Morgan Dave
Alzheimer Research Laboratory, Department of Molecular Pharmacology and Physiology, School of Basic Biomedical Sciences, College of Medicine, 12901 BB Downs Blvd. MDC Box 9, University of South Florida, Tampa, FL 33612, USA.
Exp Neurol. 2007 Jun;205(2):330-5. doi: 10.1016/j.expneurol.2007.03.006. Epub 2007 Mar 14.
Transgenic mouse models of amyloid deposition consistently demonstrate impaired performance on certain tasks of learning and memory. The article by Zhang et al. (2006) demonstrates reductions in dentate gyrus neurogenesis in a murine model of amyloid deposition which is linked to the deposition of amyloid and not overexpression of transgenes. Neurogenesis plays at least a facilitatory role in the formation of memory, the nature of which is only beginning to emerge. Thus, it seems reasonable to propose that the memory deficits found in the amyloid precursor protein transgenic mouse models of amyloid deposition result, at least in part, from reduced rates of hippocampal neurogenesis. The possible relationship to memory loss in Alzheimer's dementia is also discussed.
淀粉样蛋白沉积的转基因小鼠模型在某些学习和记忆任务中始终表现出功能受损。Zhang等人（2006年）的文章表明，在淀粉样蛋白沉积的小鼠模型中，齿状回神经发生减少，这与淀粉样蛋白的沉积有关，而非转基因的过度表达。神经发生在记忆形成中至少起促进作用，其本质才刚刚开始显现。因此，提出在淀粉样蛋白沉积的淀粉样前体蛋白转基因小鼠模型中发现的记忆缺陷至少部分是由于海马神经发生速率降低所致似乎是合理的。还讨论了与阿尔茨海默病痴呆症记忆丧失的可能关系。
