[accu200]

Haing a progressive disease makes me look for hope.
Reading the research going on ,I have come to the conclusion a cure may be found,but probably not in my lifetime.So looking thru this website ,I developed my own hope.Believing Iron may be a factor in the distruction that leads to PD,I cut back on Iron intake took B2 and Curcumin.It was stated that India has a low incidence of PD and eats a lot of curry cntaining Curcumin.I read that the Farci people in India have one of the highest incidences of PD.Wonder if they eat curry?
A while back I was at a Fox Foundation meeting where they announced that they were funding a Chinese research project on the neuroprotection properties of Green Tea.Wonder if anybody heard of any results.
4 years ago a reseach project on Coenzyme Q10 claimed it had neuroproteectivite qualities.Is it not strange that 4 years latter there has been no phase 3 study to give a difinitiveanswer to the question of it's benefits.
I have a chronic mucus problem and periodically take Robitussin DM to relieve the symptoms.I was amzed that when I had the Mucus problems my PD was better.Maybe it was the DM.

[stevem53]

I think it was the DM..Ive been taking a small amount of DM before bedtime everynight for a about 2 or 3 weeks, and Ive felt reasonably well everyday ever since..The symptoms on my left side have about disappeared

[steffi 001]

I am asking because recently my medication is not as effective as it has been.I have waited a while before coming to the conclusion that I may be getting used to them,therefore they are less effective.I guess I didn`t want to face this but...at one time I could guage when to take my next dose without my body taking a huge dive.Nowadays I take a dose and without fail,I am unable to function on any level other than to sit down and wait for my limbs to move.This invariably takes an hour at least...and is happening at an alarming rate.
I have tried Q10 and found it helpful but expensive.
I am interested in this DM product.Might it be worth giving it a go?

[Jaye]

Steffi, what you describe, if I understand correctly, is called "wearing off" before the next dose. The meds are just as effective--you don't habituate to them the way you do to an opiate or a pseduo-opiate such as dextromethorphan--but you have fewer brain cells. Remember the substantia nigra is 80% gone before we start showing "parkinsonism" symptoms. We have a progressive, degenerative brain disorder. If something is neuroprotective it stops or slows the progression, maybe a teensy bit, but so far nothing has been proven to be neuroprotective. Notice I say "proven," which means by science, not "thought to be," which would mean by individual observation, conjecture, and guessing amounting to pseudoscience. Of course a good diet gives you better chances at health, and exercise has been proven to slow progression of symptoms.

Spend as much as you like on fads. Just don't expect them to slow your PD. And if your meds are wearing off, tell your doctor. Sinemet is not toxic and may even be neuroprotective [Langston], but smoothness of delivery is important in avoiding motor complications such as dyskinesia. You may need Comtan or an agonist or one of the newe drugs to stretch out and smooth your current meds.

This is not my opinion, but a report of scientific knowledge to date. I welcome corrections.

Jaye

[steffi 001]

You know I have only just visited the hospital and feel that nothing really has been taken on board.I stretch out my visits so I know I am not a bother to them...I just would have expected a bit more interest after such a lengthy gap since my previous appointment.I saw a PD nurse,not the neuro.She was lov ely but has only increased my rop ,not suggested anything remotely like you have done.
I am also wondering if a recent 24 hour bug is takiing its toll.I feel fluey and totally listless.
I think a visit to the GP armed with your suggestions,Jaye,might be an idea...so thanks for replying.I have something to work on now.

x

[EnglishCountryDancer]

I notice you live in the U.K as I do.We all contribute to the National Health Service and you are entitled to see a neurologist regularly.So phone up and ask for an appointment.It is easy to slip through the net. The Parkinson Society have a very good help line.Sometimes you have to push for what you deserve.Perhaps you are just too nice.

[EnglishCountryDancer]

I notice that you say that you stretch out your times between visits but N.I CE guidelines say you should be seen at least six monthly.In this area my husband sees a neurologist every six months and can see a specialist Parkinsons nurse as often as he wants
On another tack :if you have had this virus which makes you feel overwhelmingly tired and gives you a cough your symptoms will be worse.I am, I hope, a fit and healthy person and only had a mild dose and it has made me feel exhausted after very little effort,low and depressed..You usually sound so upbeat and it is sad to hear you so unlike yourself.Thinking of you.

[caya]

Hi !

