Guest guest Posted June 28, 2001 Report Share Posted June 28, 2001 This is an excerpt taken from a research paper on opiodes in autism. Note the last sentence referring to DPP-IV replacement. Let me know if you differ with this hypothesis. Thankyou. Carlson Dipeptydal peptidase deficiency: Alan Friedman and colleagues have pioneered the potential role of DPP IV deficiency in autism. Some have gone so far as to suggest that DPP-IV deficiency may explain all of the abnormalities seen in autism. Dipeptidyl peptidase IV (DPP-IV) is a serine peptidase that removes N-terminal dipeptides sequentially from polypeptides having unsubstituted N-termini provided the penultimate residue is proline. The only known enzyme to break down casomorphine, dipeptidyl peptidase IV or DDP-IV, appears to be absent or reduced in autistic children. The gene for this enzyme is distal to other suspected autism genes on 2 and Q of 7 and is expressed in the kidney, the small intestine, the liver, the blood-brain barrier, and has involvement in T-Cell activation. Also found in the urine were undigested food particles, suggesting a leaky gut syndrome. Mice with the a defective casomorphine enzyme gene will die if not on a gluten free diet. Later we will discuss the possible role of glutein and cassein in autism, and the elimination of these substances from the diet as a treatment. The toxicity of gluten and cassein may result from the lack of DPP IV. Thus, DPP deficiency may be important in explaining opioid excess. DPP IV has a number of different names. When it is present on the surface of a T-cell it is called CD26. Dr. Friedman postulates that DPP-IV is either absent via a genetic mechanism (probably through two recessive genes) or that the enzyme has been inactivated, possibly through autoimmune mechanisms (a theory of autism which we will cover later). It has been postulated that people, autistic from birth, produce no DPP-IV, and those who developed normally and then regressed, had their DPP-IV inactivated through an acquired mechanism (such as auto-immunity). One such compound is dermorphin, a mu-opioid agonist that acts as an hallucinogen. Another is deltorphin II. Some researchers theorize that these compounds appear because the enzyme which cleaves certain peptide bonds (DPP IV) is either missing or inactivated. Gluten and casein are two of the proteins from which these opioids can be produced. There may be additional proteins for which this is true as well. Theories of Potential Therapies for DPP IV Deficiency [unevaluated]: If DPP IV deficiency results in autism, what can be done? If the enzyme is missing, replacing it should solve the deficiency. DPP IV is found on intestinal mucosal cells, epithelial cells in the GU tract, and on the surface of T-cells. It might be possible to hook the DNA sequence coding for DPP IV onto some type of delivery mechanism (such as a plasmid) and infuse the plasmids into the patient so that the desired sequence would be incorporated into the patient's DNA. Another alternative is stem cell therapy or live cell therapy. Injected cells might produce DPP IV which would migrate to areas in which it is needed. If the enzyme is inactivated by an autoimmune mechanism, replaced enzyme would probably be inactivated as well.Get more from the Web. FREE MSN Explorer download : http://explorer.msn.com Quote Link to comment Share on other sites More sharing options...
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