Alzheimer’s disease (AD) is a slowly progressive disease of the brain that is characterized by loss of memory and eventually by disturbances in reasoning, planning, language, and perception. Alzheimer’s disease is the most common cause of dementia — a group of brain disorders that cause the loss of intellectual and social skills. The bottom line is, in Alzheimer’s disease, the brain cells degenerate and die, causing a steady decline in memory and mental function.
Many scientists believe that Alzheimer’s disease results from an increase in the production and/or accumulation of a specific protein (beta-amyloid protein) in the brain that leads to nerve cell dysfunction/death. Moreover, some studies about this disease have shown an increased concentration of zinc and copper ions in the brain of patients with Alzheimer’s disease.
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 certain rage receptors and leads to damage of nerve cells and cerebral arteries. L-carnosine blocks and inhibits the activity of β-amyloid and in this way protects nerve tissue from developing dementia.
Articles published by one of the most prominent scientists in the field of mitochondrial dysfunction emphasize the importance of oxidative stress in the development of AD. Oxidative stress and mitochondrial damage are the early signs of AD, with ROS being a critical component of the disease pathogenesis (Wang, Wang, Perry, Lee, & Zhu, 2014; Wang, Zhao, Ma, Perry & Zhu, 2020; Lee et al, 2012). Karnozin Extra exhibits stronger antioxidative potential in comparison to sole L-carnosine.
Moreover, carnosine protects brain cells by its neutralizing the 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 a universal cell protector and plays a 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 neurodegenerative 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, the 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 the prevention of Alzheimer’s diseases.
Carnosine also works preventively 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.
Important to read! Are all L-Carnosine containing supplements the same? Click on the link for more information.
Corona, C., Frazzini, V., Silvestri, E., Lattanzio, R., La Sorda, R., Piantelli, M., … & Sensi, S. L. (2011). Effects of dietary supplementation of carnosine on mitochondrial dysfunction, amyloid pathology, and cognitive deficits in 3xTg-AD mice. PloS one, 6(3), e17971.
Caruso, G., Caraci, F., & Jolivet, R. B. (2019). Pivotal role of carnosine in the modulation of brain cells activity: Multimodal mechanism of action and therapeutic potential in neurodegenerative disorders. Progress in neurobiology, 175, 35-53.
Grasso, G. I., Bellia, F., Arena, G., Satriano, C., Vecchio, G., & Rizzarelli, E. (2017). Multitarget trehalose-carnosine conjugates inhibit Aβ aggregation, tune copper (II) activity and decrease acrolein toxicity. European journal of medicinal chemistry, 135, 447-457.
Lee, H. P., Pancholi, N., Esposito, L., Previll, L. A., Wang, X., Zhu, X., … & Lee, H. G. (2012). Early induction of oxidative stress in mouse model of Alzheimer disease with reduced mitochondrial superoxide dismutase activity. PloS one, 7(1), e28033.
Wang, X., Wang, W., Li, L., Perry, G., Lee, H. G., & Zhu, X. (2014). Oxidative stress and mitochondrial dysfunction in Alzheimer’s disease. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 1842(8), 1240-1247.
Wang, W., Zhao, F., Ma, X., Perry, G., & Zhu, X. (2020). Mitochondria dysfunction in the pathogenesis of Alzheimer’s disease: Recent advances. Molecular Neurodegeneration, 15, 1-22.