Dr. Alfred Goldberg, PhD
Harvard Medical School
Interview Date: January 7, 2016
Dr. Goldberg’s knowledge and discoveries about proteasome inhibitors, used to treat multiple myeloma, are making the development of new drugs against ALS possible. His insight about cellular mechanisms can be used for both ALS and multipule myeloma; but it opposite ways. One disease needs a proteasome inhibitor, one disease needs a proteasome activator. His studies using this target are about to start on ALS mouse models. Dr. Goldberg explains how new ideas coming from other areas of research are giving a great deal of hope.
ALS Crowd Radio Show with Dr. Goldberg
Jenny: Welcome to ALS Crowd Radio, a show helping ALS patients understand the latest in research. My name Jenny Ahlstrom and I am co-hosting a show today with Seth Christensen.
Seth: Good morning, everyone.
Jenny: Today, our show is about a unique topic taking a drug that is currently approved for something else particularly cancer in this case and applying it to a different disease like ALS. For today, we have Dr. Alfred Goldberg with us. We welcome you Dr. Goldberg.
Dr. Goldberg: Thank you. Pleased to be here.
Jenny: Let me give an introduction for you to begin with. Dr. Alfred Goldberg is a Professor of Cell Biology at Harvard Medical School, where he has been on the faculty for his entire academic career. His important discoveries have concerned the biochemical mechanisms and physiological regulation of protein breakdown in cells and the importance of this process in human disease. His laboratory first demonstrated the non-lysosomal ATP-dependent pathway for protein breakdown, now termed the ubiquitin-proteasome pathway. They first described the roles of the 26S and 20S proteasomes in the degradation of ubiquitinated proteins and discovered the ATP-dependent proteases responsible for protein degradation in bacteria and mitochondria.
In addition, their lab has elucidated their novel biochemical mechanisms and mode of regulation Also of wide impact have been Dr. Goldberg’s studies showing that the ubiquitin-proteasome pathway is critical in the clearance of misfolded aggregation-prone proteins, in the excessive protein breakdown causing muscle atrophy in many disease states, as well as in antigen presentation to the immune system. He and his colleagues also first introduced proteasome inhibitors widely used as research tools (e.g. MG132), and he initiated the development of the proteasome inhibitor, Bortezomib/Velcade, now used worldwide for the treatment of multiple myeloma.
Dr. Goldberg received his AB degree in Biochemistry and his PhD in Physiology in 1968 from Harvard University, after attending Cambridge University as a Churchill Scholar and Harvard Medical School. His research accomplishments have been recognized with many honors, including the Novartis-Drew Award for Biochemical Sciences, Severo Ochoa Award (New York Univ), Knobil Prize for Medical Research (Univ Texas), the Gabbay Award for Biotechnology and Medicine (Brandeis Univ.), the Gordon Alpert Prize for Medical Research (Harvard Univ) and the Ernst Beutler Prize for Basic Research (American Hematological Society).
He is a Fellow of the American Academy of Arts & Sciences and a member of the National Academy of Medicine and the National Academy of Sciences. He has also received honorary doctoral degrees from Cold Spring Harbor Laboratories (Watson Graduate School), the University of Maastricht and University of Barcelona and is among the 1% most cited authors in the life sciences.
Welcome again Dr. Goldberg.
Dr. Goldberg: Thank you. I’m happy to be here. How can I help you?
Jenny: Well, I think I’d like to give a little background about how we discovered you. I am a Multiple Myeloma patient who runs a foundation and have an advocacy group for Myeloma which is a blood cancer and I attended the recent American Society in Hematology meeting in Orlando Florida where you were receiving an award and giving a presentation. I know it was intended for a scientific audience. I understood a part of it but not all and I was very impressed in the thing that just gave me chills at the end as that you said this drug that has been used in cancer for over a decade and now multiple proteasome inhibitors are coming out for cancer and multiple myeloma specifically.
