"Alzheimer’s Disease Prevention -- Carnosine has also been proven to reduce, or completely prevent, cell damage caused by beta amyloid, one of the prime protein risk factors for Alzheimer’s disease. The presence of beta amyloid leads to damage of the nerves and arteries of the brain. Carnosine blocks and inactivates beta amyloid, in effect, protecting neural tissues against dementia. The key is that carnosine not only prevents damaging cross-links from forming in proteins, it eliminates cross-links that have previously formed, thus restoring normal membrane function in cells. This is true not only in the brain, but in all the organs of the body.
There is, however, one gap in carnosine’s usefulness -- lipofuscin. Lipofuscin is a pigment commonly found in aging brains and in other tissues such as the skin. By itself, it is not dangerous but merely a byproduct of harmful reactions, such as free-radical damage and protein/aldehyde damage, that have already taken place. In the case of aldehydes, for example, when you supplement with carnosine, it quickly binds with the aldehydes, preventing them from damaging the proteins. The byproduct of this reaction is lipofuscin. So once again you have inactive lipofuscin compounds, but this time as the result of preventing protein damage. In a sense, with carnosine you trade protein damage for lipofuscin. This, however, can lead to another problem. If enough lipofuscin accumulates over time (a process accelerated when you supplement with carnosine), it can interfere with proper cellular and organ functions. It’s important, therefore, to continually remove the lipofuscin so it doesn’t build up, and that’s were DMAE comes in. "
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There is, however, one gap in carnosine’s usefulness -- lipofuscin. Lipofuscin is a pigment commonly found in aging brains and in other tissues such as the skin. By itself, it is not dangerous but merely a byproduct of harmful reactions, such as free-radical damage and protein/aldehyde damage, that have already taken place. In the case of aldehydes, for example, when you supplement with carnosine, it quickly binds with the aldehydes, preventing them from damaging the proteins. The byproduct of this reaction is lipofuscin. So once again you have inactive lipofuscin compounds, but this time as the result of preventing protein damage. In a sense, with carnosine you trade protein damage for lipofuscin. This, however, can lead to another problem. If enough lipofuscin accumulates over time (a process accelerated when you supplement with carnosine), it can interfere with proper cellular and organ functions. It’s important, therefore, to continually remove the lipofuscin so it doesn’t build up, and that’s were DMAE comes in. "
Like & Share (G.Shyam)
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thanks for feedback, hope from U to share this!