2012 Research Report

Dr. Howard Lincoln Snyder (H. L.) was a well-respected and beloved physician in Winfield from 1904 and until his death on August 16, 1940.  Dr. H. L. had the foresight to understand that medicine was on the verge of experiencing great advances and growth.  He believed that this could occur only through medical research, delving into the complexities of diseases. It was this conviction that prompted Mr. And Mrs. William Moorer to generously contribute the first $5,500, which was used by Dr. Cecil Snyder and others in the Winfield community to establish a fund to form the H. L. Snyder Medical Foundation (HLSMF).  This fund has grown to over $8 million today.

HLSMF is a nonprofit organization funded by private and public donations, dedicated to biomedical research and the dissemination of information.  Located at 1407 Wheat Road in Winfield, Kansas, the Foundation’s goals are to provide support for exceptional research at world-class research institutions, and to provide scholarships for local students going into the medical field.  Our research efforts are currently directed at providing an extra boost for research nearing a significant discovery as well as providing support for very basic research studying mechanisms involved in pathophysiologic processes of human disease.

Since closing our laboratory in 2004, we have been supporting research at four different institutions detailed below. Our support does not include salary for principle investigators, but rather is used to buy equipment, supplies or technical support.

2012 Medical Research Report

SEUNG KIM, MD, PHD

Professor, Developmental Biology

Member, Stanford Cancer Institute

Seung Kim, MD, PhD, professor of developmental biology, received both his medical and doctoral degrees from Stanford and has been on the Stanford faculty since 1998. He focuses on understanding pancreatic cell growth, differentiation, and function. Dr. Kim’s work could result in novel diagnostic and therapeutic strategies for diabetes.

Diabetes

The pancreas, a vital organ of the digestive and endocrine systems, produces digestive enzymes as well as the hormone insulin. Important to Dr. Kim’s research are the beta cells that are found in the islets of the pancreas and produce insulin. Without adequate insulin production, blood sugar levels can become dangerously high, a condition known as hyperglycemia that can cause organ damage or even coma and death. Type 1 diabetes is caused by a failure to produce insulin, while type 2 diabetes is caused by combined deficits in the body in responding to and making insulin. Each type has been linked to reductions in insulin-producing beta cells.

Dr. Kim is working on isolating and analyzing human fetal pancreas cells, including stem cells and the insulin-producing cells that they give rise to when they differentiate. He uses bioinformatics to discern signaling pathways that may regulate the differentiation of these pancreatic cells. He is studying the various pathways that regulate the development of the pancreas, many of which also regulate the functioning of the pancreas in adults. Signaling errors in these pathways can result in diabetes and pancreatic cancer. 

Dr. Kim has identified a molecular signaling pathway that drives the growth and maturation of young human beta cells in mice and humans. The pathway had been shown to be important in the growth and development of many cell types, including immune cells and neurons, but this is the first time it has been shown to be involved in the development of human beta cells. A major step forward both in understanding how human beta cells develop and become functional, this finding should allow Dr. Kim to apply knowledge of the normal maturation process of the pancreas to creating substitute or replacement cell types for therapy in diabetes. It may clear the way to generating functional beta cells in a laboratory dish for transplant into a human patient or to coax a diabetic’s non-functioning beta cells to begin dividing and producing insulin. 

Dr. Kim and his colleagues found that mice in which the pathway was genetically inactivated secreted less insulin, had fewer beta cells, and died within about 12 weeks of birth from severe diabetes; in contrast, stimulating the pathway increased the expression of genes required for insulin storage and secretion in islet cells from young mice. Because beta cells in the pancreas undergo most of their maturation and growth from birth until about age 10, investigations of this pathway in humans is dependent on Dr. Kim’s network of organ donation professionals who can provide him with a child’s pancreas when it becomes available. He has then extracted the islet cells, which has allowed him to show that exposing these young human islet cells to an inhibitor to this pathway significantly reduced their proliferation. Understanding how to switch islet cell growth on and off may also lead to new therapies for rare pancreatic islet cancers called neuroendocrine tumors.

Dr. Kim and Gerald Crabtree, MD, the David Korn, MD, Professor of Pathology and professor of developmental biology, are trying to develop new drugs to treat diabetes based on this work. Dr. Kim’s continuing research is focused on how to translate his findings into the ability to control human beta cell proliferation in a therapeutic way.

