SRF Summer Scholars Program

The SRF Summer Scholars Program offers undergraduate students the opportunity to conduct biomedical research to combat diseases of aging, such as cancer, Alzheimer’s, and Parkinson’s Disease. Under the guidance of a scientific mentor, each Summer Scholar is responsible for his or her own research project in such areas as genetic engineering and stem cell research. The Summer Scholars Program emphasizes development of both laboratory and communication skills to develop well-rounded future scientists, healthcare professionals, and policy makers. Students participating in the program will hone their writing skills via periodic reports, which are designed to emulate text scientists commonly must produce. At the end of the summer, students will have the opportunity to put all of their newly developed communication skills into practice at a student symposium.

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Summer Scholars Program Training Goals

SRF Education undergraduate programs primarily are designed to address two pressing needs in STEM education: the availability of novel, inquiry-based research opportunities and scientific communication skills. Whether a student plans to pursue postgraduate studies or apply for a research position at a pharmaceutical company, practical experience is key. However, research opportunities are limited at some colleges, and specific fields of research, such as tissue engineering, may be completely absent.

SRF Education sets itself apart from many other training programs with its focus on the development of scientific communication skills in addition to enhancing laboratory and critical thinking skills. Over the course of its educational programs, participants are guided through practical writing assignments that simulate documents scientists are often asked to produce, such as grant proposals. The communication training culminates in a formal presentation at a symposium where participants present the results of their work to their peers and mentors.

Program Learning Objectives Include:

  • Planning and executing an independent research project
  • Learning new technical skills
  • Explaining scientific concepts to a non-scientific audience
  • Submitting a simple grant proposal
  • Presenting results to peers in a formal scientific symposium

Qualifications

  1. Applicants should have some biologically-related prior research experience.
  2. Although GPA will be a consideration, there are no formal GPA requirements.
  3. There are no specific major requirements. Students of any major may apply, provided they can demonstrate experience relevant to the project in question.
  4. As noted in the Eligibility Requirements section, you must be currently enrolled as an undergraduate student to be eligible for the program. Dual undergrad/grad programs are acceptable, but students who already possess an undergraduate degree are not eligible to participate in the program. The only exception to this rule are students who have graduated during the fall, winter, or spring terms of the 2019-2020 academic year.
  5. There are no restrictions to class standing. Freshman, sophomores, juniors, seniors, and fifth year seniors are all eligible to apply.

Important Dates

  1. The online application will be available on this website on October 15, 2019.
  2. Completed applications are due at NOON on Wednesday, January 15, 2020 (12 pm PST 1/15/20). Be sure to ask for your letter of recommendation well in advance to provide sufficient time for it to be submitted.
  3. Finalists will be contacted by March 31, 2020.

Start Date and Duration

  1. Most host institutions can accommodate any start date in May or June to accommodate both semester- and quarter-system students.
  2. The internship lasts between 10 and 12 weeks, depending on host institution.

Compensation

  1. Stipend rates will be based upon levels used by government agencies, such as the NIH and NSF.
  2. Summer Scholars are not eligible for benefits.

Housing

  1. Students participating in the program need to locate their own housing. Advice can be provided by SRF and the host lab. A stipend will be provided to cover room and board costs.

Review the following to confirm your eligibility to participate in the program:

  1. This program is designed for undergraduate students. Only students who are currently pursuing an undergraduate degree or students who receive their undergraduate degree the during the fall, winter, or spring terms of the 2019-2020 academic year are eligible for the 2020 SRF Summer Scholars Program.
  2. Students currently enrolled in a master’s, doctoral, medical, or similar postgraduate degree granting program are ineligible to apply. Similarly, any applicant who has already earned a postgraduate degree is ineligible to apply.
  3. Students enrolled in a dual undergrad/grad program are eligible provided the undergraduate degree (i.e. B.S., B.A., or equivalent) has not yet been conferred.
  4. The applicant must be enrolled at a university in the United States. Special circumstances, such as established exchange programs, will be considered on a case-by-case basis. U.S. citizens studying abroad are also eligible to apply.
  5. Applicants must be eligible to receive a stipend. Students who are studying abroad in the U.S. will need to participate in the Summer Scholars Program through a Curricular Practical Training (CPT) for off-campus employment. Unfortunately, due to the length of time required for approval, we will no longer be able to accept Optional Practical Training (OPT) for off-campus employment. We recommend checking with your department to determine if CPT approval is an option and what forms you need to complete prior to applying to SRF Summer Scholars Program. Verification of your eligibility will be required before a position can be confirmed. You can learn more about CPT requirements here. It will be incumbent upon the student to provide the necessary documentation to participate, not SRF or the host institution.