But you saw a use for them in Neurological Disorders like Parkinson’s or MS or ALS. I have to say, it really electrified me to ask you about the application of a currently FDA approved drug for another disease like ALS. So maybe you want to start by giving us a background of your work on proteasome inhibitors for myeloma and then the work that you have done understanding how to apply these other disease states.
Dr. Goldberg: Well, I’d be delighted to spend time on both topics but I should make it clear from the outset that there’s a little misunderstanding. The drugs that are being used for myeloma that affect the proteasome, we are not developing for neurodegenerative diseases such as ALS. The insights and the knowledge about the proteasome is making possible progress in development of drugs against ALS, we believe. The information in the cellular mechanisms are the same but the drugs themselves will have to be different. I will explain that a little more clearly I hope.
Our work for many years has been concerned about basic cellular processes. What happens when cells make a mistake in protein assembly? What happens if cell proteins get damaged or if there’s a mutation that happens for example in many ALS patients and is happening all the time to generate cancers? The cells make a protein at fails to function or even fold up correctly and we’re interested in how evolution has enabled us ourselves to recognize those proteins and destroy them, at least destroy them most of the time.
This protection mechanism which we have been studying the biochemistry of is basically a cellular sanitation system in which cells have the ability to recognize an abnormal protein and destroy it, eliminate it the way a good vacuum cleaner will do to clean problems in our household. So we’re interested in how cells were able to recognize the abnormal proteins and destroy them selectively and we discovered this structure we named the proteasomes which is where the destruction takes place.
Now, in one kind of disease, multiple myeloma, is the cancer with uncontrolled growth of cells, normally make antibodies. These are the plasma cells that produce protective antibodies in all of us. In the myeloma patients unfortunately, these cells have become cancerous and they do two things. They grow like mad and they happen to generate an abnormal protein that your physicians monitor. What we have found is that the drugs that we were developing to block the proteasome actually interfere with that, the cellular sanitation system in the myeloma cells where they already have so many abnormal proteins that take the accumulation of the misfolded proteins and kills them, in other words, the proteasome inhibitors Carfilzomib, Bortezomib. Now the new one is Ixazomib are interfering with the cell sanitation system which drive cells into basically a non-functional suicidal mode.
It has turned out that the very basic process that we were trying to understand and for which we were developing inhibitors is particularly sensitive to this kind of drug. When we were developing it, we actually didn’t understand it. The drugs were tried against many cancers and the myeloma responded dramatically for many patients. That’s the basis for the development of these two or three drugs. It’s also the basis for their combination therapies with other drugs. But the point is really that myeloma is a cancer where the cells are producing a huge amount of garbage protein.
Because the garbage breakdown mechanism is blocked, they’re not viable and we can help patients in this fashion. That’s why these drugs have been successful. Is that at all clear and we could talk about the neurological disease afterwards. But is that pathological mechanism and is the drug action clear or can I do a better job of explaining it?
Jenny: Oh, I think you did an excellent job explaining it.
Seth: Dr. Goldberg, how successful have these drugs been in myeloma?
Dr. Goldberg: Well, it all depends. Myeloma is still a terrible disease as you’re a listening audience or as Jenny can tell you much better than I. Or, my wife is a physician and I hear about the cases where the drugs are not as successful. But certainly, the longevity of the patients has been dramatically increased and the cocktails, that is the mixtures of two or three drugs with different modes of action, has been able to add years to the life of what used to be viewed as a hopeless disease.
The exact benefits are almost hard to say because new and improved ways of using these drugs keep emerging and this real reason to believe that from what’s in the pipeline of many drug companies, there are going to be further improvements even over the present mixtures. But I think this is one now, one of the more successfully treated cancers for many patients, for most patients certainly compared to the way that disease was ten years ago. Others can attest to that better than I because I am still the basic science. I’m the grandfather of the drug. I don’t give it to patients or see patients. I think the statistics are very clear that it has been very successful but certainly not as successful as we would hope and there are always improvements left to be done.