Dr. Kim’s summer mentoring of Jared Albright, a student selected by the Snyder Foundation to intern in the Kim lab at Stanford, was a smashing success. The project Mr. Albright undertook, with guidance from Dr. Kim and from James Lee, PhD, in the Kim lab, was to produce a viral-based reporter to enable purification and assessment of human beta-cells in islets. The materials produced by Albright and Dr. Lee were recently tested and found to successfully label human islet beta-cells. In addition, one-on-one mentoring and career development discussions between Dr. Kim and Albright occurred through the internship, and it is hoped this will have a lasting valuable impact on Mr. Albright's education.



Dr. Chih-Pin Liu, City of Hope, Beckman Research Institute

It is well known that effector cells of the immune system remain ready to destroy diseased cells and defend the body from bacteria and other invaders. These soldier cells normally leave healthy cells alone, however, because the immune effector T (Teff) cells are tightly controlled by special agents called regulatory T (Treg) cells. Therefore, it is important for the immune system to keep a well-balanced Teff and Treg cell population. 

For type 1 diabetes, the number of Teff cells significantly increase in the body and the Treg cells lost control of the larger number of Teff cells. The increased population of Teff cells begin attack and destroy target islet cells in the pancreas that produce insulin, which is required by our body to digest sugar into energy. As a result, the level of sugar is elevated in the body leading to severe and life-threatening complications.

The main purpose of our study in the past year has been to determine if novel methods and genes can be identified to effectively suppress Teff cells that cause type 1 diabetes and/or enhance the function of Treg cells.  It is expected that the novel findings obtained from these studies will help us translate our novel findings to the clinics and examine whether by targeting the identified novel gene targets and/or by expanding functionally very potent autologous human Treg cells can be used to therapeutically inhibit progression of type 1 diabetes and prevent rejection of islet grafts.

Specific purpose of study: Targeting pathogenic Teff and Treg cells to inhibit diabetes

Understanding the genetic and signaling mechanisms controlling the functional determination of these Teff cells should help maintain immune tolerance and suppression of insulin producing islet cell destruction by Teff cells.  In order to address these questions, we have performed the state-of-the-art comparative gene array analyses of Teff cells vs. Treg cells.  Our results have shown that several hundred genes are either up- or down-regulated in autoreactive Teff cells compared to those in Treg cells. Therefore, these novel results show that Teff cells and Treg cells express a distinct gene profile suggesting varied genetic programs may be responsible for the different function of these T cells. However, the genes responsible for the functional determination of Teff cells vs. Treg cells remain unclear. 

After intensive bioinformatics analyses, we have selected only a few candidate genes for further studies. Among them, the F-box protein Skp2 (S-phase kinase-associated protein 2) is a critical component of the SCFSkp2 ubiquitin ligase complex and may be an oncogene regulating cell division and proliferation. Previous studies suggest that Skp2 is the E3 ubiquitin ligase unit responsible for the timely degradation of several proteins, such as p21, p27KIP1 p57 and p130, that play a critical role in regulating cell division cycle. Recent studies have demonstrated that Skp2-konckout mice are viable and do not show an altered incidence of cancer. On the other hand, increased expression of Skp2 was observed during the proliferation of T-cell leukemia cells and T lymphoma cells, leading to Skp2-mediated tumor suppressor ubiquitylation and increased cell cycling activity. Beyond these, the role of Skp2 in T cells and, in particular, its role in regulating the function of Teff cells and Treg cells, remains unknown.

To examine whether Skp2 may play a role in regulating Teff cells or Treg cells, initial results from our preliminary studies have shown that Skp2 and Foxp3, a marker for Treg cells, are reciprocally expressed in CD4+Foxp3- T cells vs. CD4+Foxp3+ Treg. Based on these findings, we hypothesized that Skp2 may play an important role in regulating the function of autoreactive Teff cells vs. Treg cells during the pathogenesis and development of type 1 diabetes. 

In our studies to address this hypothesis, we have demonstrated that Skp2 down-regulation reprograms and converts diabetogenic Teff cells to potent Foxp3+ Treg cells at least partly through regulation of cell cycle control genes.  In addition, Skp2-down regulation leads to significantly decreased expression of inflammatory cytokines including IFN- and increase of anti-inflammatory cytokines including IL10 and TGF-. In contrast, over-expression of Skp2 in Foxp3+ Treg cells attenuates Foxp3 expression and abolishes their suppressive function. These results suggest that Skp2 may control Treg cell function through control of Foxp3 expression. 

