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Standing Committee on Health and Ageing
Dementia: early diagnosis and intervention

KELIN, Dr Katarina, Medical Fellow, Eli Lilly Australia Pty Ltd

MISKEL, Mr Chris, General Manager, Australia and New Zealand, Eli Lilly Australia Pty Ltd


CHAIR: I welcome witnesses from Eli Lilly Australia Pty Ltd. Although the committee does not require you to speak under oath, you should understand that these hearings are formal proceedings of the Commonwealth parliament. Giving false or misleading evidence is a serious matter and may be regarded as a contempt of parliament. I invite you to make a brief opening statement.

Mr Miskel : We thank the committee for the invitation to come and spend time with you today. We very much appreciate it. For those of you who are not familiar with Eli Lilly, we are a global research based company, having grown from a simple company founded in 1876. We opened operations here in Australia in 1960. We provide medicines to patients around the world to treat cancer, mental illness issues, diabetes, osteoporosis, men's health and heart disease. We have an extensive research and development program and we are currently investigating close to 70 different potential treatments in autoimmune conditions and in some of the same conditions where we already have products, such as cancer, diabetes, depression and a range of other disorders.

The decision by the committee to inquire into dementia and particularly early diagnosis and intervention is very welcome. I do not doubt that the committee will have heard very much about the likely significant growth of the incidence of dementia, including the most common form, which is Alzheimer's disease. The onset of symptoms indicating dementia presents many difficult choices. The various forms of dementia are often hard to diagnose, and levels of knowledge concerning the subject vary from doctor to doctor. The motivation to diagnose dementias in the absence of treatment which addresses the disease as opposed to the symptoms also varies between doctors. There is also a question as to the motivation to be diagnosed in those circumstances.

We wrote our submission to the inquiry because we thought it important that the committee understand that there are a number of organisations around the world seeking to discover ways to better diagnose and treat Alzheimer's disease. Success by any of these organisations will help reduce the barriers to early diagnosis and therefore early intervention. Lilly is one of those organisations. We have been involved in research in Alzheimer's disease for many years. Through its research labs, Lilly has invested enormous amounts of time, resource and effort to, first, better understand this highly complex disease and, second, find effective treatments. We have worked alongside world-leading scientists and clinicians and, most importantly, we have worked side-by-side with patients and their carers, who have invested their hopes in Lilly's efforts.

At times this has been very challenging. Lilly has experienced significant failure in this area. Recently, Lilly was near the end of its investigation of an experimental compound, so it was in phase 3. The hope for this molecule was that it would modify the disease or slow its progression. Unfortunately, in August 2010, the phase 3 clinical trials into that compound, called semagacestat, were halted as it was clear that the compound was not living up to its early promise. The outcome was extremely disappointing for all concerned but particularly for patients and their carers who had participated in those trials. Though frustrating, this is not unusual. Despite the setbacks, Lilly remains committed to finding better treatments. There are many reasons for this, but the best reason is the hope of making a patient's life better. Lilly has another Alzheimer's molecule that has reached phase 3 clinical trials, and its early promise has been to progressively remove from the brain the amyloid beta plaque associated with Alzheimer's disease. The outcome, if the results are successful, will be to slow down the progress of the disease and give patients more time—time to deal with the implications of the disease, time with loved ones and time to live their lives. But, until the trial's results report, we will not know if we have succeeded and we will not know to what extent the treatment will impact on the disease. We hope to get the trial data later this year and, needless to say, many people both inside and outside Lilly are waiting to hear the results.

Like other organisations working against the disease, we are sharing our hard-won insights with our partners, including governments around the world. A key concern of many is that, facing the potential size of the affected population, appropriate provision is made to ensure access to whichever molecule or molecules prove to be effective. The current Lilly molecule would be delivered via monthly infusion, and we are working to understand the future facilities that would be needed to provide infusion services in Australia and the future framework that would support that work. It would likely be significant. We would urge the committee to consider the Alzheimer's infrastructure and service needs in future healthcare planning systems, and Lilly is ready to share in that task.