Jenny: Well it is a basic drug class that’s always used now in myeloma treatments no matter what type of treatment combination therapy, you always have a proteasome inhibitor added to that treatment in my experience.
Dr. Goldberg: I think that is definitely true and the combination of those drugs with the imids and glucocorticoids, I think well over 95% shows some benefit. But for how long, it depends on genetic factors we don’t understand probably. But the improved ways of using are continually emerging thanks for the effort of many physicians.
Seth: Great. Can you clarify for those of us new to this space. Do the drugs interfere with a haywire process, or are they more targetet at restoring the natural order of a healthy cell?
Dr. Goldberg: Well, if I understand the question, these are very selective drugs. They are not like the traditional chemotherapy where patients or every cell in the body that’s dividing patients to not see loss of hair or have the GI problems — These are specifically affecting one structure in a cell and myeloma cells are particularly sensitive. At the moment, the success has been with treatment of myeloma. For other malignancies or rather even hematological malignancies, we were hoping they would probably be more successful than they have been so far. Much of that is still understudied.
Now, I’m not sure if that answered your question though.
Seth: Yeah. My question in general is about that vacuum cleaner you mentioned. Are we restoring a broken vacuum cleaner or are we —
Dr. Goldberg: Oh, I understand now. Yes. Now, that’s a very profound question. In fact, we are not in this case restoring a broken vacuum cleaner. We are making a vacuum cleaner stop working in the cell without a vacuum cleaner dies. The reason the myeloma problem is, why those cells are particularly affected, is because they are making all the garbage. The rest of our cells are doing very well. This is definitely saying, let’s take away the vacuum cleaner in the myeloma cells instead of them taking over the body are dying. That’s good. This is the case where the offending cells are very sensitive to a drug.
Now, this is in real contrast to the areas we’re working on now for neurodegenerative diseases such as ALS but also in Alzheimer’s and in Parkinson’s, cells that have functioned very well for many years specifically neurons, either neurons in a spinal cord. If it’s ALS or neurons in our brains, if it’s Alzheimer’s, they are accumulating specific abnormal proteins inside of them. That’s causing the cells to stop functioning and eventually die.
In other words, the proteasomes, the pathway that we have been studying works very well in most of us until our 70s or 80s in getting rid of the garbage. There is something that goes wrong in either the brain or the spinal cord of patients that in these diseases causes the accumulation of toxic amounts of abnormal proteins that precipitate out in the cells. What we’re talking about in this as our challenge and what our lab is working on to these diseases is the exact opposite of myeloma. We want the garbage collection system to work even better. We want to eliminate these proteins just like we did when we were young. That is a scientifically harder thing. To make a better vacuum cleaner, you have to really understand how it works.
To mess it up or stop it from functioning, you only have to understand a little. The past ten years and in the last couple of years, we think we have learned a lot about the pathway and then we have some exciting new hints on how we can activate the proteasome so we can enhance the garbage collection and presumably stop the progression of these diseases if the research is successful. It looks very encouraging in the test tube at the moment. Now the point is to go to animals and humans with specific drugs. But we have a rationale that looks very promising that we didn’t have in the past.
Is that distinction clear? Because I certainly didn’t want in my lecture to say that the kind of impression I may have given because it was a short talk. We are working. We are focusing on the neurodegenerative diseases but it’s not with the same molecules. It’s with the same target. It’s the same concern with the proteasome.
Jenny: I think I jumped ahead too much making that connection. What you’re saying is using the current drugs would possibly have the opposite effect of what you want.
Dr. Goldberg: You have really gotten a very important point. Using the present drugs, it might have been — have very negative consequences and we worried about this 12 years ago when we developed the first proteasome inhibitors. In those drugs like Carfilzomib, Bortesomib, Ixazomib actually do not get across through the blood brain barrier. They will not cause the same problems that you might see. Maybe I should explain this.
