Carnosine for nerve protection

• Alzheimer's disease and mild cognitive impairment
• Parkinson's disease
• Epilepsy and schizophrenia
• Autistic spectrum disorders
• Stroke, vascular cerebral disorders

Carnosine is a universal neuroprotectant

Evolution has ensured, that healthy and young brain nerve cells contain enough carnosine for protection against damage and degenerative changes. As described above, the protective properties are mainly related to the antioxidant effects of carnosine and prevention of glycation and carbonylation. Carnosine in addition protects proteasomes that are part of a major mechanism of removing harmful carbonylated proteins. Carnosine simply stops the protein deformation process and “paves” the way to the prevention and slowdown of Alzheimer's disease and other kinds of demention and mild cognitive impairment.

The oxidative stress and degenerative processes described above prevail in a large volume in chronic brain diseases, Alzheimer and Parkinson´s disease, epilepsy and schizophrenia. Glycation denatures proteins and phospholipids with following AGEs production, that are a “fuel” for oxidation of cell membrane lipids.

Oxidative stress increases the PLA2 enzyme activity, which disrupts the cell membrane's fatty acids, causing impairment of membrane integrity, resulting in severe cell malfunction through to its extinction. All these harmful reactions together break the function of neurotransmitters. Carnosine reduces, not only oxidative stress, but also the malignance of following or concomitant processes (glycation, carbonylation, AGEs) Carnosine also acts directly as a neurotransmitter, anticonvulsant and chelating agent  (heavy metals binding). Carnosine thus becomes a universal substance, protecting against neurological and psychiatric syndromes and disorders. Alzheimer's disease is a MCI-mild cognitive impairment. It is a degenerative brain disease that causes progressive memory impairment and cognitive impairment. The disease slowly and relentlessly attacks nerve cells in all parts of the cerebral cortex, as well as their surrounding structures, resulting in the inability of the patient to control emotions, distinguish mistakes, errors and patterns, coordinate motions and the ability to remember. In the final stages of the disease, the patient experiences complete memory loss as well as all mental functions. There is no treatment known, and the medicines used are so far inefficient. Notwithstanding the progressive destruction of the nerve cells, it is possible to detect a wide spectrum of further abnormalities occurring in dead patients with Alzheimer's, including the extracellular deposit of amyloid beta protein and microscopical plaques and tangles in the brain cells. Experimental trials proved that carnosine is able to reduce or completely inhibit the cell damage caused by the toxic effect of amyloid - a typical protein associated to Alzheimer's. Amyloid beta reacts with specific RAGE receptors, causing damage to both nerves and brain arteries. Carnosine blocks and inactivates amyloid beta, protecting the nerve tissues against the development of dementia. Moreover, carnosine protects brain cells by neutralizing the highly toxic substance - alpha-beta-unsaturated akrolein aldehyde - which is formed during polyunsaturated lipids peroxidation. This substance most likely acts as a “toxic second messenger“ during oxidative destruction of cell membranes.

Current studies have shown that toxic unsaturated crotonaldehyde is involved in the further process of protein and phospholipids (especially cell membranes) destruction - carbonylation, lipid peroxidation. Because carnosine fights all aldehydes, there is an opportunity to explain its further effect as a significant preventive factor in Alzheimer's and other oxidative stress related diseases. Carnosine also prevents other Alzheimer's mechanisms. Some studies proved incidences of an increased zinc and copper ions concentration in patients' brain cells. These ions probably change the chemical structure of normal beta-amyloid and cause its toxicity. Mildly acid pH is required for this change to bind zinc and/or copper ions to beta-amyloid. These conditions (acidic environment and increased amounts of zinc and copper) generally occur as part of an inflammatory response to local damage. Carnosine, as a zinc and copper chelator, is able to remove these metals from the organism. This may be another important function of carnosine in preventing and slowing the progress of Alzheimer's and other degenerative brain disorders.

Mild cognitive impairment MCI

This disorder is currently described as a change-over between healthy perception aging and dementia. MCI studies consider a significant cause of this disorder multiplicity, together with the statement of underestimation of some common processes (e.g. cerebrovascular disease).  However, in such a multiplicity, it is difficult to detect prevalence, prognosis and eventual benefits of treatment. In this case, carnosine offers its strong neuroprotective effect as an ideal supplement for those with a suspicion of MCI or its initial stages.

Parkinson's disease

As a final reason, on an atomic level, there are toxic free radicals and their toxic metabolites, destructing certain brain cells. Hydrogen peroxide and tetracanoylphorbolacetate  are radicals capable of predominant brain cell destruction. Carnosine is able to prevent this formation and thus protect the brain cells against damage. Furthermore, so-called Lewy's bodies in the brain of patients with Parkinson's accumulate a substance called alpha-synuclein that accelerates the progress of the disease. Alpha-synuclein is formed under the condition of oxidative stress - and carnosine is able to reduce the oxidative stress as well as alpha-synuclein accumulation. Therefore, carnosine is already recommended as a supplementary treatment for Parkinson's.

Epilepsy and schizophrenia

These chronic diseases also belong to a large group of diseases where oxidative stress and carbonylation are involved in brain cell damage. Because carnosine effectively suppresses both of these reactions, it becomes a suitable treatment supplement for these  patients. Recent studies proved that carnosine has a significant anticonvulsant effect.

Autistic spectrum disorders

It was quite a sensation, when Dr. Michael Ches, a neurologist, published the results for autistic disorders treatment (autism and Asperger syndrome). Since 2001, nearly 1000 autistic children have been treated with carnosine. As mentioned, 80 to 90 % improved significantly during the 8 weeks after treatment began. According to Dr. Chez, carnosine acts in the frontal parts of the brain, combining its effect with the effect of nerve transducers acting in the deep parts of the brain.

Notable results of this treatment were also confirmed by the parents of the autistic children, even after the first week of the treatment. There was improvement not only in the communication area, but also in behaviour and social contacts.

Dr. Chez also discovered improvement in the treatment of dyslexia, mainly in the reading skills area and the attention level. In addition, Dr. Chez made a double-blind study in 31 autistic children with similar results. 400 mg carnosine was delivered without observing any side effects.

Stroke

Laboratory experiments proved that carnosine supplementation protects brain cells from ischemia caused damage, that occurs during or following the sudden closure of one of the cerebral arteries (stroke, ictus). One of the studies demonstrated 67% rat mortality after an ischemic incident. Mortality in the group supplemented by carnosine (started before the stroke) reached only 30%. Another study confirmed similar results - mortality after an ischemic attack declined from 55 % to 17%. This confirms that carnosine is a beneficial supplement for the secondary prevention of a stroke.