Therefore, our results support the conclusion that Skp2 can act as an important molecular and functional switch between Teff and Treg cells. It is anticipated that proper control of Skp2 expression in these functionally distinct T cells is likely critical for inducing/maintaining immune tolerance in animals and humans. Identification of molecular and cellular mechanisms regulating the expression and function of Skp2 and its associated genes in Tpath or Treg would help us understand how to improve cell-based immunotherapy to prevent or treat autoimmune diseases like type 1 diabetes.

 Publication: Wang, D., Qin, H., Du, W., Shen, Y.-W., Lee, W.-H., Riggs, A.D., Liu, C.-P. 2012. Inhibition of Skp2 reprograms and converts diabetogenic T cells to Foxp3+ regulatory T cells. Proc. Natl. Acad. Sci. USA. 109:9493-9498.



Dr. Phillip Kantoff, The Lank Center for Genitourinary Oncology, Dana-Farber Cancer Institute

Dana-Farber’s Lank Center for Genitourinary Oncology, led by Philip Kantoff, MD, provides compassionate care and the most effective therapies for patients with prostate, kidney, bladder and testicular cancers, as well as many other rare and common cancers.  Patient care at the Lank Center is fueled by ongoing discovery, and accordingly the Lank Center is home to a host of physician-researchers who are committed to conducting cutting-edge clinical, translational, and basic research.   
 
Through its generous support of the Hahn and Freedman Laboratories within the Lank Center, the H.L. Snyder Medical Foundation has been a strong ally in the Center's ultimate goal of developing effective treatments for patients with genitourinary cancers.   
                
Lank Center-wide research highlights from 2011 include significant developments toward the discovery of new biomarkers, targets and targeted therapies in prostate cancer, as well as progress in the identification of genes that drive metastasis in bladder cancer.  In the target discovery arena, prostate cancer research conducted in the Lank Center resulted in the publication of a seminal paper this past February (Nature. 2011 Feb 10;470(7333):214-20) which described the first whole genome sequencing analysis of human prostate cancers.  The authors of this study identified potentially new prostate cancer drug targets and oncogenes, gleaned valuable insights about prostate tumor biology, and also were able to form hypotheses about which cellular processes within the prostate are likely going awry during tumor formation.  In addition to discovering novel drug targets, an effort to identify actual drug like chemicals that bind to the known prostate cancer target TMPRSS2-Erg is being performed by Lank Center scientists, and has yielded two small molecule inhibitors that will be further studied for their clinical and investigational utility.  

Another important area of prostate cancer research is learning how to distinguish indolent from aggressive cancers as soon as possible after diagnosis.  Drawing upon a large prostate tumor "biospecimen bank" at the Lank Center, researchers have designed a promising study to compare RNA sequences from prostate tumors of long term survivors with tumors from those who have died from this disease; sequencing and analysis of these samples are now underway.  In the field of bladder cancer research, Lank Center clinical scientists seek to further understand the genetic basis of metastasis.  They have thus far identified three chromosomal regions associated with metastasis in a cohort of 100 patients and are now homing in on pinpointing actual genes that underlie metastasis in bladder cancer.   
                
Drs. William Hahn and Matthew Freedman have each contributed to aspects of the above referenced investigations.  In addition, funding from the H. L. Snyder Medical Foundation has specifically enabled the progress made in the key projects described below.   

William Hahn, MD, PhD - Associate Professor of Medicine, Dana-Farber Cancer Institute/Harvard Medical School Co-Director, Center for Cancer Genome Discovery,      Dana-Farber Cancer Institute

William Hahn, MD, PhD is co- Director of the Center for Cancer Genome Discovery at the Dana-Farber Cancer Institute, where he is also the Deputy Chief Scientific Officer and the Chief of the Division of Molecular and Cellular Oncology. He is also Associate Professor of Medicine at the Harvard Medical School.  Having published over 40 peer-reviewed articles in the last two years, Dr. Hahn is at the forefront of Dana-Farber’s efforts to understand the genetic underpinnings of cancer diagnosis and treatment.  His work on Project Achilles, which uses the world’s most sophisticated collection of tools to analyze gene function, has led to the identification of some of the genetic mutations that are the most promising targets for cancer therapeutics.  As part of this project, he, along with colleagues from the Broad Institute of Harvard and MIT, examined cells from over 100 tumors, including 25 ovarian cancer tumors, to unearth the genes upon which cancers depend. They found that one of these genes is altered in a significant fraction of ovarian tumors — nearly one-fifth of those surveyed in the study. Another collaboration with colleagues  the  Broad Institute and MIT’s Koch Institute for Integrative Cancer Research, has resulted in groundbreaking work which identified  vulnerabilities in cancer genes that were a consequence of genomic instabilities; these findings can now be leveraged to investigate potential targeted therapies—treatments that target a the specific  mutated cancer-causing gene.  In addition, he has published an important study showing that the suppression of three specific genes could lead to prostate cancer.  Dr. Hahn’s cutting edge work has already has —and will continue to have— a game-changing effect on the way we are able to diagnose and treat cancer. 