If you have any questions regarding your eligibility for the program, you may contact SRF Director of Education Gregory Chin at [email protected].

Below is an alphabetical list of the Principal Investigators (PIs) and their 2019 Summer Scholar research projects. Participating labs and specific research projects are similar but vary slightly from year to year. The 2020 Summer Scholar research project options will be announced when the 2020 application period opens on October 15, 2019.

Principal Investigator: Julie Andersen, PhD

Buck Institute for Research on Aging

Start Date: May or June

Neurofibrillary tangles are a defining hallmark of both Alzheimer’s and Parkinson’s disease and they or similar aggregates also appear in the neuronal cytoplasm in other neurodegenerative diseases of old age. One possibility for their formation is that these tangles arise from an autophagic “traffic jam” caused by lysosomal inactivation. Lysosomal autophagy is an important mechanism by which cells rid themselves of such proteotoxic aggregates. Restoration of lysosomal function therefore constitutes an attractive candidate target for these disorders. As part of funded research from the SENS Foundation, we have established human tau P30L mutant versus wildtype-expressing neurons as an in vitro model of disease to test whether restoration of lysosomal function can prevent or reverse the formation of toxic tau aggregates. We determined using this model that low-dose (0.1 microM) application of a pharmacological accelerator of autophagic flux, K604, decreases levels of phosphorylated tau and protects against neurite retraction associated with the P30L model, even following their formation. We now propose to use this model to test newly identified lysosomal rejuvenating factors recently identified by our laboratory as part of a compound library screen for such compounds. These could potentially serve as novel therapeutics for the treatment of Alzheimer’s and Parkinson’s disease.

Principal Investigator: Amutha Boominathan, PhD

SRF Research Center

Start Date: May or June

Mitochondria are the power plants of the cell and are also the only cellular organelle that possess their own DNA in mammals. In humans, mitochondrial DNA (mtDNA) codes for 13 important proteins, which all assemble into the oxidative phosphorylation relay. Mutations in mtDNA occur as a consequence of constant exposure to reactive oxygen species produced by the mitochondrial energy generation process as well as mistakes in mtDNA replication. These mutations accumulate over time due to inefficient repair mechanisms and compromise respiratory chain function. Inherited and acquired mutations in mtDNA result in impaired energy generation and are the cause for several pathologies such as Leber’s hereditary optic neuropathy (LHON), Myoclonic Epilepsy with Ragged Red Fibers (MERRF), Kearns-Sayre syndrome and Leigh syndrome.

 

At SENS Research Foundation, we are in the early stages of creating an exciting and innovative system to repair mitochondrial mutations. Using the allotopic approach, we have identified specific targeting elements/ sequences that can improve expression of these essential genes from the nuclear DNA and their transport to the correct location in mitochondria. The summer intern selected will get the opportunity to design and test a library of constructs in model patient cell lines with specific mutations to mtDNA. The ability of re-engineered genes to rescue function will be evaluated through various techniques, such protein gels, qPCR and activity assays, with the potential of extending the studies to animal models.

Principal Investigator: Judith Campisi, PhD

Buck Institute for Research on Aging

Start Date: May or June

Cellular senescence is a basic aging process by which a cell undergoes a permanent arrest of cell division. Far from simple arrest, senescent cells are metabolically active – producing a vast array of secreted molecules that can drive pathology in the tissue microenvironment and potentially – systemically. Diabetes is a major risk factor for the development of several age-related degenerative conditions, including a form of kidney failure (diabetic nephropathy). Kidneys from diabetic patients and mice show accumulation of senescent cells – suggesting that senescence may drive kidney disease in response to diabetes. The Summer Scholar will work on a project to characterize the senescent state of kidney-derived proximal tubule epithelial cells (PTECs) in a tissue culture model. Key goals of this project include determining what pathways are activated by hyperglycemia that result in the senescence arrest; identifying and quantitating the factors secreted by these senescent cells; and assessing the effects of these secreted factors on other kidney cell types.

Principal Investigator: Lisa Ellerby, PhD

Buck Institute for Research on Aging

Start Date: May or June

The potential project will involve modeling disease and aging in human induced pluripotent stem models. The Ellerby laboratory has established a number of disease models of Huntington’s disease, Parkinson’s disease and aging. We have developed different methods to identify novel therapeutic targets for HD and aging. The intern will generate models of disease and evaluate therapeutic targets to validate these for treatment of the disease.

