Carnosine may help you remain . . .

Agelessly Agile
New findings show carnosine to significantly enhance
movement-associated neurology
By Will Block

Do you, do you, do you, do you want to dance?
— Bobby Freeman

antasize for a moment what it would be like to suffer a brutal accident and become severely quadriplegic. You have not merely lost the use of your four limbs. You are totally paralyzed and no longer free to move. How devastating and tragic! Nonetheless, you would be making a mistake to believe that avoiding vile accidents will eliminate the possibility of movement loss. In fact, many people develop movement disorders, which can be just as debilitating—albeit in different ways. And even if you never suffer from a classified movement disease, the gradual loss of agility is part of the aging process.

Fortunately, as with all aging mechanisms, science is finding answers to the problems of waning mobility. Thus, it is increasingly possible to maintain the freedom of movement that we lose with age. Or recover some of what we lose from disease. Or perhaps even to advance beyond what is supposed to be “normal” movement function.

Movement Disorders Are Widespread

Movement disorders include such neurological conditions as akinesia (lack of movement), spasms, tremor, chorea (rapid, involuntary movements), ballismus (violent involuntary rapid and irregular movements) and dystonia (in which sustained muscle contractions cause twisting and repetitive movements or abnormal postures). Altogether, these afflictions affect millions of individuals, many of whom have turned to drugs and neurosurgery for the past 50 years. Reluctantly … because it’s an uphill battle with limited benefits and significant side effects. These are management techniques that have no hope for abolishing the conditions. Yet at last there is good news, with a growing interest in new approaches that herald higher expectations.

The Core of Motor Malfunctions

The chronic neurodegenerative illness known as Parkinson’s disease (PD) is the big headliner in movement disorders because it encompasses so many symptoms. PD is characterized by the progressive loss of dopaminergic neurons in the substantia nigra. It is within this core area of the brain (and elsewhere within it, including the ventral tegmental area) that the neurotransmitter dopamine is produced. Although dopamine also operates as a neurohormone (released by the hypothalamus to regulate prolactin in the pituitary), its principal role involves motor coordination, along with important roles for memory and reward. Whenever you do something that makes you feel good, that reward feeling is due to the release of dopamine.

As PD develops, dopaminergic neurons die in the substantia nigra, and when the attrition reaches 70–80%, the symptoms which characterize the disease appear, including uncontrollable tremors, rigidity, bradykinesia (slowdown in movement), and postural imbalance.1 While a precise understanding of the causation of PD is not at hand, what we now know is that the disease is driven by both genetic and environmental factors, the combined thrust of which is the development of oxidative stress in certain areas of the brain.

In its early stages, PD is closely associated with mitochondrial dysfunction,2 reactive oxygen species (ROS) accumulation,3 and apoptotic (cell suicide) signals in the substantia nigra.4 At the same time, the growing death of dopaminergic neurons causes the release of high amounts of free dopamine, which oxidize readily.5 Attending this, ROS are generated, which in turn worsen the oxidative stress status of the substantia nigra.

As the degeneration process of PD continues, the antioxidant system weakens, with levels of the most important endogenous antioxidants diminishing.6 To counter this, drug protocol replaces lost dopamine with agonists (receptor enhancers), including DOPA-containing drugs (e.g., levadopa), and MAO B inhibitors such as selegiline (aka L-deprenyl). MAO B stands for monoamine oxidase of the type B variety. Found in blood platelets, MAO B breaks down dopamine. It is important to emphasize that because of severe side effects, rendering treatment nearly ineffective, the goal what is called DOPA drug therapy is limited to symptomatic improvement (however slight) and not altering the course of the disease.

On the Stage of Neuroprotection

Consequently, nutrients that can be shown to offer benefits for movement disorders, such as antioxidants and neuroprotectors, are entering the spotlight. The neuropeptide carnosine (ß-alanyl-L-histidine) has been considered as an adjunctive therapy for PD, and alone as a tool in its own light. Found in the body and brain, carnosine is natural. Among its useful properties, it has been shown to be neuroprotective in several experimental models of brain ischemia.7 This has enabled researchers to predict that carnosine might be useful as a treatment for brain injury in both PD and Alzheimer’s disease.

The chronic neurodegenerative illness
known as Parkinson’s disease (PD)
is the big headliner in movement
disorders because it encompasses
so many symptoms.