In reference to the Phase 3 Trial for CoQ10........it is BEGINNING in April, next month. The Parkinson's center where my MDS practices and teaches is one of the facilities involved in the CoQ10 trials. They are all quite excited about it. Dr. Clifford Shults of the University of California San Diego who has pioneered the CoQ10 research died of Cancer two months ago. His illness complicated the project for a few months but it is back on go now. Stay tuned.

Caya

[reverett123]

As we all know there is a range of opinion on this subject and there is a case to be made for both ends of the spectrum. I have no desire to disabuse anyone's faith in science or the current research community or anything else. One's belief, whether in alternative or mainstream, gives hope and hope is vitally important. With that disclaimer:

As even a few researchers are beginning to point out, PD research entered a cul-de-sac 30 years ago and little has emerged since. The problem of funding is just one part. The net truth is that there is little hope for a cure in time for us. But it is also true that there is much that offers promise but not profit. No one is going to knock on our neuro's door and give ink pens with "green tea" printed on them.

Another part of the problem is that the majority of the research is focused on the "Standard Model" of PD as "a genetic predisposition combined with an environmental insult" killing dopamine producing neurons in the substantia nigra. That is a simplistic view of a complex problem and it is bottling up research dollars in that cul-de-sac. Why? One possible factor is that the American PD community alone spends about ten billion dollars a year on meds!!!

So, I and others spend hour upon hour combing the Net looking. And there are things that make big differences for me. And they have research behind them, not always from US labs. I recommend nothing, not a doctor, etc. But I consider the following as the most promising:

1) the combo of alpha-lipoic acid and acetyl-L-carnitine and L-carnosine. I have stopped this trio hree or four times in the last few years and each time have been forced to admit it was an error. Restarted and noticed improvement in just days. Because this one is so important I am going to attach a file that is a collection of Medline abstracts.

2) Green tea extracts do so much that it is impossible to cover here but one thing in particular is that they calm down the inflammatory response in our brains that kills the neurons

3) essential fatty acids are proving more and more important. Not only because of their role in brain structure but more importantly, their role in cell signaling, the very essence of our being.

There are others, including the DM, but I will limit myself to these three standouts because they have research to back them, have proven safe and effective, and I have tested them on my own little brain and survived.

There are risks everywhere. Sinemet? Requip? Selegeline? They tell us they tested each one and found it safe. They don't make a point of the fact that the testing was only weeks or months, that a lot of people had bad experiences, and that they never tested them together. I take all three. Now THAT"S a white rat!

-Rick

[reverett123]

I just found that the file format "rar" is not known to vbulletin! Kind of surprising. So, I'll do it the old fashioned way....

Summary: Alpha Lipoic Acid, Acetyl-L-Carnitine, L-Carnosine

1- Accelerates nerve regeneration.
2- Improves nerve conduction.
3- Acts to preserve normal enteric peptide balance.
4- Restores mitochondrial function.
5- Improves cognition.
6- Synergizes with fatty acids.
7- Acts against glycation (Lewy bodies).



1: Endocr Res. 1997 Feb-May;23(1-2):27-36.

Acetyl-L-carnitine effects on nerve conduction and glycemic regulation in
experimental diabetes.

Soneru IL, Khan T, Orfalian Z, Abraira C.

Extended Care & Geriatrics Service (181C), Hines VA Hospital, Illinois 60141,
USA.

