Low molecular weight glycosaminoglycan C3 attenuates AF64A-stimulated, low-affinity nerve growth factor receptor-immunoreactive axonal varicosities in the rat septum
详细信息 查看全文
- 作者：Dudas ; Bertalan ; Rose ; Michael ; Cornelli ; Umberto ; Hanin ; Israel
- 关键词：Disorders of the nervous system ; Degenerative disease ; Alzheimer's??????miscellaneous ; Alzheimer's disease ; Animal model ; p75NTR ; Neurodegeneration
- 刊名：Brain Research
- 出版年：2005
- 出版时间：February 1, 2005
- 年：2005
- 卷：1033
- 期：1
- 页码：34-40
- 全文大小：305 K
文摘
Glycosaminoglycans (GAGs) play a pivotal role in the pathogenesis of Alzheimer's disease (AD). Although, as we have shown earlier, a low molecular weight GAG, C3, protects against ethylcholine aziridinium (AF64A)-induced cholinergic damage, and against A??-induced tau-2-immunoreactivity (IR), the mechanism of the neuroprotective effect of GAGs is not yet known. Several clues exist. Previous studies in rats revealed that continuous NGF infusion (icv) after AF64A injection increases septal ChAT and AChE activities. Moreover, C3 increases axonal outgrowth in the rat hippocampus, raising the possibility of a NGF-receptor mediated neuroprotection. Furthermore, it has been reported that NGF expression is increased in the septum following AF64A administration.