We would like the committee to know that there are many dedicated organisations working hard to discover ways to better diagnose and treat people with Alzheimer's disease. If any of these efforts succeed, there will be a significant impact on the drive to diagnose. There will be new possibilities for meaningful intervention and, having worked hard to fight this disease for so long, we hope that Lilly can play a part. Thank you.

CHAIR: Thank you. I might start with a question. In your submission you note that with the standard of treatment guidelines for medical practitioners in treating people with dementia there is concern about lack of standard procedures. Why is this when dementia is so prevalent in our community?

Dr Kelin : I will try to respond to that question. Alzheimer's disease is a progressive neurodegenerative illness. The prevalence of this illness is rising, and that is obviously a concern for all people involved in this situation. Current treatments that are available are not the cure for illness, and that is really disappointing. There is no cure for Alzheimer's disease. The current treatments that are available are so-called symptomatic treatments that are able to address symptoms that patients experience with Alzheimer's disorder, but they do not affect the underlying mechanism or underlying pathology of the disease. What we hope for with our product, solanezumab, is that it will be possible to slow the rate of progression of the illness and in that way change the course of the whole illness.

CHAIR: Thank you.

Mr WYATT: I am mulling over what you have said in terms of the research that you have undertaken and the plaque within the brain. What future hope do you see in that identification of the plaque and the protein make-up of that that there might be a potential piece of work that will either lead to medication that will slow that process down or, alternatively, prevent the growth of plaque so that it impacts in the way that it does?

Dr Kelin : That is, again, a question that it is best to answer through trying to explain the exact mechanism that we hope solanezumab will be working by. In the brains of people with Alzheimer's, there is a protein that all of us have, amyloid protein. In people who do not have Alzheimer's, that protein has a typical metabolic path. However, with people with Alzheimer's something goes wrong and that protein changes and transforms into what is called beta-amyloid. Those beta-amyloid proteins have a tendency to link together—to clump together—and they form the plaque, which is sort of an insoluble congregation of those proteins and some other debris which is found in the brain. What will solanezumab potentially do in slowing the rate of progression? It will sort of vacuum up—suck up—those soluble beta molecules before they actually aggregate in a plaque, and in that way it will prevent the progression of illness. So it is not directly attacking the plaques which are already formed—people may have those for years before the symptoms—but it will work in eliminating soluble ones and preventing them from aggregation.

Mr LYONS: Does this drug reduce the pressure in the brain as well?

Dr Kelin : Well, pressure is probably not the key element in the pathology of Alzheimer's disease. The key thing is that amyloid is changed. It becomes unknown to our organism and, being changed, it forms the plaque, which is actually one of the hallmarks of Alzheimer's disease. Although we do not know clearly what causes the illness, we have known for quite some time that those plaques are actually the hallmark. They are found in all brains analysed post mortem of people who have Alzheimer's.

Mr WYATT: You do not know the trigger yet for offsetting?

Dr Kelin : Sorry, what do you mean?

Mr WYATT: The trigger for changing the protein into a new chemical composition.

Dr Kelin : It is something that scientists are working really hard on. We do not know why that happens. Maybe just in the last 10 or 12 years some enzymes have been identified that are in our brain. In a so-called normal brain, or a brain free of Alzheimer's, there is an enzyme, alpha, which does that job in the metabolism of the protein, and everything works perfectly well, with no cognition decline. And then recently there have been discovered another two proteins called beta and gamma proteins that actually snip off the bits and pieces of that protein, change their structure and take that protein to that pathological path. Why is that happening? We do not know.

Mr WYATT: There is no DNA profiling that shows that there might be a factor that triggers that?

Dr Kelin : No. It is not known to science why it is happening. We know that, in some people who have a genetic predisposition potentially for that, Alzheimer's disease may happen more frequently or be more prevalent, but why it happens at that particular moment we do not know.