Acetyl-L-Carnitine (ALC), an activator of carnitine, can accelerate nerve
regeneration after experimental surgical injury in rats. In this study, we
examined the ability of ALC to improve nerve conduction velocity and its effect
on intravenous glucose tolerance test in streptozotocin-induced diabetic rats.
Diabetic (blood glucose > 200 mg%) and normal animals were treated
intraperitoneally for four weeks with ALC, 50 mg/Kg/d and 150 mg/Kg/d. Nerve
conduction velocity was measured by direct exposure of sural nerve. Two-hour
IVGTT was studied by measuring plasma glucose, insulin and free fatty acids
after intravenous injection of glucose, 1.75 gm/Kg/body weight in animals
treated either with ALC 150 md/Kg/d or saline alone. Six weeks of STZ-induced
diabetes resulted in impairment of nerve conduction velocity in animals injected
with saline (16.05 +/- 1.09 m/s), as compared to saline-treated normals who did
not receive streptozotocin (31.0 +/- 0.84 m/s, p<0.0005). Diabetic animals
treated with ALC, 150 mg/Kg/d, preserved near normal nerve conduction (27.10 +/-
1.42 m/s), compared with the saline-treated diabetic animals (p < 0.0005), but
diabetic animals treated with ALC, 50 mg/Kg/d, had a non-significant increase in
nerve conduction (23.68 +/- 1.6). ALC treatment had no effect on fasting or
post-intravenous plasma glucose in normal or diabetic rats, although it
moderately reduced baseline and 40 minute insulin levels (p < 0.02) in normal
rats as compared with their saline-treated counterparts. ALC treatment lowered
baseline free fatty acids in normal (p < 0.04) and diabetic (p < 0.03) animals,
and the 60 minute levels in the normal group only (p < 0.003). CONCLUSION: ALC
at a dose of 150 mg/Kg/d given for one month, produced near normalization of
nerve conduction velocity in streptozotocin-induced diabetes with no adverse
effects on glucose, insulin or free fatty acid levels.

PMID: 9187536 [PubMed - indexed for MEDLINE]



1: Metabolism. 1995 May;44(5):677-80.

Acetyl-L-carnitine corrects the altered peripheral nerve function of
experimental diabetes.

Lowitt S, Malone JI, Salem AF, Korthals J, Benford S.

Department of Pediatrics, University of South Florida, Tampa, USA.

Acetyl-L-carnitine (ALC) has been shown to facilitate the repair of transected
sciatic nerves. The effect of ALC (50 mg/kg/d) on the diminished nerve
conduction velocity (NCV) of rats with streptozotocin (STZ)-induced
hyperglycemia of 3 weeks' duration was evaluated. The aldose reductase
inhibitor, sorbinil, which is reported to normalize the impaired NCV associated
with experimental diabetes, was used as a positive control. Aldose reductase
inhibitors are thought to have an effect by decreasing peripheral nerve sorbitol
content and increasing nerve myo-inositol. Treatment of STZ-diabetic rats with
either ALC or sorbinil resulted in normal NCV. Sorbinil treatment was associated
with normalized sciatic nerve sorbitol and myo-inositol; ALC treatment did not
reduce the elevated sorbitol levels, but sciatic nerve myo-inositol content was
no different from nondiabetic levels. Both ALC and sorbinil treatment of
STZ-diabetic rats were associated with a reduction in the elevated
malondialdehyde (MDA) content of diabetic sciatic nerve, indicating reduced
lipid peroxidation. The beneficial effects of sorbinil and ALC on the altered
peripheral nerve function associated with diabetes were similar, but their
effects on the polyol pathway (frequently implicated in the pathogenesis of
peripheral neuropathy) were different.

PMID: 7752919 [PubMed - indexed for MEDLINE]


1: Int J Clin Pharmacol Res. 1992;12(5-6):225-30.

Peptide alterations in autonomic diabetic neuropathy prevented by
acetyl-L-carnitine.

Gorio A, Di Giulio AM, Tenconi B, Donadoni L, Germani E, Bertelli A, Mantegazza
P, Maccari F, Ramacci MT.

Department of Medical Pharmacology, Faculty of Medicine, University of Milan,
Italy.

Autonomic neuropathy and gastrointestinal problems are among the most common
complications of diabetes. In this report it is shown that a possible
correlation between the two disorders might exist, since diabetes causes a
profound alteration of the peptidergic innervation of the gut. It is reported
that 14 weeks after diabetes induction with alloxan the levels of substance P
and methionine-enkephalin are markedly reduced throughout the intestine, while
vasoactive intestinal polypeptide content is dramatically increased. Therefore
the enteric innervation of diabetic animals is completely disorganized, with
some systems undergoing atrophy and others undergoing hypertrophy. Treatment of
diabetic animals with acetyl-L-carnitine prevents the onset of the marked
peptide changes described above. The results suggest a potential for
acetyl-L-carnitine in the treatment of autonomic neuropathies.

PMID: 1284498 [PubMed - indexed for MEDLINE]



1: Brain Res. 2002 Apr 5;932(1-2):70-8.

L-carnitine accelerates the in vitro regeneration of neural network from adult
murine brain cells.

Athanassakis I, Zarifi I, Evangeliou A, Vassiliadis S.

