Check GAD antibody positivity with the Diamyd anti-GAD RIA plate*

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Mark Atkinson, Ph.D.,is an AmericanDiabetes AssociationProfessor for DiabetesResearch, and theDirector of the Centerfor Immunology andTransplantation at theUniversity of Florida. Atkinson was amongstthe first groups of researchers to identifythe value of measuring immune responsesagainst GAD, and to describe the whiteblood cell response against this protein inpersons with the disease. Atkinson holdspositions on a number of scientific advisoryboards/research panels including theJuvenile Diabetes Foundation Inter-national(JDFI), the American Diabetes Associationand the National Institutes of Health (NIH).While Atkinson’s current research extends tounderstanding the molecular immunologicaland genetic mechanisms underlying the formationof diabetes, his primary researchgoal lies in the development of an effectivemethod for preventing insulin-dependentdiabetes. Professors Atkinson and NoelMaclaren were first to file a US patent forGAD and diabetes therapy which is exclusivelylicensed by Diamyd Medical.More Effective Methods forpreventative Interventionβ cell MassLower Accuracy inDisease PredictionHigher Accuracy inDisease PredictionLess Effective Methodsfor PreventativeInterventionOnset of OvertType 1 DiabetesAbility to Predict Type 1DiabetesAbility to Predict Type 1DiabetesType 1 Diabetes: a Dilemmafor Clinical TreatmentTMark Atkinsonhroughout much of the lastdecade, guarded hope existedthat an agent capable of preventingor reversing Type 1diabetes would be uncovered.As of today, such an agentdoes not unequivocally exist. As a result, manyhave addressed the question ‘why?’ The answers tothis question are many; some of which are readilyaddressable, others are by their nature more inherentlydifficult. Among the latter obstacles facingthe diabetes prevention field is a situation that hasbeen referred to as the ‘treatment dilemma’. Awide body of evidence, both in animal models ofType 1 diabetes as well as in persons with or – atincreased risk for – the disease, supports thenotion that the most effective interventions willbe those that are begun early in the autoimmunedisease process. In contrast, the process of diseaseprediction [that is, using immunologic (e.g. GADautoantibodies), genetic (e.g. HLA types), andmetabolic (e.g. glucose tolerance tests) markers ofthe disease to identify risk for eventual diseasedevelopment] is most accurate in the period closeto the onset of overt diabetes. As a result, a conflict(both ethical and clinical) exists wherein themost effective forms of therapy may involve theearly treatment of subjects in a period in whichdisease prediction is less accurate; a situation thathas positioned the need for a safe and benignform of therapy against treating persons who maynever develop Type 1 diabetes. The identificationof such an idealized agent has thus far provenextremely difficult to uncover.Yet another challenge relates to properlyaddressing, in combination, the questions of “whodo we treat” and “what agent will we use”? In theory,attempts to prevent Type 1 diabetes will mostlikely address two distinct populations. The firstwould involve therapy of high-risk individuals (e.g.GAD/islet autoantibody positive relatives of aproband with Type 1 diabetes) or those who alreadyhave one form of the disease (e.g. LADA subjects).The second would be that of a generalpopulation approach such as is common practicefor vaccinations against infectious disease. Bothmodels have inherent strengths and weaknesses interms of therapeutic intervention. In the lattermodel, a safe and benign therapy capable of interrruptingadverse immune events/environmentalagents (e.g. a vaccine) or alterations in lifestyle providingavoidance of disease risk factors (e.g. diabetogenicdietary components) would ideally beimplemented while the costs associated with screeninggeneral populations forms a barrier. Indeed,one could speculate that in designing preventativemeasures within the general population, the diseasefrequency and unpredictable time of onsetform major obstacles that screening would be eliminatedand vaccination would become universal.Performing clinical trials in increased-risk populationsor those already diagnosed with the diseasemay prove more cost effective (in terms of a trial)and efficient, yet in terms of humanitarian benefit,it could be argued that the general populationapproach may ultimately be more importantas approximately 85% of newly-diagnosedpatients have no family history of the disease.A final barrier for this discussion is the lack ofobvious candidates for the next round of largeprevention trials. As a result, current interest isdirected at studies involving recent-onset Type 1diabetes and LADA patients for the purpose ofidentifying new and perhaps more promisingagents such as diamyd . If diamyd is shown to beclinically effective, then prospective, randomizedcontrolled studies with appropriate statisticalpower and objective endpoints can be designedand prevention strategies in different populationgroups at different stages of the disease processcan be undertaken. Not only will these studiesascertain potential efficacy and safety, but shouldalso lead to greater insight into disease pathogenesis.page 32 dmccad june 2003
Diamyd S-100ß ConcentrationMeasurement ELISADetermination of S-100β protein concentrations in serum is used in neurologyto assess the extent of brain damage in stroke, in head injuries, during extracorporealcirculation and during circular arrest.It is also used for follow-up and prognosis of malignant melanoma.Diamyd, Inc has developed prototype ELISA kits for detecting the presence ofS-100ß protein in human serum/plasma.Diamyd S-100ß-antibody ELISAS-100β autoantibodies have recently been shown to be a possiblemarker for autoimmune diabetes. An article (Nature 2003*) shows evidencethat islet cell death is related to autoreactive T- and β-cellresponses to neighbouring peri-islet Schwann cells, which express S-100β protein. Diamyd, Inc has developed prototype ELISA kits fordetecting the presence of autoantibodies to S-100ß protein in humanserum/plasma. The ELISA uses visual detection (requires a visibleplate reader that measures absorbance at 492 nm).page 32www.diamyd.comproducts@diamyd.compage 21dmccad june 2003
Page 4 and 5: forewordResearch Scientists through
Page 6 and 7: The Story ofGADRobert Dinsmoor1975R
Page 8 and 9: Åke Lernmark, MD, Ph.D., and his c
Page 10 and 11: theory, the immune system mistakenl
Page 12 and 13: GAD Back to the Future…Åke Lernm
Page 14 and 15: 100GAD in GraphsGAD65 DNA vaccinati
Page 16 and 17: In Nature, Anything that CanHappen
Page 18 and 19: References1. Baekkeskov, S., et al,
Page 20 and 21: GAD in GraphsIncidence of diabetes
Page 22 and 23: References1. Quinn A, et al,MHC cla
Page 24 and 25: References1. Tisch, R., et al,Induc
Page 26 and 27: Vaccination with GAD PlasmidSuppres
Page 28 and 29: GADGAD in GraphsGAD ELISPOT outperf
Page 30 and 31: GAD in GraphsA1004 wks of age% Inci
Page 34 and 35: GAD in GraphsIL-4 (pg/ml)2501007550
Page 36 and 37: References1. Kobayashi T, et al,Isl
Page 38 and 39: References1. A.Falorni, et al,Radio
Page 40 and 41: References1. Chattopadhyay, S., et
Page 42 and 43: Diamyd’s Commercial Development o
Page 44: T cell GAD65For use of GAD in immun

Check GAD antibody positivity with the Diamyd anti-GAD RIA plate*

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