles of Alzheimer's disease, where these normally soluble proteins assemble into amyloid-like filaments. Tau inclusions are also found in a number of related disorders. Genetic studies have shown that dysfunction of amyloid-beta or tau is sufficient to cause dementia. The ongoing molecular dissection of the neurodegenerative pathways is expected to lead to a true understanding of disease pathogenesis. 相似文献
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Although neurodegenerative diseases such as Alzheimer's disease are not classically considered mediated by inflammation or the immune system, in some instances the immune system may play an important role in the degenerative process. Furthermore, it has become clear that the immune system itself may have beneficial effects in nervous system diseases considered neurodegenerative. Immunotherapeutic approaches designed to induce a humoral immune response have recently been developed for the treatment of Alzheimer's disease. These studies have led to human trials that resulted in both beneficial and adverse effects. In animal models, it has also been shown that immunotherapy designed to induce a cellular immune response may be of benefit in central nervous system injury, although T cells may have either a beneficial or detrimental effect depending on the type of T cell response induced. These areas provide a new avenue for exploring immune system-based therapy of neurodegenerative diseases and will be discussed here with a primary focus on Alzheimer's disease. We will also discuss how these approaches affect microglia activation, which plays a key role in therapy of such diseases. 相似文献
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Role of Alzheimer's protein is tangled 总被引:1,自引:0,他引:1
J L Mark 《Science (New York, N.Y.)》1987,238(4832):1352-1353
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Alzheimer's drug trial put on hold 总被引:1,自引:0,他引:1
J L Marx 《Science (New York, N.Y.)》1987,238(4830):1041-1042
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Finch CE 《Science (New York, N.Y.)》1985,230(4730):1107
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Alzheimer's disease is a synaptic failure 总被引:1,自引:0,他引:1
Selkoe DJ 《Science (New York, N.Y.)》2002,298(5594):789-791
In its earliest clinical phase, Alzheimer's disease characteristically produces a remarkably pure impairment of memory. Mounting evidence suggests that this syndrome begins with subtle alterations of hippocampal synaptic efficacy prior to frank neuronal degeneration, and that the synaptic dysfunction is caused by diffusible oligomeric assemblies of the amyloid beta protein. 相似文献
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G Kolata 《Science (New York, N.Y.)》1986,232(4749):448-450
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Defect in Alzheimer's is on chromosome 21 总被引:1,自引:0,他引:1
D M Barnes 《Science (New York, N.Y.)》1987,235(4791):846-847
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Brain protein yields clues to Alzheimer's disease 总被引:1,自引:0,他引:1
J L Marx 《Science (New York, N.Y.)》1989,243(4899):1664-1666
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J L Marx 《Science (New York, N.Y.)》1988,241(4872):1432-1433
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NGF and Alzheimer's: hopes and fears 总被引:3,自引:0,他引:3
J Marx 《Science (New York, N.Y.)》1990,247(4941):408-410
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Pennisi E 《Science (New York, N.Y.)》1999,286(5440):650-651