Dr. Hahn has published 49 papers in national journals between January 2010 and August 2012, many of which have cited the HL Snyder Medical Foundation as providing partial support for the research.

Matthew Freedman, MD - Assistant Professor, Dana-Farber Cancer Institute and Harvard Medical School

Matthew Freedman, MD, is an Associate Physician at Dana-Farber Cancer Institute, Assistant Professor at Harvard Medical School, and Associate Member of the Broad Institute.  In addition, he is an investigator for the Howard Hughes Medical Institute.  His work cuts across the Cancer Genetics and Prostate Cancer Programs, and has contributed tremendously to the understanding of the DNA regions that do not code for genes (or proteins). Until recently, the study of cancer genetics mainly focused on the regions of DNA that code for genes. Newer studies point to the importance of these non-genic regions that were previously referred to as ‘junk DNA’. In fact, most of the DNA changes that increase the risk of cancer are located in these less-studied regions.
 
Dr. Freedman has articulated a strategy to study the non-genic pieces of the human genome to understand the root causes of cancer. This work has revealed that the non-genic regions, which help to regulate gene levels, are critical mediators of cancer initiation.  Using cutting edge techniques, his group was recently able to study genome folding in three dimensions, allowing Dr. Freedman and his team to link known DNA variants that elevate cancer risk to MYC, a well-known cancer-causing gene. This not only improves the prospects for new targeted therapies, but also introduces a new method for studying the genetics of cancer.  Even more recently, his group has linked another set of non-protein coding areas to their target genes, making progress towards Dr. Freedman’s ultimate goal of defining the genes and pathways that initiate cancer pathogenesis. This work necessitates utilizing techniques and methods that are often applied to questions in other scientific fields.  His expertise in the laboratory combined with his innovative problem solving skills have distinguished Dr. Freedman as an exceptional physician-scientist, and a valuable resource to those seeking answers cancer’s most intractable questions.

Dr. Freedman is very prolific in publishing his work.  Between January 2010 and August 2012, he has published 21 articles in national peer reviewed journals, many of which cite the HL Snyder Medical Foundation as providing partial support for the research.


JUDITH SHIZURU, MD, PHD

Associate Professor, Medicine (Blood and Marrow Transplantation) 

Member, Stanford Cancer Institute

Judith Shizuru, MD, PhD, associate professor of medicine (blood and marrow transplantation), received both her medical and doctoral degrees from Stanford and has been on the faculty at Stanford since 1997. Dr. Shizuru’s long-term goals are to solve some of the major challenges of bone marrow transplant therapy. 

Transplantation

Bone marrow transplantation is a powerful form of cellular therapy that has the capacity to cure many different diseases, from severe forms of cancer to genetic disorders of blood formation to diseases of the immune system, such as childhood diabetes or multiple sclerosis. Its challenges include eliminating the toxic side effects of the irradiation and drugs necessary for successful blood stem cell transplantation. Another challenge is the potentially deadly complication of graft-versus-host disease, which develops when immune cells in a donor graft mistakenly attack recipient tissues. Dr. Shizuru has pursued the approach of isolating and transplanting only pure blood-forming stem cells, rather than mixed cell populations contained in standard bone marrow grafts. By transplanting only pure blood-forming stem cells, the graft-versus-host disease complication can be avoided. 

Dr. Shizuru has also shown that when a patient receives purified blood-forming stem cells from a donor, the immune system that the patient redevelops is tolerant of all tissues subsequently transplanted from that donor as well as the recipient’s native tissue. Thus, pre-transplantation of blood-forming stem cells from a donor to a patient would prevent the patient’s immune system from rejecting subsequent organ, tissue, or even tissue stem cell transplants from that same donor. This pre-transplantation could potentially replace the regimen of lifelong immunosuppressive drugs now used to prevent transplant rejection. An additional benefit of transplanting purified blood-forming stem cells is the avoidance of graft-versus-host disease in the recipient.