Carsnosine, the safety of which has been established,* crosses the blood-brain barrier readily because of its hydrophilic nature. In the brain and body, its concentration varies substantially depending on the type of tissue. Other studies have found that carnosine protects SOD (superoxide dismutase, an important group of antioxidants made in the body) from oxidative damage in both in vitro and in vivo conditions.8,9 And recently, carnosine was found to protect mice with MPTP-induced (senescence accelerated) Parkinsonism.10 At the same time, carnosine taken at 100 mg/kg of body mass per day improved neurological symptoms, prevented activation of MAO B, and decreased proteins and lipid oxidation.11

*Its LD50 (the lethal dose for 50% of rodents) is about 20 g/kg of body mass, which renders it quite safe.

Tango Outdoes Exercise for Preserving Mobility

How about dancing? Now that’s a real part of life … until we lose the agility and body consciousness that makes it easy and a sheer delight. Could there be way to enable us to continue dancing on into our later years? The answer is yes, according to a recent study that followed the progress of Parkinson’s disease (PD) patients, noted to loose functional mobility more rapidly than those without it.1

What the study found was that dance, and specifically Tango, may be the right strategy for improving functional mobility deficits in people who are frail and elderly. Comparing the effects of two movement programs—Tango or exercise classes—19 subjects with PD were randomly assigned to either group. After 20 Tango or exercise classes, an evaluation was done and compared with one done a week before the study started. While both groups showed significant improvements according to one standardize scale for evaluating PD, the Tango group showed significant improvements on another scale. While the exercise group did not improve on this measure, the Tango group showed a trend toward improvement on the “Timed Up and Go” test that was not observed in the exercise group.

Another study by the same authors compared the effects of Tango, Waltz/Foxtrot, Tai Chi, and No Intervention (NI) in patients with PD regarding their health-related-quality-of-life (HRQoL). Seventy-five persons with PD were assigned to the four groups of either of two dances, Tai Chi, or the NI group. After 20 lessons (or 13 weeks for the NI group), Tango significantly improved mobility, social support and the outcome of a PD questionnaire. While there were no HRQoL advances noted in the Waltz/Foxtrot, Tai Chi or NI groups, Tango triumphed again. The authors attributed this to Tango’s ability to address balance and gait deficits social interaction context that requires working closely with a partner. Wanta dance?


  1. Hackney ME, Kantorovich S, Levin R, Earhart GM. Effects of tango on functional mobility in Parkinson's disease: a preliminary study. J Neurol Phys Ther 2007 Dec;31(4):173-9.
  2. Hackney ME, Earhart GM. Health-related quality of life and alternative forms of exercise in Parkinson disease. Parkinsonism Relat Disord 2009 Mar 27. [Epub ahead of print]

Carnosine for Adjunctive Therapy

This led the researchers of a recent study to see if carnosine could add to the usual basic treatment for PD.12 Thirty-six patients with trembling-rigid and trembling manifestations of PD (20 males and 16 females; ages 46–68 years) in early- to late-stages of the disease took part in the trial. None of the patients had chronic systemic diseases, and the registered period of the disease was from 2.5 to 16 years. Twenty healthy subjects served as controls; their average age was 42.0 (±6.7 years).

Using a standard Parkinson’s disease rating system, mentality and behavior, activity of daily living, motor examination, and complication of therapy were measured. This rating system was focused in on specific parameters, including extremity rigidity, leg agility, activity of daily living, motor examination, and so forth. The measuring physician was blinded to the treatment protocol to prevent the possibility of bias.

As the study began, the PD patients were distributed into two groups balanced for age, duration of disease, and neurological symptoms. The first group contained 16 patients who received only the basic therapy at individualized doses—DOPA-containing drugs, agonists of dopamine receptors, and amantadines (antiviral drugs). The other group, consisting of 20 patients, received the basic therapy plus carnosine (0.5 g, three times daily for a total of 1.5 g/day). The treatment lasted for 30 days.

Several biochemical parameters were measured before and after the treatment: MAO B and Cu/Zn-SOD, measured in platelets and in red blood cells, respectively; protein carbonyls in blood plasma; and iron-induced lipoprotein oxidation in blood lipoproteins.

Carnosine Improves Neurological Status

The iron-induced lipoprotein oxidation test was designed to measure the rate of oxidation and thus to characterize the antioxidant state of the patients’ blood before and after treatment. Initially, the level of neurological symptoms of patients corresponded to 38.9 points on the scale use, but after 30 days this level decreased to 32.5 points in the basic therapy group. However, in the group with basic therapy combined with carnosine it was 24.9 points, a 36% drop. The patients receiving just the basic protocol only dropped 16.5%. This represented a significant efficiency of treatment, and thus carnosine, as an additional treatment, significantly improved the neurological state of the patients.