Department of Biology, University of Crete, P.O. Box 2208, 714-09 Heraklion,
Crete, Greece. athan@biology.uoc.gr

The development, growth and regeneration of nerve cells remain an unresolved
issue. The up-to-date reported brain repair mechanisms are numerous and evidence
suggests that, apart from the required trophism, tropism, microenvironment and
specificity of the brain, a plethora of chemical, physiological and
immunological compounds can contribute to such events. Among these compounds, we
concentrated our interest on L-carnitine (L-Cn), which regulates the
beta-oxidation of long chain fatty acids necessary for brain development,
myelinization and growth. In contrast to fetal brain cells that grow easily in
culture, adult brain cells show limited neurogenesis. Here, using adult brain
cells from experimental mice, we show that although L-Cn does not improve their
proliferative activity in short-term cultures, it accelerates the growth and
differentiation of neurons, astrocytes, oligodendrocytes and ependymal cells
from neurospheres in long-term cultures. Thus, the formation of a confluent
neural network requires a 2-month period in culture. These observations provide
new insights for in vivo use of L-Cn to support brain cell development in cases
of injury or brain degenerative diseases.

PMID: 11911863 [PubMed - indexed for MEDLINE]


1: Ann N Y Acad Sci. 2004 Nov;1033:108-16.

Delaying the mitochondrial decay of aging with acetylcarnitine.

Ames BN, Liu J.

Nutritional Genomics Center, Children's Hospital Oakland Research Institute,
Oakland, CA 94609, USA. bames@chori.org

Oxidative mitochondrial decay is a major contributor to aging. Some of this
decay can be reversed in old rats by feeding them normal mitochondrial
metabolites, acetylcarnitine (ALC) and lipoic acid (LA), at high levels. Feeding
the substrate ALC with LA, a mitochondrial antioxidant, restores the velocity of
the reaction (K(m)) for ALC transferase and mitochondrial function. The
principle appears to be that, with age, increased oxidative damage to protein
causes a deformation of structure of key enzymes with a consequent lessening of
affinity (K(m)) for the enzyme substrate. The effect of age on the
enzyme-binding affinity can be mimicked by reacting it with malondialdehyde (a
lipid peroxidation product that increases with age). In old rats (vs. young
rats), mitochondrial membrane potential, cardiolipin level, respiratory control
ratio, and cellular O(2) uptake are lower; oxidants/O(2), neuron RNA oxidation,
and mutagenic aldehydes from lipid peroxidation are higher. Ambulatory activity
and cognition decline with age. Feeding old rats ALC with LA for a few weeks
restores mitochondrial function; lowers oxidants, neuron RNA oxidation, and
mutagenic aldehydes; and increases rat ambulatory activity and cognition (as
assayed with the Skinner box and Morris water maze). A recent meta-analysis of
21 double-blind clinical trials of ALC in the treatment of mild cognitive
impairment and mild Alzheimer's disease showed significant efficacy vs. placebo.
A meta-analysis of 4 clinical trials of LA for treatment of neuropathic deficits
in diabetes showed significant efficacy vs. placebo.

PMID: 15591008 [PubMed - indexed for MEDLINE]


1: Diabetologia. 1998 Apr;41(4):390-9.

Effects of alpha-lipoic acid on neurovascular function in diabetic rats:
interaction with essential fatty acids.

Cameron NE, Cotter MA, Horrobin DH, Tritschler HJ.

Department of Biomedical Sciences, University of Aberdeen, Scotland, UK.

Elevated oxidative stress and impaired n-6 essential fatty acid metabolism
contribute to defective nerve conduction velocity (NCV) and perfusion in
diabetic rats, which may be corrected by free radical scavenger and
gamma-linolenic acid (GLA) treatments. Alpha-lipoic acid (LPA) has antioxidant
actions and both LPA racemate (racLPA) and GLA treatments produced benefits in
clinical neuropathy trials. The aims were to study LPA action on neurovascular
function in diabetic rats and to investigate potential interactions for
co-treatment with GLA and other essential fatty acids. After 6 weeks of
diabetes, 2 weeks of racLPA treatment corrected 20% sciatic motor and 14%
saphenous sensory NCV deficits. The ED50 for motor NCV restoration was
approximately 38 mg kg(-1) day(-1). racLPA also corrected a 49% diabetic deficit
in sciatic endoneurial blood flow. R and S-LPA enantiomers were equipotent in
correcting NCV and blood flow deficits. Treatment of diabetic rats with low
doses (20 mg kg(-1) day(-1)) of racLPA and GLA, while having modest effects on
their own, showed evidence of marked synergistic action in joint treatment,
completely correcting motor NCV and blood flow deficits. This was also noted for
the novel compound, SOC0150, which contains equimolar proportions of LPA and GLA
(ED50 9.3 mg kg(-1) day(-1), containing 3.5 mg LPA). NCV effects also showed
marked synergism when racLPA:GLA ratios were varied over a 1:3-3:1 range. In
contrast, a compound containing LPA and the n-3 component, docosahexaenoic acid,
showed similar activity to LPA alone. Thus, LPA-GLA interactions yield drug
combinations and compounds with an order of magnitude increase in efficacy
against experimental diabetic neuropathy and are worthy of consideration for
clinical trials.

PMID: 9562342 [PubMed - indexed for MEDLINE]


1: Laryngoscope. 2002 Nov;112(11):2076-80.

Lipoic acid in the treatment of smell dysfunction following viral infection of
the upper respiratory tract.

Hummel T, Heilmann S, Huttenbriuk KB.

Department of Otorhinolaryngology, University of Dresden Medical School,
Germany. thummel@rcs.urz.tu-dresden.de

OBJECTIVES/HYPOTHESIS: The study aimed to investigate the potential therapeutic
effects of alpha-lipoic acid in olfactory loss following infections of the upper
respiratory tract. Possible mechanisms of actions include the release of nerve
growth factor and antioxidative effects, both of which may be helpful in the
regeneration of olfactory receptor neurons. STUDY DESIGN: Unblinded, prospective
clinical trial. METHODS: A total of 23 patients participated (13 women, 10 men;
mean age 57 y, age range 22-79 y; mean duration of olfactory loss, 14 mo; range,
4 to 33 mo); 19 of them were hyposmic and 4 had functional anosmia. Alpha-lipoic
acid was used orally at a dose of 600 mg/day; it was prescribed for an average
period of 4.5 months. Olfactory function was assessed using olfactory tests for
phenyl ethyl alcohol odor threshold, odor discrimination, and odor
identification. RESULTS: Seven patients (30%) showed no change in olfactory
function. Two patients (9%) exhibited a moderate decrease in olfactory function;
in contrast, six patients (26%) showed moderate and eight patients (35%)
remarkable increase in olfactory function. Two of the 4 patients with functional
anosmia reached hyposmia; 5 of 19 hyposmic patients became normosmic. Overall,
this resulted in a significant improvement in olfactory function following
treatment (P =.002). At the end of treatment parosmias were less frequent (22%)
than at the beginning of therapy (48%). Interestingly, recovery of olfactory
function appeared to be more pronounced in younger patients than in patients
above the age of 60 years (P =.018). CONCLUSIONS: The results indicate that
alpha-lipoic acid may be helpful in patients with olfactory loss after upper
respiratory tract infection. However, to judge the true potential of this
treatment, the outcome of double-blind, placebo-controlled studies in large
groups of patients must be awaited, especially when considering the relatively
high rate of spontaneous recovery in olfactory loss after upper respiratory
tract infection.

PMID: 12439184 [PubMed - indexed for MEDLINE]


1: Diabetes Care. 2006 Nov;29(11):2365-70.

Oral treatment with alpha-lipoic acid improves symptomatic diabetic
polyneuropathy: the SYDNEY 2 trial.

Ziegler D, Ametov A, Barinov A, Dyck PJ, Gurieva I, Low PA, Munzel U, Yakhno N,
Raz I, Novosadova M, Maus J, Samigullin R.