Principal Investigator: Jennifer Garrison, PhD

Buck Institute for Research on Aging

Start Date: May or June

As animals age they exhibit correlated recognizable and predictable changes to their physiology. These changes occur nearly synchronously across multiple tissues. Alterations in neuromodulatory signaling that lead to disruption of homeostasis may be one mechanism by which these concerted changes occur during aging. We want to understand how neuromodulators influence behavior and aging. Our lab develops new methods to monitor and manipulate signaling in living animals and to identify the fundamental enzymes that regulate inter-tissue communication. The goal of this project will be to characterize the role of intermediate filaments during aging in a C. elegans model.

Principal Investigator: Pankaj Kapahi, PhD

Buck Institute for Research on Aging

Start Date: May or June

Circadian rhythms are diurnal cycles of behavior (sleep/activity) and oscillations in cellular functions that are vital for maintaining homeostasis. Aging is accompanied by a gradual loss of circadian rhythm function and dampening in downstream rhythmic processes. Disruption of circadian clocks has been linked to accelerated aging and is a risk factor for several age-related diseases. Several studies show that disruption of circadian rhythms, genetically or through chronic jet-lag paradigms, is associated with neurodegeneration, obesity, and other age-related pathologies. However, the mechanisms by which circadian clocks influence aging and tissue homeostasis remain poorly understood.

 

The circadian system, similar to a free-swinging pendulum, maintains a rhythmic balance that slows over time as the animal ages. Our overall hypothesis is that dietary restriction (DR) slows aging by providing a push to the pendulum that increases the amplitude allowing the rhythmic motion to last longer. We base this on our previous findings showing that DR enhances circadian gene amplitude and that disruption of clocks abrogates the lifespan extension by DR. Similarly, in mice, high fat diet has been shown to dampen circadian rhythms, and circadian clocks are required for the lifespan extension upon calorie restriction. The goal of this lab is to understand the mechanisms by which DR enhances circadian amplitude and to identify the major clock output pathways that are important for tissue homeostasis and extending healthspan.

 

Approach: Our analysis of the DR circadian transcriptome revealed a significant enrichment for genes involved in the phototransduction cascade. Consistently, behavioral assays show that flies on DR show greater sensitivity to light. In this project, the Summer Scholar will test the hypothesis that DR enhances circadian amplitude by enhancing the light signals to the clock. Furthermore, the student will test whether DR delays the visual senescence observed in flies. We will use a combination of dietary and light manipulations in conjunction with genetic manipulations of the circadian clock and phototransduction genes in the fly eye to test their impact on circadian amplitude, visual senescence, and lifespan. Our experiments will address the importance of phototransduction in mediating some of the protective effects of DR.

Principal Investigator: Gordon Lithgow, PhD

Buck Institute for Research on Aging

Start Date: May or June

Dr. Lithgow’s lab is focused on understanding the role of aging in the origins of age-related chronic disease. Specifically, his lab has led the field in the identification of pharmacological interventions in aging. The Lithgow lab utilizes molecular genetics, biochemistry and a range of leading edge technologies, including proteomics and metabolomics. His team utilizes the microscopic worm, C. elegans, which ages rapidly but exhibits many characteristics of human aging. Using this model, the lab has identified scores of chemical compounds that suppress disease phenotypes and extend lifespan. Many of these compounds promote protein homeostasis, which usually fails during normal aging and is also a factor in diseases such as Alzheimer’s and Parkinson’s.

 

Current Research Projects:

 

  1. Identifying chemical compounds (natural and synthetic) that promote proteostasis and extend healthspan and lifespan. The lab has identified scores of compounds with one or more of these properties and are working to understand their mechanisms of action. The lab is collaborating on mouse experiments testing the effects of these compounds on neurological disease and age-related bone loss.
  2. Determining the extent to which age-related accumulation of metals contribute to aging and disease pathology. We are manipulating metal levels in C. elegans using drug-like compounds.
  3. Investigating tissue-to-tissue signaling in the regulation of the mitochondria unfolded protein response.
  4. The lab is also part of a consortium, the Caenorhabditis Intervention Testing Program along with Monica Driscoll’s lab (Rutgers) and Patrick Phillips lab (Univ. of Oregon). The consortium is an NIA funded program to establish standard conditions for testing chemicals for effects on longevity and healthspan with a view to identifying robust interventions in aging for future pre-clinical and clinical research.

Principal Investigator: Jeanne Loring, PhD

The Scripps Research Institute

Start Date: May or June

The Loring lab is focused on harnessing the power of pluripotent stem cells for regenerative medicine. We believe that cells derived from pluripotent stem cells will revolutionize medicine and lead to longer and healthier lives. We are looking for a Summer Scholar to work on our cell therapy project for Parkinson’s disease in which induced pluripotent stem cells from Parkinson’s patients are used to derive dopaminergic neurons, the same neurons which are lost in the brains of Parkinson’s patients. The aim of this Summer Scholar project is to evaluate whole-genome gene expression profiles from dopaminergic neurons derived from 10 different patient lines.