To be specific, the carnosine-treated group was found to have improved locomotion, with reduced rigidity of extremities and hand movements, by 32–38% compared to the basic therapy group. One of the most important clinical signs of Parkinsonism is hypokinesia and carnosine—while not achieving “clinical significance” because there were so few patients in the study—clearly demonstrated its tendency to improve hypokinesia.

The carnosine-treated group
was found to have improved
locomotion, with reduced rigidity of
extremities and hand movements,
by 32–38% compared to the
basic therapy group.

Carnosine Improved Leg Agility Two-Fold

Symptoms of supination (the excessive rotation of the forearm and hand, and the corresponding excessive movement of the foot and leg) improved two-fold with carnosine, as did easiness of leg movements (rapid, alternating movements of hands and leg agilities), compared with the basic therapy group.

Also, the typical “finger taps” test (where the patient taps thumb with index finger in rapid succession), as well as rigidity of both extremities, and trembling, showed similar improvement in both groups of patients. Thus, in this test, carnosine had no advantage.

However, everyday activity measure improved significantly more in the carnosine treated patients. This is important because it enables more independent self-service (daily life activity improved by 32% in the carnosine-treated group). Also, motor skills were improved by 34% owing to carnosine treatment. Furthermore, carnosine displayed no negative side effects nor was it found to be incompatible with basic therapy.

Upon analyzing MAO B, it was found that levels were elevated in both therapies. Yet neurological symptoms improved, leading the researchers to conclude that the rise in MAO B activity is controlled by the intrinsic antioxidant defense system.

Carnosine Boosts Endogenous Antioxidant Protection

It was also found that Cu/Zn-SOD levels were decreased in the group receiving basic therapy, whereas it was increased in the carnosine group. SOD is a key enzyme of antioxidant defense, but the decrease in the basic group was not judged significant. Nevertheless, Cu/Zn-SOD is one of the important directions of therapeutic effect of carnosine. In fact, another study has shown that carnosine protects SOD from oxygen starvation in rats.9 Yet, there are contradicting data in the literature about SOD activity in PD patients, some reporting decreases, while some showing increases of SOD activity compared to healthy donors. However, the researchers’ data suggests that some success in the treatment can be achieved without effect on SOD, whereas therapy resulting in restoration of SOD may be more efficient.

Carnosine Protects Cellular Proteins Against Oxidation

When the level of protein carbonyls in healthy donors and the different groups of PD patients was compared, the amount of oxidized protein molecules increased in PD patients but was not changed during basic therapy. However, the carnosine protocol resulted in noticeable decreases in protein carbonyls, which is in good correlation with the ability of carnosine to protect cellular proteins against oxidation.

With pronounced SOD restoration,
which is suppressed in PD patients,
carnosine demonstrated significant
neuroprotective action on PD. These
findings suggest the value of carnosine
for other movement disorders.

Measuring the iron-induced oxidation in the blood of PD patients showed that the initial level of hydroperoxides was not changed by basic therapy, although carnosine decreased the oxides, but it was not statistically significant. This indicates that carnosine effectiveness not only protects SOD, but other important molecules that can oxidize.

Carnosine for Other Movement Disorders

In the final analysis, the study clearly demonstrated the efficacy of carnosine when used as a nutritional supplement to increase the success of basic therapy on PD patients. Even through MAO B didn’t change, there were positive changes in neurological symptoms. With pronounced SOD restoration, which is suppressed in PD patients, carnosine demonstrated significant neuroprotective action on PD. These findings suggest the value of carnosine for other movement disorders.

High levels of carnosine depend on the carnosine synthase enzyme and supplies from dietary resources (meat and fish). Yet it is difficult to get enough in the typical American diet; supplementation is required. Carnosine protects cells and tissues as an direct result of its antioxidant activity and through its ability to protect cells and tissues against oxidative stress by protection from oxidation of SOD and other proteins, as well as lipids.

As to other possible mechanisms (and applications), in recent studies carnosine prevented aldehyde modification of proteins (suggesting a use in Alzheimer’s disease),13 disaggregated proteins damaged by oxidative modification (substantiating its use for cataracts),14 and to prevented protein carbohydrate cross-linking (suggesting its use for conformational diseases).15

Looking to the Future

It is known that carnosine levels in tissues are decreased under stress conditions. Indeed, this is associated with diminished thresholds for physical exercise exhaustion, increased aging, and the consequential lowering of resistance to disease. This is why, in animal models of oxidative stress, carnosine demonstrates efficient protection of the brain against oxidative injury. Similar mechanisms are probably working in the human body as the study at hand demonstrates. In combination with basic therapy for PD, carnosine may be a path to improving efficacy while decreasing toxic effects of over-loading with DOPA-containing drugs.

