When I was trying to decided if gluten, casein, and ovalbmin were functioning as serpins, serine protease inhibitors, I looked at all serpins.
I had wanted to show that Candida could cause autoimmune disease by switching between a yeast and a mold state. The notion of root halting came from a golf course grass experiment at Ohio state. That corn gluten halted not just grass seed from sprouting roots but had blocked a parasitic mold from creating hyphals. I wanted to know if gluten, casein, and ovalbumin halted root growth.
I started to look at serpins as off growth switches thus i pondered if serine proteases were on root growth switches.
I looked at the maspin of breast cancer which when lost caused out of control cellular growth. In breast cancer there are several "on" switch proteases.
I looked at neuroserpin. Did it halt the growth of nerves? I did not find an answer. I did not find a specific target protease. What I did find was APP. When clipped it became the notorious amyloid plaques but the normal function of the regular protein was unknown. APP was a serine protease so could it be an on growth switch?
I suddenly viewed Alzheimer's differently. Everyone views it as a state of brain cell death but what if the brain cell was actually trapped in a state of growth first? Were the nerve axons growing like roots?
Early onset Alzheimer's disease is common in the mother's of downs syndrome children. This seemed to indicate a mitochondria problem. We have, the good, the bad and the ugly mitochondrias and perhaps the ugly ones are involved in Alzheimer's. We know that some of these mother's have mitochondria that do not function well because they passed on poor functioning mitochondria to their children.
During normal synaptogenesis the mitochondria move to the axon tips of the neurons. Axon growth would not be possible if the mitochondria do not make it there to supply the energy. When the mitochondria of Alzheimer's disease mouse models were recently illuminated the mitochondria were not reaching the synapse. Is early Alzheimer's a failure of the mitochondria to support growth?
Late onset Alzheimer's involves the apoE genotype which means the lipid supplier, the one that carries the lipid wall building supplies to the nerve becomes important. Most people have apoE3 but those with late stage Alzheimer's have apoe4. We know as we age our dietary absorption decreases and with the growth already choking with a bad apoE4 delivery man perhaps nerve growth is slowly dwindles? The use of statin drugs have been said to cause a memory dysfunctional state in patients perhaps by limiting the lipids. So far this could make sense, in order for a nerve to grow it needs supplies.
So how does APP fit in and end up as plaques in both cases?
Is APP a growth on switch? Studies have been done in mice which show that in young mice with app knocked out seem fine but the older mice that seem to have issue. Consider that young mice or even kids have a rapid state of nerve growth and pruning whereas adults have a slower state of growth and not so much pruning. Perhaps app is the growth switch of the adults? The app knock out mice did have sparse spinal nerves compared to normal mice. When does the production of APP actually start? when we become adults? Is that why this is a disease of adults?
How do all the theories converge to explain the app becoming cleaved and becoming the amyloid plaques we find in Alzheimer's patients? What could actually be happening? Nerve growth factor induces the expression of app. App then creates a growth state which can be shut off by neuroserpin. If something goes wrong with the state of growth would the nerve attempt to make more of the "on switch" which is app? does the nerve says it needs to grow and keeps sending the app growth switch but the lack of supplies or the lack of energy cause the app to be broken down instead? Could it be that amyloid plaques are a result of stunted growth not a cause of the nerve failure?
That Alzheimer's is not so much a disease of cell death but a failure of cell growth?
Okay i have drifted off topic, but this is a blog and i am allowed to do that. I will end with an interesting thought about mitochondria moving. In fireflies the off and on glow is controlled very quickly by NO acting on their mitochondria. Wouldn't it be neat if the mitochondria can control their own locomotion with their own NO synthase? ahhh I think too much some days.
Other thoughts:
There are things that can enhance memory which one could look at as greasing the gears of the mitochondria. Vitamin E and omega fats are not just the insulation of cells but they are the main ingredient of the inner mitochondria membrane. Vitamin E does not just protect the omega fats from oxidation but stabilizes the membrane instead of cholesterol, something that i think is currently over looked in the field. That omega fats require vitE to work. Low levels of vit E are associated with poorer memory as we age.
Parkinson's has currently been viewed as a mitochondria disease in that PURL has been indicated. Purl is a rhomboid protease involved in the morphology of mitochondria. This would not stop the functioning of the mitochondria rather make transport of them down the axon more difficult. Purl might be breaking a large mitochondria suv into smaller mitochondria coopers....so to speak...thus a sporatic energy supply. I don't know if any one has looked into that but it makes me wonder. If Resveratrol is now said to induce mitochondria biogenesis and has been shown to extend the lifespan of yeast and flies....could it counter the problem in Parkinson's somewhat?
I hope this inspires people out there to think...literally...may Alzheimer's be a fixable state of growth error?
