Thursday, February 02, 2012 11:49:32 AM
Neuro would be the one to ask, but there is a long shot AD program from an Australian company called Prana (PRAN). Their hypothesis is that in AD, neuronal zinc and copper ions build up excessively in the synaptic cleft, and interact with beta amyloid to form toxic oligimers. Prana's 'Metal Protein Attenuating Compounds' (MPACs) prevent the interaction of synaptic zinc and copper with A-beta to prevent the A-beta from becoming toxic.
Concerning metals and AD, I always wondered if heavy metals like lead and mercury could have had a role in the emergence of AD. People spent many decades breathing in auto fumes full of tetraethyl lead, and we are exposed to mercury from power plants, vaccines, etc. The appearance of Alzheimer's has coincided with the widespread cummulative exposure to these heavy metals.
Prana -
>>> with increasing age, the normal tight regulation
of metal transport and localization in the brain weakens. Notably, that the normal mechanisms of pumping Zinc and Copper back into neurons (after an electrical signal passes from one neuron to another) become fatigued resulting in a buildup of metals in the synaptic cleft (the narrow space between communicating neurons). This phenomenon has been modelled using transgenic mice in which neuronal zinc reuptake has been disrupted causing a dramatic decline in cognition which is completely restored by drugs which replenish neuronal zinc (11 ). In the ageing brain, as a consequence of copper and zinc pooling in the synaptic cleft, A-beta that is normally released into the same synaptic space, has a high chance of interacting with the metals to form oligomers which are toxic to neurons, leading to cognitive impairment (8). This toxic effect is further exacerbated as copper and zinc required for normal synaptic transmission are bound up within the accumulating amyloid mass. <<<
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