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Carnosine Research in Age-Related & Neurological Conditions


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Recent research indicates that L-Carnosine may have protective and preventive properties for conditions related to aging (including cataracts, Parkinsons and Alzheimers).  L-Carnosine research related to these conditions is given below.  For information on our Liquid Carnosine Plus supplement, please click here.  

Laboratory research on cell life indicates that L-Carnosine has the ability to rejuvenate cells approaching old age, restoring normal appearance and extending celluar life span.  Cataracts are also believed to result from the gradual accumulation of damaged tissues and L-Carnosine is believed to help by binding to receptor sites where damage normally occurs, preventing further damage.  

Carnosine, Glycation and Aging

Carnosine Intefering with Aging Process

 

Recent research is indicating that an intrinsic part of the aging process involves damaged structures and tissues that gradually accumulate in the body through a destructive process called “glycation”.   Glycation is the binding of a protein molecule to a glucose molecule resulting in the formation of damaged, nonfunctioning structures, known as AGES (Advanced Glycation End products).  Glycation alters protein structure and decreases biological activity.  For example, glycation contributes to the aging of skin, contributing to wrinkles and age spots.  Many age-related diseases such as arterial stiffening, cataract and neurological impairment are at least partially attributable to glycation.

Cataracts are likely to form as a result of glycation, while glycation inhibitors, like carnosine protect against the damage. There are also anecdotal reports that carnosine may relieve some forms of macular degeneration and may protect against glaucoma.  

The L-Carnosine molecule chemically resembles the receptor sites in the body that glycation normally attacks.  It appears to researchers that L-Carnosine sacrifices itself to spare normal glycation targets, preventing damage.  L-Carnosine also bolsters proteolytic pathways, helping the body to rid itself of damaged, useless glycated proteins. Carnosinylation (the process where carnosine combines with denaturated molecules) tags glycated proteins for cell removal.   The following diagram shows L-Carnosine's role in interfering in the glycation process by quenching carbonyl compounds and and AGES.

Parkinsons and Nerve Cell Die-Off

Nerve Cell Receiving Excitatory Signal and Firing

Over-excitation of the nerves in the brain causes the nerve cells to excessively fire (constantly transmit chemical/electrical impulses without stopping) exhausting the nerve cells and resulting in their dieing off.  As we age, the body is less effective at protecting itself against cellular damage and efforts to protect, remove by-products of cellular metabolism  (through  the ATP energy cycle), repair and replace damaged cells.  Over time, more and more nerve cells die off. 

If enough nerve cells die off this can result in the development neurological conditions.  If enough of the areas of the brain that produce dopamine die off during the overall nerve cell die-off process, Parkinsons Disease may arise.  

Calming neurotransmitters, such as GABA act as a brake after a nerve has fired, causing the nerve to stop firing, and preventing the deadly over-firing. L-Carnosine promotes the production of GABA and protects the GABA producing receptor sites in the brain, which in turn, may provide protection against the die-off of dopamine producing nerves in the substantia nigra area of the brain.  The combination of Liquid L-Carnosine Plus, which contains Carnosine and Zinc, plus Alpha-Lipoic Acid, enables the body's ATP energy cycle to work more efficiently, prolonging the life of cells, helping cells to eliminate toxins and by-products of metabolism.  

Alzheimers - Accumulation of Cellular Debris, Impaired Memory Formation and Nerve Cell Die-Off

In a study of Alzheimer's patients, at Georgetown University, headed by William Rebeck, it was found that two receptors found on the surface of nerve cells may play a part in difficulty in forming new memories and in triggering die-off of nerve cells. These receptors are APOE and NMDA and are linked to form a single molecular unit, called the APOE/NMDA receptor site.  The APOE and NMDA receptors are joined together by a protein called PSD95, often found in connections between nerves (synapses). The APOE/NMDA receptor site causes the nerve cell to fire when any one of the following bind molecules/chemicals bind to it:  the APOE protein, the NMDA protein, or glutamate.

In order to make and store a memory, the NMDA receptor on a nerve cell must be triggered to cause the cell to fire for a sufficiently long time, producing a long-lasting synaptic response that ultimately results in the storing of a new memory.

The APOE protein that binds to the APOE receptor is believed to transport cellular debris as the result of normal metabolism or injury away from cells in the brain, moving debris to areas where it can be completely removed from the brain.  There are eight different APOE receptor types.  APOE receptor 2 type (ApoEr2 ), is believed to be critical to the development and operation of a normal brain.  

An APOE protein variant called APOE4 is linked to Alzheimer's and is believed to less be efficient at removing cellular debris from the brain than APOE2 or APOE3 variants.  Because it is less efficient, the brain secretes more of the APOE4 protein to do this job.  Unfortunately, when excessive amounts of APOE4 bind to the APOE receptors at the APOE/NMDA receptor sites in the brain, the APOE4 protein interferes with the ability of the NDMA receptors to make and store new memories. Rebeck's team theorizes that the clogging of receptors with APOE4 prevents glutamate from activating the processes necessary to form memories. 

If too much APOE binds to the APOE/NMDA receptor site two things can happen:  

1.  The receptor site becomes over-stimulated and continuously fires, causing the nerve cell to die off.  (Monosodium glutamate (MSG) can also act as a neurotoxin, triggering the over-firing of nerve cells.  I hypothesize that the reason MSG makes food taste better is that it over-stimulates the nerve cells in the mouth and on the tongue.)

2.  The receptor site turns down its activity, not responding to stimulus, resulting in the inability of NMDA to stimulate the nerve cell, interfering with the formation of memories.  Rebeck theorizes when brain damage occurs, this causes areas of the brain to shut down to protect itself, resulting in the brain not thinking too much in effected areas.

If excessive levels of APOE4 the protein cannot clear up the accumulating damage in the brain, the ability to make new memories is increasingly lost. The accumulating damage takes the form of the beta amyloid structures found in the brains of Alzheimer's patients.  

L-Carnosine is believed to reduce or prevent cell damage in the brain caused by beta amyloid, in part, by protecting the protein that removes damaged proteins from brain cells and preventing the accumulation of damaged structures within the brain.  It also helps to prevent nerve cells from over-firing by promoting the production of the calming neurotransmitter, GABA.  

In Conclusion 

Because Carnosine promotes calming neurotransmitters that  prevent over-firing of the nerves, binds to receptor sites on nerves that would otherwise become over-excited, and helps scavenge and eliminate cellular debris, Carnosine is proving to be of nutritional support for a variety of conditions including learning disabilities, aging-related conditions, and neurological conditions. 

There is also a study currently taking place in the the use of Carnosine for individuals with schizophrenia and bi-polar conditions - initial results appear to be promising.  We have also had received feedback from individuals suffering from depression indicating improved mood, when using Liquid Carnosine Plus in combination with one of our methylated B Vitamin supplements.