 
Treatment of Severe Combined Immunodeficiency Disease

Children with severe combined immunodeficiency disease (SCID), or the “bubble boy” disease, are treated with transplantation. These children are born without a functional immune system and are therefore extraordinarily susceptible to serious infections. If not treated, most die by the age of two. Bone marrow transplantation is the only established cure for this disease. Unfortunately, the likelihood of a successful cure is reduced by the way transplants are currently performed. Prior to transplantation with healthy donor cells, the defective cells in these children are killed with toxic chemotherapy or irradiation, which can themselves be life-threatening. 

Focusing on the treatment of children with SCID, Dr. Shizuru is testing the use of a protein—a monoclonal antibody directed against molecules expressed on blood stem cells—to remove diseased or dysfunctional blood and immune system stem cells. Used prior to transplantation, this antibody would eliminate the faulty cells without the use of toxic treatments. Experiments in mice have shown that the antibody allows the animals to more readily accept the subsequent transplant with few to no side effects. 

SCID is a relatively rare disorder; however, if the planned trial succeeds for these children, it will open the door to transplanting pure blood-forming stem cells to treat all genetic diseases of the blood-forming system without high-dose chemotherapy or irradiation. This treatment could apply to patients with sickle cell and Mediterranean anemias—and even juvenile diabetes, lupus, multiple sclerosis, and rheumatoid arthritis.

Breast Cancer Treatment

Dr. Shizuru has done a long-term study of women at Stanford with stage 4 breast cancer that is reviving a decade-old debate about high-dose chemotherapy as a treatment option. She and her colleagues found that a significantly greater proportion of patients who received the aggressive treatment approximately a dozen years ago, followed by a rescue with their own, specially purified blood stem cells that had been purged of cancer, survived compared with those who were rescued with unmanipulated blood grafts.

This study is the first to analyze the long-term outcomes of women who received their own (autologous) stem cells that had undergone this purification process. High-dose chemotherapy followed by autologous blood stem cell transplantation was largely discarded at the end of the 1990s because interim analyses of several then-ongoing phase 3 clinical trials suggested it produced no better outcomes than other forms of treatment. However, women in this study received blood stem cells that had been prepared very differently, and the research suggests that the high-dose therapy strategy can be modified to include the use of cancer-free purified blood stem cells that will yield better overall outcomes in women with advanced breast cancer.

High-dose chemotherapy is considered to be an aggressive treatment because, in addition to killing cancer cells, it also destroys a patient’s blood-forming system. Such patients therefore need to be rescued with stem cells that can restore blood production, which includes red blood cells, platelets, and infection-fighting white blood cells. Unfortunately, cancer cells often stow away in the blood and may cause an eventual relapse.

As a result, in the mid-1990s Stanford researchers wondered if there was a way to overcome this problem. They opted to use antibodies that recognized newly identified markers on the surface of the blood stem cells to purify the stem cells away from regular blood and from any roving cancer cells. They then used this purified population of stem cells in women with metastatic breast cancer. 

Dr. Shizuru’s research team has now compared this experimental group to a group of women who received identical chemotherapy treatments during the same period but who received unmanipulated, peripheral blood. The results demonstrate significantly better overall and progression-free survival in those patients who received cancer-free stem cells. The Stanford blood and marrow transplant group is planning a larger clinical trial of the treatment in the summer or fall of 2013.

These important findings will serve as a basis for future trials not only for breast cancer but also for other cancers in which autologous transplants are used to enable high-dose chemotherapy. 


Dr. Berl R. Oakley - University of Kansas / BioScience Department / Irving S. Johnson Distinguished Professor






2012 Research Report with Charts




KARL DEISSEROTH, MD, PHD
D. H. Chen Professor
Professor, Psychiatry and Behavioral Science
Professor, Bioengineering
Member, Bio-X

Karl Deisseroth, MD, PhD, the D. H. Chen Professor and professor of psychiatry and behavioral science and of bioengineering, received both his medical and doctoral degrees from Stanford and has been on the faculty since 2005. He focuses on developing optical, molecular, and cellular tools to observe, perturb, and re-engineer brain circuits. He also sees patients in the psychiatry department with autism spectrum, anxiety, and depression.
In 2006, Dr. Deisseroth coined the word “optogenetics” to describe his invention of technology by which nerve cells in living animals are rendered photosensitive in order to allow action in these cells to be turned on or off by different wavelengths of light. Dr. Deisseroth’s optogenetic technology has made his stunning research on autism, schizophrenia, and anxiety possible. In each case, he has been able to use light to switch on and off behavior in mice. 

