Mechanism of Alzheimer's disease: arguments for a neurotransmitter-aluminium complex implication.
Identifieur interne : 000A68 ( Ncbi/Curation ); précédent : 000A67; suivant : 000A69Mechanism of Alzheimer's disease: arguments for a neurotransmitter-aluminium complex implication.
Auteurs : R. Deloncle [France] ; O. GuillardSource :
- Neurochemical research [ 0364-3190 ] ; 1990.
English descriptors
- KwdEn :
- Aluminum (metabolism), Aluminum (toxicity), Alzheimer Disease (etiology), Alzheimer Disease (metabolism), Alzheimer Disease (physiopathology), Blood-Brain Barrier, Brain (physiopathology), Down Syndrome (physiopathology), Humans, Neurotransmitter Agents (metabolism), Parkinson Disease (physiopathology).
- MESH :
- chemical , metabolism : Aluminum, Neurotransmitter Agents.
- chemical , toxicity : Aluminum.
- etiology : Alzheimer Disease.
- metabolism : Alzheimer Disease.
- physiopathology : Alzheimer Disease, Brain, Down Syndrome, Parkinson Disease.
- Blood-Brain Barrier, Humans.
Abstract
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.
PubMed: 1982955
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