In experiments, treatment with carnosine
was found to reduce or completely prevent cell damage caused by beta amyloid,
the substance found in the brain of Alzheimer's disease patients. Beta amyloid
can interact with certain RAGE receptors causing damage to the nerves and arteries
of the brain. Carnosine blocks and inactivates beta amyloid, so it protects neural
tissues against dementia.
Moreover, carnosine protects the brain cells
by fighting the highly toxic alpha, beta-unsaturated aldehyde acrolein which is
formed during the peroxidation of polyunsaturated lipids, raising the possibility
that it functions as a 'toxicological second messenger' during oxidative cell
injury (Burcham et al. 2000).
research also confirms that the toxic unsaturated aldehyde crotonaldehyde (CA)
contributes to carbonylation resulting in protein damage during lipid peroxidation
(Fontaine et al 2002). As carnosine combats all aldehydes, it offers another
explanation for its benefits in prevention of Alzheimer´s disease and other
conditions with oxidative stress.
Metal chelation by carnosine may prevent
and slow down Alzheimers.
Some laboratory studies have reported
excessive amounts of metal ions such as zinc, copper in Alzheimer´s brain.
Such ions may possibly change the chemical architecture of normal beta amyloid,
making it more harmful. A mildly acidic environment appears to be important in
the process that binds these metals to beta amyloid. Experts observe that such
conditions (acidic environment and higher levels of zinc and copper) commonly
occur as part of the inflammatory response to local injury. Carnosine has the
unique ability to chelate copper, zinc and other metals, and to remove them from
the body, as explained above in the section Metal Chelation. This may be an important
function of carnosine in preventing and slowing down Alzheimer´s and other
degenerative brain disorders.