Optogenetics involves selectively bioengineering specific types of nerve cells so that they respond to light. Then, by delivering pulses of light via optical fibers to specific brain areas, researchers can target particular nerve-cell types and particular cell-to-cell connections or nervous pathways leading from one brain region to another. Because the fiber-optic hookup is flexible and pain-free, the experimental animals’ actual behavior as well as their brain activity can be monitored.

Autism and Schizophrenia

Autism spectrum disorder and schizophrenia each affect nearly one percent of all people. At present, there are no good drugs for mitigating the social-behavioral deficits of either disorder. While they differ in many ways, each syndrome is extremely complex, involving diverse deficits, including social dysfunction. Dr. Deisseroth has been able to switch on, and then switch off, social-behavior deficits in mice that resemble those seen in people with autism and schizophrenia, thanks to optogenetics allowing him to precisely manipulate nerve activity in the brain. 

Dr. Deisseroth’s work with optogenetics is the first demonstration that elevating the brain’s susceptibility to stimulation can produce social deficits resembling those of autism and schizophrenia, and that then restoring the balance can ease those symptoms. 

Animals in whose medial prefrontal cortex excitability had been optogenetically stimulated lost virtually all interest in engaging with other mice to whom they were exposed. In contrast, the normal mice were much more curious about one another. Boosting their excitatory nerve cells largely abolished their social behavior, and the brains of these mice showed the same gamma-oscillation pattern that is observed among many autistic and schizophrenic patients. Dr. Deisseroth believes that these results suggest that what is observed in animals could be relevant to people.

Anxiety

Anxiety is a poorly understood but common psychiatric disease. More than one in four people, in the course of their lives, experience bouts of anxiety symptoms sufficiently enduring and intense to be classified as a full-blown psychiatric disorder. In addition, anxiety is a significant contributing factor in other major psychiatric disorders from depression to alcohol dependence. Dr. Deisseroth sees patients with anxiety disorders in his clinical practice.

Most current anti-anxiety medications work by suppressing activity in the brain circuitry that generates anxiety or increases anxiety levels. Many of these drugs are not very effective, and those that are have significant side effects. The discovery of a novel circuit whose action is to reduce anxiety could translate into an entirely new strategy of anti-anxiety treatment for patients. 

Using optogenetics, Dr. Deisseroth and his colleagues have discovered a brain circuit that eases anxiety. One advantage of this state-of-the-art technology is that it allows researchers to tease apart the complex circuits that compose the brain so these can be studied one by one. 

Stimulation of a distinct brain circuit that lies within the amygdala, the brain structure typically associated with fearfulness, produces not fear but the opposite effect. Dr. Deisseroth employed a mouse model to show that stimulating activity exclusively in this circuit enhances animals’ willingness to take risks, while inhibiting its activity renders them more risk-averse. This finding could lead to new treatments for anxiety disorders.

Depression

Depression is one of the leading causes of disability worldwide and involves combinations of the inability to enjoy life, hopelessness, psychomotor retardation, anxiety, and social withdrawal. However, virtually nothing is known about what makes the depressed brain fail to work well. One consequence of this situation is that psychiatrists are not able to design truly new, safe, and effective treatments.

Dr. Deisseroth is using optogenetics to study depression, and he has succeeded in identifying neural circuits that underlie the devastating and life-threatening depression symptoms of hopelessness and the inability to enjoy rewarding experiences. This work has helped psychiatrists and neuroscientists to understand the fundamental circuit pathology of depression and its treatment.
Dr. Deisseroth’s work shows encouraging potential for translation to treatment of his patients in the clinic for those suffering from autism and schizophrenia, anxiety, and depression.

                
      Since the H. L. Snyder Medical Foundation started supporting Dr. Deisseroth research in 2004, he has had 68 publications. Moreover, his Optogenetics method was awarded “Method of the Year” in 2010.   
                
      For an excellent presentation of what his work entails, see the YouTube presentation: