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I do not claim to know the full extent of where this is heading, but thought someone else may find it of interest if only as a (possible) extra fact to know. I searched the site, and found no other references to the study. Basically, carnosinase is pretty low in MS compared to normals and even other CNS diseases.

Normals - 161
Epilepsy - 148
MND - 155

Parkinsons - 109
Multiple Sclerosis - 82.5
Cerebrovascular accident - 74.6 (interesting, while still not wishing to cross-post...)


Serum carnosinase activities in central nervous system disorders

Serum carnosinase activity was assayed in five groups of patients with neurological disorders. Enzyme activities in patients with idiopathic epilepsy (mean ± S.E.M., 148 ± 11 nmol/ml per min) and motor neurone disease (155 ± 15 nmol/ml per min) were similar to the control group (161 ± 7 nmol/ml per min). Reduced serum carnosinase activity was observed in patients with Parkinson's disease (109 ± 11 nmol/ml per min, P < 0.005), multiple sclerosis (82.5 ± 10.0 nmol/ml per min, P < 0.005) and patients following a cerebrovascular accident (74.6 ± 5.4 nmol/ml per min, P < 0.001) compared with the control group. Carnosinase activity, 5–10% of that found in serum, was detected in CSF samples. The cause of reduced serum carnosinase activities in central nervous system disorders is unclear, although anoxic damage to carnosinase-producing cells or disruption of the blood-brain barrier may be responsible.

http://www.ncbi.nlm.nih.gov/pubmed/8033354

Carnosine is comprised of the amino acids "histidine" and Beta-alanine.

MS patients lack numerous essential amino acids, due to a lack of protease. Protease are the enzymes that digest dietary proteins and release essential amino acids.

In the following study from Mayo College of Medicine the researchers stated that an “array of studies” implicate protease in multiple sclerosis pathogenesis.


Curr Top Microbiol Immunol. 2008;318:133-75.
The multiple sclerosis degradome: enzymatic cascades in development and progression of central nervous system inflammatory disease.
Scarisbrick IA.
“An array of studies implicate different classes of protease and their endogenous inhibitors in multiple sclerosis (MS) pathogenesis based on expression patterns in MS lesions, sera, and/or cerebrospinal fluid (CSF). Growing evidence exists regarding their mechanistic roles in inflammatory and neurodegenerative aspects of this disease…”


In the following study the researchers found an association between “subnormal” plasma histidine levels and impaired protein hydrolysis in patients with MS.
(Altern Med Rev 2000;5(3):224-248.)


Transdermal histamine in multiple sclerosis,
part two: A proposed theoretical basis for its use.
George Gillson, MD, PhD,
Jonathan V. Wright, MD, Elaine DeLack, RN,
and George Ballasiotes, BSc, Pharm

“…Here we include preliminary findings on the impairments of digestion and assimilation in MS patients seen in a private clinic. Although only a small number of patients was surveyed, an association was found between impaired gastric acid production, impaired protein hydrolysis, and subnormal plasma histidine levels in patients with MS. Impaired digestion might, therefore, impair the ability of MS patients to synthesize histamine…Various mechanisms of action are suggested, including:..pancreatic enzyme secretion…We also discuss the observed failure of digestive function in MS…”

You can trace every valid scientific finding and symptom of MS directly back to these missing pancreatic enzymes. The subnormal levels of histidine would explain the low levels of carnosinase.