Experimental studies have shown that carnosine can reduce or completely prevent cell damage whose cause is the toxic effect of amyloid, a protein characteristic of Alzheimer’s disease. β–amyloid reacts with a certain RAGE receptors and leads to damage of nerve cells and cerebral arteries. Karnozin Extra blocks and inhibits the activity of β-amyloid and in this way protects nerve tissue from developing dementia.
Moreover, carnosine protects brain cells by its neutralizing effect of an extremely toxic substance, α-β-unsaturated aldehyde of acrolein, which is formed during the peroxidation of polyunsaturated lipids. Since carnosine fights all types of aldehydes, this gives answer why Karnozin Extra is universal cell protector and plays preventive role in Alzheimer’s disease and other diseases associated with oxidative stress.
Carnosine levels are significantly lower in patients with Alzheimer’s and other neuro-degenerative disorders, suggesting either that carnosine deficiency contributes to the disease, or, more likely, that the disease symptoms are manifesting slower by using carnosine. In either case, addition of carnosine could be expected to eliminate much of the cellular toxicity that contributes to these diseases, which is why animal and human studies now suggest an important role for carnosine usage in prevention of Alzheimer’s diseases.
Carnosine also works preventive on mechanisms that accompany Alzheimer’s disease. Zinc and copper ions probably change the chemical structure of the normal β-amyloids and they are the reason for their toxicity. This change requires a slightly acidic environment to bind zinc ion and/or copper with a β-amyloid. These conditions (acidic medium and the increased concentration of ions of zinc and copper) are present as part of an inflammatory reaction at the place of damage. Carnosine, as an excellent chelator of copper and zinc (and other metals), is able to remove these heavy metals from the body. This may indicate another important function of carnosine in preventing and delaying the progress of Alzheimer’s disease and other degenerative brain diseases.