Thanks for listening,
Angela Biggs
I had wanted to show that Candida could cause autoimmune disease by switching between a yeast and a mold state. The notion of root halting came from a golf course grass experiment at Ohio state. That corn gluten halted not just grass seed from sprouting roots but had blocked a parasitic mold from creating hyphals. I wanted to know if gluten, casein, and ovalbumin halted root growth.
I started to look at serpins as off growth switches thus i pondered if serine proteases were on root growth switches.
I looked at the maspin of breast cancer which when lost caused out of control cellular growth. In breast cancer there are several "on" switch proteases.
I looked at neuroserpin. Did it halt the growth of nerves? I did not find an answer. I did not find a specific target protease. What I did find was APP. When clipped it became the notorious amyloid plaques but the normal function of the regular protein was unknown. APP was a serine protease so could it be an on growth switch?
I suddenly viewed Alzheimer's differently. Everyone views it as a state of brain cell death but what if the brain cell was actually trapped in a state of growth first? Were the nerve axons growing like roots?
Early onset Alzheimer's disease is common in the mother's of downs syndrome children. This seemed to indicate a mitochondria problem. We have, the good, the bad and the ugly mitochondrias and perhaps the ugly ones are involved in Alzheimer's. We know that some of these mother's have mitochondria that do not function well because they passed on poor functioning mitochondria to their children.
During normal synaptogenesis the mitochondria move to the axon tips of the neurons. Axon growth would not be possible if the mitochondria do not make it there to supply the energy. When the mitochondria of Alzheimer's disease mouse models were recently illuminated the mitochondria were not reaching the synapse. Is early Alzheimer's a failure of the mitochondria to support growth?
Late onset Alzheimer's involves the apoE genotype which means the lipid supplier, the one that carries the lipid wall building supplies to the nerve becomes important. Most people have apoE3 but those with late stage Alzheimer's have apoe4. We know as we age our dietary absorption decreases and with the growth already choking with a bad apoE4 delivery man perhaps nerve growth is slowly dwindles? The use of statin drugs have been said to cause a memory dysfunctional state in patients perhaps by limiting the lipids. So far this could make sense, in order for a nerve to grow it needs supplies.
So how does APP fit in and end up as plaques in both cases?
Is APP a growth on switch? Studies have been done in mice which show that in young mice with app knocked out seem fine but the older mice that seem to have issue. Consider that young mice or even kids have a rapid state of nerve growth and pruning whereas adults have a slower state of growth and not so much pruning. Perhaps app is the growth switch of the adults? The app knock out mice did have sparse spinal nerves compared to normal mice. When does the production of APP actually start? when we become adults? Is that why this is a disease of adults?
How do all the theories converge to explain the app becoming cleaved and becoming the amyloid plaques we find in Alzheimer's patients? What could actually be happening? Nerve growth factor induces the expression of app. App then creates a growth state which can be shut off by neuroserpin. If something goes wrong with the state of growth would the nerve attempt to make more of the "on switch" which is app? does the nerve says it needs to grow and keeps sending the app growth switch but the lack of supplies or the lack of energy cause the app to be broken down instead? Could it be that amyloid plaques are a result of stunted growth not a cause of the nerve failure?
That Alzheimer's is not so much a disease of cell death but a failure of cell growth?
Okay i have drifted off topic, but this is a blog and i am allowed to do that. I will end with an interesting thought about mitochondria moving. In fireflies the off and on glow is controlled very quickly by NO acting on their mitochondria. Wouldn't it be neat if the mitochondria can control their own locomotion with their own NO synthase? ahhh I think too much some days.
Other thoughts:
There are things that can enhance memory which one could look at as greasing the gears of the mitochondria. Vitamin E and omega fats are not just the insulation of cells but they are the main ingredient of the inner mitochondria membrane. Vitamin E does not just protect the omega fats from oxidation but stabilizes the membrane instead of cholesterol, something that i think is currently over looked in the field. That omega fats require vitE to work. Low levels of vit E are associated with poorer memory as we age.
Parkinson's has currently been viewed as a mitochondria disease in that PURL has been indicated. Purl is a rhomboid protease involved in the morphology of mitochondria. This would not stop the functioning of the mitochondria rather make transport of them down the axon more difficult. Purl might be breaking a large mitochondria suv into smaller mitochondria coopers....so to speak...thus a sporatic energy supply. I don't know if any one has looked into that but it makes me wonder. If Resveratrol is now said to induce mitochondria biogenesis and has been shown to extend the lifespan of yeast and flies....could it counter the problem in Parkinson's somewhat?
I hope this inspires people out there to think...literally...may Alzheimer's be a fixable state of growth error?
Thanks for listening,
Angela Biggs