FRCPE, Deutsche Diabetes-Klinik, Deutsches Diabetes-Zentrum, Leibniz-Institut an
der Heinrich-Heine-Universitat, Auf'm Hennekamp 65, 40225 Dusseldorf, Germany.
dan.ziegler@ddz.uni-duesseldorf.de

OBJECTIVE: The aim of this trial was to evaluate the effects of alpha-lipoic
acid (ALA) on positive sensory symptoms and neuropathic deficits in diabetic
patients with distal symmetric polyneuropathy (DSP). RESEARCH DESIGN AND
METHODS: In this multicenter, randomized, double-blind, placebo-controlled
trial, 181 diabetic patients in Russia and Israel received once-daily oral doses
of 600 mg (n = 45) (ALA600), 1,200 mg (n = 47) (ALA1200), and 1,800 mg (ALA1800)
of ALA (n = 46) or placebo (n = 43) for 5 weeks after a 1-week placebo run-in
period. The primary outcome measure was the change from baseline of the Total
Symptom Score (TSS), including stabbing pain, burning pain, paresthesia, and
asleep numbness of the feet. Secondary end points included individual symptoms
of TSS, Neuropathy Symptoms and Change (NSC) score, Neuropathy Impairment Score
(NIS), and patients' global assessment of efficacy. RESULTS: Mean TSS did not
differ significantly at baseline among the treatment groups and on average
decreased by 4.9 points (51%) in ALA600, 4.5 (48%) in ALA1200, and 4.7 (52%) in
ALA1800 compared with 2.9 points (32%) in the placebo group (all P < 0.05 vs.
placebo). The corresponding response rates (>/=50% reduction in TSS) were 62,
50, 56, and 26%, respectively. Significant improvements favoring all three ALA
groups were also noted for stabbing and burning pain, the NSC score, and the
patients' global assessment of efficacy. The NIS was numerically reduced. Safety
analysis showed a dose-dependent increase in nausea, vomiting, and vertigo.
CONCLUSIONS: Oral treatment with ALA for 5 weeks improved neuropathic symptoms
and deficits in patients with DSP. An oral dose of 600 mg once daily appears to
provide the optimum risk-to-benefit ratio.

PMID: 17065669 [PubMed - indexed for MEDLINE]



1: Sci Aging Knowledge Environ. 2005 May 4;2005(18)e12.

Carnosine: a versatile antioxidant and antiglycating agent.

Reddy VP, Garrett MR, Perry G, Smith MA.

Department of Chemistry, University of Missouri-Rolla, Rolla, MO 65409, USA.
preddy@umr.edu

Carnosine (beta-alanyl-L-histidine) has recently attracted much attention as a
naturally occurring antioxidant and transition-metal ion sequestering agent. It
has also been shown to act as an anti-glycating agent, inhibiting the formation
of advanced glycation end products (AGEs). Through its distinctive combination
of antioxidant and antiglycating properties, carnosine is able to attenuate
cellular oxidative stress and can inhibit the intracellular formation of
reactive oxygen species and reactive nitrogen species. By controlling oxidative
stress, suppressing glycation, and chelating metal ions, carnosine is able to
reduce harmful sequelae such as DNA damage. AGEs are known contributors to the
pathology of Alzheimer's disease, and carnosine therefore merits serious
attention as a possible therapeutic agent.

Publication Types:
Review

PMID: 15872311 [PubMed - indexed for MEDLINE]



1: Ann N Y Acad Sci. 2006 May;1067:369-74.

Would carnosine or a carnivorous diet help suppress aging and associated
pathologies?

Hipkiss AR.

Centre for Experimental Therapeutics, William Harvey Research Institute, Barts'
and the London School of Medicine and Dentistry, UK. alanandjill@lineone.net

Carnosine (beta-alanyl-L-histidine) is found exclusively in animal tissues.
Carnosine has the potential to suppress many of the biochemical changes (e.g.,
protein oxidation, glycation, AGE formation, and cross-linking) that accompany
aging and associated pathologies. Glycation, generation of advanced
glycosylation end-products (AGEs), and formation of protein carbonyl groups play
important roles in aging, diabetes, its secondary complications, and
neurodegenerative conditions. Due to carnosine's antiglycating activity,
reactivity toward deleterious carbonyls, zinc- and copper-chelating activity and
low toxicity, carnosine and related structures could be effective against
age-related protein carbonyl stress. It is suggested that carnivorous diets
could be beneficial because of their carnosine content, as the dipeptide has
been shown to suppress some diabetic complications in mice. It is also suggested
that carnosine's therapeutic potential should be explored with respect to
neurodegeneration. Olfactory tissue is normally enriched in carnosine, but
olfactory dysfunction is frequently associated with neurodegeneration. Olfactory
administration of carnosine could provide a direct route to compromised tissue,
avoiding serum carnosinases.

PMID: 16804013 [PubMed - in process]