Other nutrients thought to be of value for movement disorders include coenzyme Q10, vitamin E, creatine, tangerine peel, cocoa, red clover, green tea (EGCG), and benfotiamine. When taken together with unfolding knowledge about the molecular and genetic mechanism of the etiology of movement disorders, 2009 may be a pivotal year and a gateway for what is to come and make us freer to move again,16 and to reach for ageless agility.


  1. Factor SA, Weiner WJ, editors. Parkinson’s Disease: Diagnosis and Clinical Management. New York: Demos Medical Publishing; 2002.
  2. Dawson TM, Dawson VL. Molecular pathways of neurodegeneration in Parkinson’s disease. Science 2003;302:819–22.
  3. Olanov CW. A radical hypothesis of neurodegeneration. Trends Neurosci 1993;16:439–44.
  4. Mouradian MM. Recent advances in the genetics and pathogenesis Parkinson’s disease. Neurology 2002;58:179–85.
  5. Jenner P, Olanow CW. Oxidative stress and the pathogenesis of Parkinson’s disease. Neurology 1996;47(suppl3): S161–70.
  6. Abraham S, Soundararajan CC, Vivekanandhan S, Behari M. Erythrocyte antioxidant enzymes in Parkinson’s disease. Ind J Med Res 2005;121:111–5.
  7. Dobrota D, Fedorova T, Stvolinsky S, Babusikova E, Likavcanova K, Drgova A, Strapkova A, Boldyrev A. Carnosine protects the brain of rats and Mongolian gerbils against ischemic injury: after-stroke-effect. Neurochem Res 2005;30:1283–8.
  8. Choi SY, Kwon HY, Kwon OB, Kang JH. Hydrogen peroxide-mediated Cu,Zn-superoxide dismutase fragmentation: protection by carnosine, homocarnosine and anserine. Biochim Biophys Acta 1999;1472:651–57.
  9. Stvolinsky SL, Fedorova TN, Yuneva MO, Boldyrev AA. Protective effect of carnosine on Cu,Zn-superoxide dismutase during impaired oxidative metabolism in the brain in vivo. Bull Exp Biol Med 2003;135(2):151–4.
  10. Boldyrev AA, Fedorova TN, Stvolinsky SL, Borras C, Sastre J, Vina J. Chemical intervention in senescence-accelerated mice metabolism for modeling neurodegenerative diseases: an overview. In: Nomura Y. (Ed.), Senescence-Accelerated Mouse (SAM): An Animal Model of Senescence. Elsevier, Amsterdam, 2004.
  11. Boldyrev A, Fedorova T, Stvolinsky S, Stepanova M, Dobrotvorskaya I, Kozlova E, Bagyeva G, Ivanova-Smolenskaya I, Markova E, Illarioshkin S. Carnosine increases efficiency of L-DOPA therapy of parkinsonics. Parkinsonism Rel Disor 2007;13:S99.
  12. Boldyrev A, Fedorova T, Stepanova M, Dobrotvorskaya I, Kozlova E, Boldanova N, Bagyeva G, Ivanova-Smolenskaya I, Illarioshkin S. Carnosine [corrected] increases efficiency of DOPA therapy of Parkinson's disease: a pilot study. Rejuvenation Res 2008 Aug;11(4):821-7. Erratum in: Rejuvenation Res 2008 Oct;11(5):988.
  13. Hipkiss A. Could carnosine or related structures suppress Alzheimer’s disease? J Alz Dis 2007;11:229–240.
  14. Seidler NV, Yeargans GS, Morgan TG. Carnosine disaggregates glycated a-crystallin: an in vitro study. Arch Biochem Biophys 2004;427:110–5.
  15. Yan H, Harding JJ. Carnosine protects against the inactivation of esterase induced by glycation and a steroid. Biochim Biophys Acta 2005;1741:120–6.
  16. Wider C, Wszolek ZK. Movement disorders: insights into mechanisms and hopes for treatment. Lancet Neurol 2009 Jan;8(1):8-10.

Will Block is the publisher and editorial director of Life Enhancement magazine.

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