Recent research indicates that L-Carnosoine may have protective and preventive properties for Dyslexia and 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 and related autism research, please click here.  

Dyslexia Research 

According to new research, dyslexics struggle to read because even small visual or auditory distractions can throw them off.  Children with dyslexia don't filter incoming information well.  This results in their having trouble creating mental categories to identify letters and word sounds.  

This research was published in the January 2007 issue of Psychological Science.   Studies were carried out by by neuroscientist Zhong-Lin Lu, at the University of Southern California, researcher Anne Sperling of the National Institutes of Health, psychologist Franklin Manis of University of Southern California, and  department and  psychologist Mark Seidenberg of the University of Wisconsin-Madison.

USC College professors Zhong-Lin Lu (above) and Frank Manis (below) are part of a research team that has developed a new model of dyslexia.

These researchers theorize that deficit in noise exclusion may come from abnormally low levels of GABA, a neurotransmitter that helps the brain to filter out irrelevant information.  L-Carnosine, which has been shown to stimulate the production of GABA and protect areas of the brain that protect GABA, may be of benefit. . 

Autism Coach has received reports from dyslexic adults and the parents of dyslexic children using Liquid Carnosine Plus of  reduction in symptoms, a feeling of well-being, calmness, and greater focus after having taken the supplement for 2-3 weeks. 

Dyslexia affects millions of people, from 5 to 15 percent of the U.S. population.  The symptoms of dyslexia include difficulty with word recognition, directional ability and decoding  symbols.

Dr. Anne Sperling said people with dyslexia appear to have shaky mental categories for the essential sounds that make up language.  

“It’s harder to make a [language] task automatic when your categories are fuzzier than they ought to be to begin with,” she said.  “In terms of treatment, the results suggest that programs that foster the development of sharper perceptual categories for letters and letter sounds might be a good way to supplement existing dyslexia interventions,” she added.

The team’s latest study builds on results they published last year in Nature Neuroscience.  The same authors previously showed that poor readers also have trouble figuring out categories in simple card games.

Other recent studies support their theory.  Johannes Ziegler of the Universite de Provence in Marseille, lead author on a study of dyslexia and auditory noise published this year in Proceedings of the National Academy of Sciences, said his results suggest that dyslexia stems from shaky categories for the basic sounds of language (phonemes).

“In silence, information is often redundant and dyslexics get away with the perception deficit,” Ziegler said in an e-mail. “In noise, however, they can no longer compensate.

“What is important is that noisy environments are the rule and not the exception,” he added, citing a study from South Bank University in the U.K. that found average noise levels in primary classrooms to be as high as near a busy intersection.

“What Sperling and Lu’s data suggest is that the mechanism responsible for faulty phonological development is quite general and has to do with attention in a broad sense .…

Lu said there is a “lot of evidence” of learning problems from background noise. In one such study, Manis and a collaborator from UCLA found that children with dyslexia struggled to discriminate similar sounds, like “spy” and “sky,” because they weighed irrelevant differences in sounds equally with key distinctions.

Manis also cited research from Finland and the United States showing that infants with dyslexic parents lag behind their peers in forming categories for speech sounds.

Lu and his collaborators believe their studies disprove the old theory of dyslexia, which theorized that dyslexia was caused by  a deficit in processing quickly incoming sounds and visual information.   Lu and his colleagues found that the the  pathway for processing quickly incoming sounds and visual information works normally both in children and adults with dyslexia  — as long as visual or auditory background noise is low.  However, as visual distractions and background noise increases, dyslexics begin to score poorly on visual pattern tests - even when the task only requires slow processing.

These new findings bring a better understanding of and the promise of improved treatments for dyslexia.

Carnosine and Aging

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 our liquid methylated B Vitamin complex, Behavior Balance.

For information on our Liquid Carnosine Plus supplement, please click here.