Deloncle R, Guillard O
Bio-Inorganic Chemistry Laboratory, Faculty of Pharmacy, Tours, France.
Neurochem Res. 1990 Dec;15(12):1239-45. doi: 10.1007/BF01208586.
The authors are convinced that in Alzheimer's disease, as in Down's syndrome and Guam-Parkinson dementia, one may find an alteration in blood brain barrier transfer and a resultant imbalance in mineral metabolism. Metals, such as aluminium, which in vivo yield stable complexes with aspartic and glutamic acids act as previously been clearly shown with glutamic acid; they cross the blood brain barrier, and are deposited in the brain. The authors explain how amyloid protein or neurofibrillary tangles could well be produced by aluminium complex formation. Within the brain, in the form precisely of aluminium complex, L-glutamic acid is consequently unable to detoxify ammonia from neurons and to produce L-glutamin. Accumulation of ammonia is subsequently responsible for the neuronal death, affecting each and every neurotransmitter system.
作者确信，在阿尔茨海默病中，如同在唐氏综合征和关岛帕金森痴呆症中一样，可能会发现血脑屏障转运的改变以及由此导致的矿物质代谢失衡。金属，如铝，在体内会与天冬氨酸和谷氨酸形成稳定的复合物，正如之前用谷氨酸所清楚表明的那样；它们会穿过血脑屏障，并沉积在大脑中。作者解释了淀粉样蛋白或神经原纤维缠结如何很可能是由铝复合物的形成所产生的。在大脑中，正是以铝复合物的形式，L - 谷氨酸因此无法从神经元中解毒氨并产生L - 谷氨酰胺。随后氨的积累导致神经元死亡，影响每一个神经递质系统。
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