In our bodies, between the nervous system and the brain and the rest of the body is a barrier which we call the blood brain barrier that stops many drugs from entering the brain. It’s something that protects the brain against many things we view as toxins. Certainly many drugs do cross it, but many do not. The drugs that we’re talking about here do not enter the brain and therefore, there are no side effects of the kind that you have perceptibly notice. If you actually study nerves in a dish or in a test tube as we do in the laboratories, then you’re absolutely right. The drugs can cause — or would make a model of ALS, they would make a model of Alzheimer’s worse because they would make the garbage collection that minimizes disease non-functional. But this is not a worry for patients or for any humans who are taking these drugs.
Jenny: Right, because their usual drugs are completely different application.
Dr. Goldberg: They don’t enter the brain. That’s what I meant by the blood brain barrier. Those drugs, if they got into the nerves would do what you say but they don’t get across into the brain because of this barrier. We are definitely in, to think about these diseases have to study molecules that actually do get into the brain and we are doing that.
Jenny: The lessons that you have learned over this very deep extremely exceptional research is now being applied to these. What are the key lessons that you gain in the neurological diseases like ALS that really stand out to you?
Dr. Goldberg: Well, I think it’s hard to say. I think the most important point is that you learn from myeloma. From this way of thinking about the neurodegenerative diseases such as ALS is that new ideas coming from other areas are giving a great deal of hope. People studying myeloma or a blood cancers premier lymphoma would never have been worried about the proteasome or that pathway where that was a very fundamental bit of biochemistry with basic research advancing our knowledge, then molecules that could be drugs became available.
It was almost a surprise to find out the myeloma patients were so sensitive because research in myeloma hadn’t focused on this area. The same thing is true about the group of diseases to be called neurodegenerative diseases or ALS. If one just studied how nerve or muscle worked or even how memory work, you would almost, as many neurologist do, forget that the nervous system is made up of cells in very basic biochemical processes that tell us how white cells or liver cells work also apply to the nervous system.
The new insights that we’re bringing or people who think about these issues, are bringing to thinking about neurological diseases are coming from a general biological background and are a good example of the unanticipated benefit of very basic research. Whether they’ll be coming as fast as patients would like or as we would hope, that we can’t say. But these new approaches are being applied and they’re coming from outside of the traditional discipline. They’re coming from work that the NIH has sponsored as undirected research for many years and now the insights can be directed to specific diseases such as ALS.
Jenny: It’s foundational work.
Dr. Goldberg: We hope so. We hope it’s relevant someday. But we’re optimistic that we’re on the right track.
Jenny: Seth, do you have a question? I have other questions but I don’t want to prevent you from asking yours.
Seth: Yeah, Dr. Goldberg, my mind is filled with questions. I’m curious in myeloma, how long ago was the vacuum cleaner discovered and how long did it take to make a drug based on that model?
Dr. Goldberg: That’s also an important insight. I mean in broader points to discuss our research related to how cells breakdown proteins goes back. I started it in the ’70s. The field really starts growing in the ’80s or ’90s. But in the early 1990’s, we were convinced that inhibitors of the proteasome could be drugs. We did not have myeloma in mind at all. When we actually started a company, our first goal was to build up muscle, muscle atrophy for example, what you see when you injure a nerve or an ALS patient. When a nerve dies, the wasting of those muscles is a case where we have too much protein breakdown and we were able to show that excessive protein breakdown was the vacuum cleaners working too fast.
Our first goal was if we got molecules to slow down the vacuum cleaner to use this metaphor, we would have applications to build muscle and to stop the wasting you see in cancer patients, the neurodegenerative patients. Drugs were developed and the first evidence was 20 years ago that a small molecule could do this. By the early ’90s, we started a company because in the University, there was no way for basic scientists and chemists and physicians to work together and we actually had a small venture capital firm in a small company. By the mid ’90s, we were able to get molecules that look like they could be turned into drugs. The clinical trials were started in about 2003 and in truth, they were tried against cancers.
For various reasons, we knew that we could kill cancers with these drugs more easily than we could slow muscle atrophy. In other words, as the research progressed, we reoriented our research towards a different group of diseases and when it went into patients in a phase one trial, this was about 2003, 2004. Within one year, there was dramatic results and phase two approval was achieved. First as a fallback drug then a phase two was confirmed it became approved as the drug of choice in phase one. That’s really only about I think eleven years ago.
I would say from when we had real molecules to when it was widely used was about 13 or 14 years. That’s a lot longer than I think a sick patient would hope for. But for some patients, this was three or four years from when it was still an idea until it first was used as a drug. I think if an agent is really able to have an effect and the clinical trials are well designed, this process can go much quicker than it does for many drugs. But still to prove efficacy in an impartial way unfortunately takes time and sometimes science is a prolonged frustrating process. But the myeloma case, it went fairly rapidly. Does that clarify?
Jenny: I think part of Seth’s question is what you addressed. But ALS has had maybe one new drug approved in the last hundred years. And so they have a great sense of urgency to say okay, how can we get things into the clinic to try that looked like they are potentially effective. With your research that you have done on the foundational research that you have done, how long do you think it would take to try to create a small molecule, proteasome inhibitor or maybe not proteasome inhibitor, just something — yeah, a proteasome activator that would affect ALS per se.
Dr. Goldberg: Yes. This is always the kind of question that a careful scientist and a careful physician does not like to face because even though with absolutely and appropriate and natural question that they are thinking themselves. One wants to not get hopes irrationally encouraged and also wants to be realistic. The truth of the matter is, in this case, the molecules that we are investigating and find to inactive that proteasome and have effects in cells are well-known agents that is in a sense that we are not developing molecules of a kind that have never been drugs or that a totally going to require new chemistry, which occurs in many areas.
We have a lot of information we can build on and there are some molecules already available to try in cells and the test tube and already in mice. My collaborators have shown that this works in mice against a model of it’s called frontal temporal dementia. It’s an early onset Alzheimer’s condition for which there is a specific abnormal protein well-studied. And so it has been used as a model and this has already worked in a mouse. The situation here is that we are about ready to study animal models which our models of ALS. We have started such studies in collaboration with Dr. Robert Brown who is one of the persons who identified SOD1 mutants as one of the causes of ALS.
We are about to start on some such studies on a different ALS model and mouse caused by mutations in the Fos protein. We are farther along than we ever were in other projects such as the myeloma one. We’re not at the outset. We’re at a position where if animal models are encouraging and there are some pretty good animal models to try this on. Then one could consider human trials within a few years, a couple of years. This isn’t an immediate possibility but it’s much more tractable than when one reads about an exciting new gene target and one has to start with new chemistry and even develop animal models.
When it comes to the animal studies, I have to work with neurologists and we are just starting those for people who are really experts in thinking about the practicalities of handling disease models and patients also. Because we don’t have other treatments available, they’re also — It should be much easier to bring new ideas and new drugs into clinical trials which isn’t true of conditions for example where there are five competing trials and they’re harder to establish. I think there is a reason to be relatively optimistic. Although it’s hard to say that to any person, any community of patients. Physicians are very sympathetic too but don’t have miracles to offer.
Seth: Dr. Goldberg, we’ll ask about how we can help speed up that process but perhaps then I know we have a number of callers. Could you remind them how they can ask a question.
Jenny: Oh, sure. If you are online listening to the show and you’d like to ask a question to Dr. Goldberg, you can call 516-590-0362 and press 1 on your keypad.
Dr. Goldberg, I think you make a really important point that you’re not starting at the absolute onset of research. It sounds like there is a process. I’m familiar with it but I don’t know if everyone is that you do this research in the lab first and you move it to the mouse models and then you start phase one, two and three clinical trials. A new drug will have to go through that process to be able to get FDA approved. What you’re saying is you’re in the middle of that process because you’re almost to the point of starting to work in mouse models. Is that correct?
Dr. Goldberg: Yes, that’s absolutely correct and mainly because we’re building on a lot of valuable insights into this area of chemistry and to this area of biology and because the initial experiments, which have just been published, have been very encouraging. Yes, we have colleagues who work and are very expert on animal models and develop that and they will be pursuing these more translational research building on our cellular biochemical insights testing whether the ideas are really helpful. But then the question is how to optimize the utility and whether that goes quickly or not, it’s almost unpredictable.
Seth: Are there anything that the ALS community can do help speed up that model?
Dr. Goldberg: There is no question that in science, like many other things our government does or foundations do, it requires money. ALS has recently through the efforts of many patients and their families and well wishers has gotten an infusion of research funding that has been very helpful. This is the new area to me in the sense that I’m not a long term investigator in the area, long term interested. But for example, in the past year, we have applied for research grants to one group called Target ALS, one group called Project ALS, and also to Jenitech, the company which gives some funds for basic scientists.
All have chosen our projects as particularly promising in wanting to fund. We have entered from the outside without credentials in ALS directly but what looks to us and the people who have read it as a novel and exciting idea and we have gotten support. There is no question that kind of money from foundations makes the world go round. Sometimes, money comes without good applications or good ideas or good ideas that don’t work. But without those ideas, there has never really been progress.
Now, I think there are a lot of innovative ideas available to Seth. I think the small foundations have recognized that. Further support would only help without a doubt and that means more people could be working on this area. Whether we can convince companies to put resources into it or not, that would further accelerate it. That’s exactly what happened with the case of myeloma, what was looked at as a drug that was very unlikely to succeed and no one wanted to pursue it. As soon as patients were responding, then at least four companies jumped in and now there are at least four proteasome inhibitors in trials and the possibility with each step of success you would encourage shall we call financial capitalist’s interest which means more valuable research.
I think resources will only help. Now it certainly helps what we do directly and will help with the field. Thankfully our government just passed regulation to give more money to science for these diseases which had been cut back to the last few years in economic downturns but the politics seems to now be changed as both democrats and republicans realize that helping people should be a priority.
Seth: Excellent. To put a fine point on it, how can the individual members of the ALS community determine where best to focus their time and money. I know that is a bit explicit but do you have any recommendations?
Dr. Goldberg: I feel like I’m somewhat knowledgeable as a scientist. The idea of evaluating organizations or their relative strengths, I have 1) no qualifications in very good experience. My limited knowledge has left me impressed that the major foundations that exist are certainly well-motivated in doing their best. In these areas, I don’t think I can comment with any knowledge. In fact, all of you probably have much more experience with the specific foundations, what they do with the patient. In terms of specific scientific projects which are highly technical issues then I have strong opinions and I don’t think those are issues that one can distinguish one’s foundation from another from anything I know.
Dr. Goldberg: I feel very confident talking about my research but what foundations they’re doing is really someone else’s concern. But these are not — I don’t know any are organizations that aren’t doing good. Whether they are doing as best as they can, I don’t know enough.
Jenny: Well I want to make the point too that now that we have talked to many, many doctors and understand more about the lab work that’s being done at specific facilities, it’s quite possible, and happens very frequently, that people donate directly to a lab at a facility, if it’s a project that they see is very helpful. Someone could do that for you. Someone could do that for another physician or another researcher and that’s done really all the time. It’s possible.
Dr. Goldberg: Yeah, there is no question. If people with means are interested in supporting work, there is no question we would be delighted. We have young scientists in training that have careers taking off. To encourage and to go directly would certainly be something that we would welcome but it would have to be with the absolute understanding as that we are not working with patients. We are working to make treatment of patients possible one of these days.
Jenny: It’s foundational work, yes.
Dr. Goldberg: Yes. It’s definitely work that we think is important in a reason for being optimistic but it’s very hard to say anything certain in the kind of life that I lead. We know a good idea but we don’t know whether it will necessarily be beneficial.
Jenny: Well you have to take it all the way through the process. That’s part of entrepreneurship and that’s part of science. I think that’s pretty common. Anytime you have a new idea, Seth understands and we both understand the entrepreneurial process and that’s very similar. You have to take a risk to see if it will work or not.
Dr. Goldberg: Yes. This is definitely risky but I am not sure if I would call the word entrepreneurial in a sense that we’re not working for a profit the way a venture capital is — We are working for personalal reward or intellectual reward to do something helpful but these are not — Then the research we do, we don’t directly profit from. To some extent, it’s not the — This is not an entrepreneurial company. Few scientists work on that basis.
Jenny: That’s not typical. Seth, do you have another question?
Seth: No. I really appreciate your work Dr. Goldberg. I look forward to hearing more about it as we make advances in our understanding of the biology of ALS.
Dr. Goldberg: Well, if there are any specific questions that you or people listening have, I’d be glad to try answering them or putting them in touch with people who have expertise that’s relevant, if mine isn’t. If anyone is interested in supporting for the research, I’d love to talk about how that’s possible.
Jenny: Well I like to ask one last question. You mentioned earlier in the show about how new ideas coming from other areas do help people. What can be done to help support that cross disease foundational work that people like you are doing to help make those connections? I guess myeloma is a good example in that one patient, one time, they knew about Fulton and the work he was doing on angiogenesis and demanded that a certain drug be used for her husband. And it didn’t work for him but it became part of the class which is a whole class of drugs that’s now typically used with the proteasome inhibitors for myeloma.
Those type of flukes chance happening in disease, from your perspective, since you have been on a corporate side and you have also just been assigned to doing such fonation work for such a long time, how do you see those connections being improved or what could we do to speed those up or make those better?
Dr. Goldberg: What you have defined is a major challenge for education of our young scientists. It’s also a major challenge for drug companies and foundations which often gets dominated by existing expertise, people who for example have thought about myeloma or a cystic fibrosis or ALS and know as much as possibly knowable about that condition. But since they have gone to medical school or graduate school, major advances have come in about important factors that will eventually influence therapy. Those are very hard challenges.
I mean I try teaching PhDs about medical problems and we always have the challenge of teaching physicians about basic research. It’s not obvious that there is a simple solution at the moment that many of us are not struggling with that very problem. The case of individual diseases to bring, we have a neurobiologist and people interested in memory together with people who are interested in keeping cells alive. Those are very different areas of science and to get them to talk to one another may be where real insights come from. Some drug companies really are doing that continually.
Sometimes, we get buried in our own special walls with notes around it and we don’t communicate with the areas where we can have an impact. I’m not sure if there is a general way to do that. The best most open companies and the best most open foundations bring together a variety of talents and have them talk to each other whether it’s geneticists who studied those few patients with ALS repeatedly in the family, with people who are able to analyze what’s special about their genes, and then test them in a cell. Those are different expertise that you have to bring together.
In some places, it’s done routinely. In many place, it isn’t. I don’t know if I have a specific solution but realize that it is a continued challenge and try keeping our eyes open for new technologies that we might apply. I think drug companies are getting much, much better in this realm than in the past and small biotech companies have been much more innovative in this respect than drug companies in the past, which is I think a real reason for hope.
Jenny: Well, I would agree. I see that in many different diseases including ALS. I know for patients who have limited options, what you’re doing is very exciting. They are looking forward to seeing more about what you’re doing and so we hope you will keep us posted.
Dr. Goldberg: Thank you very much for the invitation. I look forward to more contact in the future.
Seth: Thank you.
Dr. Goldberg: Good bye.
Jenny: Thank you so much, Dr. Goldberg for joining us and thank you for your deep research and all the effort that you put in to helping people and curing diseases over the course of your very prestigious career.
Dr. Goldberg: Thank you very much. Bye-bye.
Jenny: Thank you so much.