MECHANISM OF ALZHEIMERS-DISEASE - ARGUMENTS FOR A NEUROTRANSMITTER ALUMINUM-COMPLEX IMPLICATION - COMMENT

被引:65
作者
DELONCLE, R
GUILLARD, O
机构
[1] FAC MED POITIERS,DEPT PHARMACOL,F-86034 POITIERS,FRANCE
[2] FAC MED POITIERS,DEPT BIOCHEM,F-86034 POITIERS,FRANCE
关键词
ALZHEIMER; BLOOD BRAIN BARRIER; ALUMINUM; GLUTAMIC ACID; AMMONIA; NEURONS; BRAIN;
D O I
10.1007/BF01208586
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:1239 / 1245
页数:7
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