bobze
Science Advisor
Gold Member
- 648
- 18
Time-Out!
Hshields, some of your stuff does seem to be a little "fringe". The possible link to Alzheimer's and prions exists, but whether it is causative is certainly speculative. And certainly saying that it is the cause is incorrect. Alzheimer's is mutlifactorial, I suspect that prion proteins or some of their homologous coding regions play a role, but other things (like tau-MAPs) are certainly involved.
Proton-While I agree that some of the linked stuff is "fringy", the link certainly exists between protein folding disorders (like Alzheimer's and Parkinson's) and prion proteins.
All prion proteins are encoded for by the organisms genome. There is more than one (probably from gene duplication events or amino acid homology which can lead to aggregate and precipitate formation) in our genomes.
I explained above, prion proteins (where not really sure what exactly they do yet--At least most of them, but probably all play integral roles in neural functions) exist in a balance between a structural isoforms. One favors alpha helices, the other beta sheets.
When the beta sheet isoform dominates, it precipitates out of solution which drives the reaction to the right and pulls more protein out of solution. This leads to plaque and fibrillary tangle formation--Which is what causes destruction of neurons.
The general equilibrium for prions looks something like;
PrP↔PrPsc**→PrPsc aggregates.
**SC was the prion protein species initially discovered in the prion disease scrapie (sheep) but "PrPsc" is now used when discussing any general form of prion protein.
Introducing PrPsc, rather than just driving the equilibrium back to the left, causes the aggregate formation--Which forces more prion protein in the equilibrium to the prion form. For reasons unknown, aggregate deposition fuels more and more aggregate deposition and ultimately leads to a prion disease.
Hshields, some of your stuff does seem to be a little "fringe". The possible link to Alzheimer's and prions exists, but whether it is causative is certainly speculative. And certainly saying that it is the cause is incorrect. Alzheimer's is mutlifactorial, I suspect that prion proteins or some of their homologous coding regions play a role, but other things (like tau-MAPs) are certainly involved.
Proton-While I agree that some of the linked stuff is "fringy", the link certainly exists between protein folding disorders (like Alzheimer's and Parkinson's) and prion proteins.
All prion proteins are encoded for by the organisms genome. There is more than one (probably from gene duplication events or amino acid homology which can lead to aggregate and precipitate formation) in our genomes.
I explained above, prion proteins (where not really sure what exactly they do yet--At least most of them, but probably all play integral roles in neural functions) exist in a balance between a structural isoforms. One favors alpha helices, the other beta sheets.
When the beta sheet isoform dominates, it precipitates out of solution which drives the reaction to the right and pulls more protein out of solution. This leads to plaque and fibrillary tangle formation--Which is what causes destruction of neurons.
The general equilibrium for prions looks something like;
PrP↔PrPsc**→PrPsc aggregates.
**SC was the prion protein species initially discovered in the prion disease scrapie (sheep) but "PrPsc" is now used when discussing any general form of prion protein.
Introducing PrPsc, rather than just driving the equilibrium back to the left, causes the aggregate formation--Which forces more prion protein in the equilibrium to the prion form. For reasons unknown, aggregate deposition fuels more and more aggregate deposition and ultimately leads to a prion disease.