Give a man a fish he eats for a day. Teach a man to fish he eats for a lifetime….and he lives longer.
Recent studies have inferred that omega fats and vitamin E do not protect against Alzheimer’s disease. However it is my opinion that these studies were conducted incorrectly since these supplements were not given together. “Researchers” have suggested that vitamin E stabilizes the omega fat phospholipid membranes instead of cholesterol. Therefore I believe vitamin E and omega fats work synergistically in the critical regions of the nerve: the synapse and the inner mitochondrial membrane.
If we look at key players we can see how nerves normally function and how these 2 regions are central.
APOE is an omega fat and vitamin E delivery man to the synapse. As we age less vitamin E is found at the synapse and we struggle to remember. APOE4 has been associated with an increased risk for Alzheimer's disease. It would be interesting to know if APOE4 delivers less vitamin E.
Amyloid is a serine protease which could be a microtubule builder at the synapse membrane. (like the serine protease Htra1 building microtubules) If the amount of omega fats at the synapse decreased or become unstable without vitamin E does less APP (amyloid) exist in the synpase? Does more amyloid end up in the mitochondria or secreted to form plaques?
Looking specifically at the omega fats of the mitochondria is there a connection between the functionality of the mitochondria and the fats? The mitochondria must be able to move to the synapse on the microtubules. Tau is a mitochondria zone controller. Tau binds to the microtubule that the mitochondria travels on locking it into regions of travel. Most vitamin E ends up in the mitochondrial inner membrane; as we age less and less vitamin E exists at the synapse. Does this destabilize the membranes? These 2 regions are critically intertwined in function.
APOE is an omega fat and vitamin E delivery man to the synapse. As we age less vitamin E is found at the synapse and we struggle to remember. APOE4 has been associated with an increased risk for Alzheimer's disease. It would be interesting to know if APOE4 delivers less vitamin E.
Amyloid is a serine protease which could be a microtubule builder at the synapse membrane. (like the serine protease Htra1 building microtubules) If the amount of omega fats at the synapse decreased or become unstable without vitamin E does less APP (amyloid) exist in the synpase? Does more amyloid end up in the mitochondria or secreted to form plaques?
Looking specifically at the omega fats of the mitochondria is there a connection between the functionality of the mitochondria and the fats? The mitochondria must be able to move to the synapse on the microtubules. Tau is a mitochondria zone controller. Tau binds to the microtubule that the mitochondria travels on locking it into regions of travel. Most vitamin E ends up in the mitochondrial inner membrane; as we age less and less vitamin E exists at the synapse. Does this destabilize the membranes? These 2 regions are critically intertwined in function.
It is my hope that if we recognize the similarities of these omega phospholipid regions we will understand how the failure of one region could affect the other. They may compete for vitamin E. They may compete for omega fats. They have the same free radical susceptibility. They may even be confused and mixed up during dysfunction thus end up with each other’s proteins.
Test post, please ignore.
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