Presence of extracellular deposits of amyloid has been determined In Alzheimer’s disease. Experimental studies have shown that carnosine can reduce or completely prevent cell damage caused by toxic effect of amyloid. β-amyloid reacts with the specific RAGE receptors, causing the damage to nerve cells and cerebral arteries.
Karnozin Extra blocks and prevents the activity of amyloid-β, and in this way protects the neural tissue against the development of dementia.
Furthermore, carnosine protects brain cells with its neutralizing effect against an extremely toxic substance, α-β-unsaturated aldehyde acrolein, which is formed during the oxidation of unsaturated fatty acids (PUFA). This substance probably acts as a “second toxicology messenger” in oxidative damage of cell membranes. Recent studies have also found that toxic unsaturated crotonaldehyde participates in the following process, destruction of protein and the phospholipids (mostly of cell membranes) – carbonylation conditioned by lipid peroxidation.
Since carnosine combats all aldehydes, the explanation of the latter activity is offered as an important factor in the prevention of Alzheimer’s disease and other diseases associated with oxidative stress.
Carnosine also acts preventively on later mechanisms that accompany Alzheimer’s disease. Some studies about this disease have shown an increased concentration of zinc and copper ions in the brain of patients with Alzheimer’s disease. These ions possibly modify the chemical structure of the normal
β-amyloid, and they are the reason for its toxicity. This change requires a slightly acidic environment in order to be caused, i.e. to bind zinc and/or copper ion with β-amyloid. These conditions (acidic medium and increased concentration of zinc and copper ions) are present as part of an inflammatory reaction at the site of damage.
Carnosine, an excellent chelator of copper and zinc (and other metals), is able to remove these metals from the organism. This may point to another important function of Karnozin Extra in preventing and delaying the progress of Alzheimer’s disease and other degenerative brain diseases.