Mr WYATT: Which part of the brain does it start in? Is there a particular area that it starts that process in?

Dr Kelin : As Alzheimer's disease is a disease of cognition primarily and affects all cognitive processes—memory, thinking, language, planning, organisation—the areas in the brain which are responsible for those particular executive functions are affected. So, if you look at where the plaques are mostly formed in the brains of people with Alzheimer's, that would be the hippocampal area and some occipital and temporal parts of our cortex.

Mr WYATT: Thank you.

Ms O'NEILL: Could you explain to me, as a non-medical professional, what infusion facilities are and the diagnostic imaging equipment that you need to use to be able to do the diagnosis for early intervention? Also, could you give a bit of an explanation about access to that in Australia and comparisons with overseas?

Dr Kelin : I can start and obviously Chris can add to that. That is, we believe, the critical part which we need to understand. Obviously, first of all, a drug has to show its efficacy to be able to be available for the patient. But, being a monoclonal antibody and a large molecule, it is delivered through infusions. So patients would receive this medication in a 30-minute infusion, coming on a monthly basis.

Ms O'NEILL: For comparison, that is a bit like getting chemotherapy treatment in a hospital, is it?

Dr Kelin : You could take that route to compare it, because oncolytics are delivered by infusion as well, but what is completely unknown is the fact that the Alzheimer's space has never had a product with infusion. We do not know still. We are working on that. We are trying to find information about it. But we do not know how this whole infusion process will sit with the Alzheimer's patient population. We have done some work in Australia to this point which is more qualitative in nature to understand the infusion landscape that we currently have, and some other therapeutic areas like rheumatology, for example, or osteoporosis have similar monoclonal antibodies that have to be delivered in infusion. But for Alzheimer's that is new. The most common infusion delivery is in oncology, as you rightly said, and they already have quite a set-up for those patients to come and receive oncolytics. However, other therapeutic areas do not have dedicated space for that. For example, a rheumatology drug would be delivered either in existing oncology and haematology units or in ambulatory day care, or in general infusion centres. Whether those centres will work for Alzheimer's is still to be really investigated further, and that is part of the process of us learning what is happening in that space. We assume that, for this sort of patient, a lot of those general infusion centres may not be quite appropriate because of the nature of the illness. Probably, again, the good scenario would be to have dedicated centres where the Alzheimer's patient can come, be diagnosed and eventually come on a regular monthly basis to get their treatment done—something like memory clinic models, which I am sure you have heard about and which exist in several states to a different degree of sophistication.

Mr WYATT: I do not have any questions at the moment. I am interested in the protein and the work that you have been doing around it, but I want to do some more reading first. I would not mind some more information to look at the detail. I am thinking of the research in Parkinson's and a couple of other neurological diseases in which they have used injections to make a slight difference. Recently on television there was a program that showed an illness—I have forgotten the illness—where, once treatment was given, patients recovered for a short period of time, but it was not sustained. I would not mind receiving from you some more detailed technical information that I can read so that, if I have other questions—

CHAIR: That is a question on notice, possibly.

Dr Kelin : Yes, we will try to make it available.

CHAIR: There being no further questions, I would like to thank you for appearing before the committee today. I am sure that if there is anything further that you wish to add, as we have just heard, you can do so. From our side of it, if there is anything else that we feel should have been raised today that has not been, we will be in touch with you to get that further information. Thank you very much for your submission and for your time. Thank you very much for your attendance, all the witnesses; the media; Broadcasting, which has kept a correct and accurate record of everything that was said today; the secretariat that are here; the staff; and the members of the public that are here as well. The next meeting of the committee will be on 25 June 2012 in Canberra. There will be some site visits this afternoon that the committee will be participating in.

Resolved (on motion by Mr Irons):

That this committee authorises publication, including publication on the parliamentary database, of the transcript of the evidence given before it at public hearing this day.

Committee adjourned at 13:08