 

The Summer Scholar should have a strong interest in computational biology and ideally some background in computer science. The tools and skills for doing much of the bioinformatics analysis will be based around the Linux operating system. A working knowledge of Linux OS and some Python or R skills is desirable, along with an ability to solve data management problems independently and on-the-fly. Industry standard tools such as the GenomeAnalysisToolkit, Amazon AWS and Firecloud will be used to get an overview of the integrity of the neurons created in-house, and hence their suitability for transplantation.

Principal Investigator: Matthew O’Connor, PhD

SRF Research Center

Start Date: May or June

This research project is geared toward performing translational research studying aging as it relates to the immune system and senescent cells. More specifically, the Summer Scholar will study how the immune system interacts with senescent cells. Research will include testing of candidate signaling protein blockers to try to induce killing of senescent cells. Another aspect of this project will involve identifying and characterizing new types of senescent cells from among the many tissue and cell types in the body. This will involve high-throughput microscopy on our robotic microscope. The research project will be a collaborative effort between SRF and the Buck Institute for Research on Aging, located in Novato, CA.

Principal Investigator: Matthew O’Connor, PhD

SRF Research Center

Start Date: May or June

This project seeks to employ a small molecule approach to remove a toxic form of cholesterol from human blood in order to combat the development of atherosclerosis. Oxysterols are non-enzymatic cholesterol oxidation products that recently have become of interest in the pathology of several diseases, including atherosclerosis. The human body has difficulty processing such cholesterols and thus they accumulate in certain types of cells and tissues over time. We are testing the ability of various drugs to remove such toxic cholesterols from human cells. This rational drug design project will involve computational, in vitro, and ex vivo experiments and measurements of the activity of various compounds that we are testing. Our goal is to create a product based on SENS damage repair concepts that can be used in human patients in the near future.

Principal Investigator: Khalid Shah, PhD

Harvard School of Medicine

Start Date: May

Cell-based therapies are emerging as a promising strategy to tackle cancer. We have developed tumor cell surface receptor targeted T cells and adult stem cells expressing novel bi-functional pro-apoptotic and immunomodulatory proteins and oncolytic viruses. Using different primary and metastatic tumor models that mimic clinical settings, we show that that engineered stem cells expressing novel bi-functional proteins or loaded with oncolytic viruses target both the primary and the invasive tumor deposits and have profound anti-tumor effects. Recently, we have reverse engineered cancer cells using CRISPR/Cas9 technology and demonstrated self-tumor tropism and therapeutic potential of receptor self-targeted engineered cancer cells. These studies demonstrate the strength of employing engineered cells and real-time imaging of multiple events in preclinical-therapeutic tumor models and form the basis for developing novel cell based therapies for cancer.

Principal Investigator: Evan Snyder, MD, PhD

Sanford Consortium for Regenerative Medicine

Start Date: May or June

We believe the study of stem cell biology will provide insights into many areas: developmental biology, homeostasis in the normal adult, and recovery from injury. Indeed, past and current research has already produced data in these areas that would have been difficult or impossible via any other vehicle. We have engaged in a multidisciplinary approach, simultaneously exploring the basic biology of stem cells, their role throughout the lifetime of an individual, as well as their therapeutic potential. Taken together, these bodies of knowledge will glean the greatest benefit for scientists and, most importantly, for patients. All of our research to date has been performed in animal models with the ultimate goal of bringing them to clinical trials as soon as possible.

 

Possible research project options include:

 

  1. Model Parkinson’s Disease (PD) using human induced pluripotent stem cells (hiPSCs)
  2. Search for molecules that confer a resistance to age-related degeneration
  3. What directs the homing of neural stem cells to areas of pathology?

Below is an alphabetical list of the Principal Investigators (PIs) and their 2020 Summer Scholar research projects.

Principal Investigator: Julie Andersen, PhD

Buck Institute for Research on Aging

Start Date: May or June

Neurofibrillary tangles are a defining hallmark of both Alzheimer’s and Parkinson’s disease, and they or similar aggregates also appear in the neuronal cytoplasm in other neurodegenerative diseases of old age. One possibility for their formation is that these tangles arise from an autophagic “traffic jam” caused by lysosomal inactivation. Lysosomal autophagy is an important mechanism by which cells rid themselves of such proteotoxic aggregates. Restoration of lysosomal function therefore constitutes an attractive candidate target for these disorders. As part of funded research from the SENS Research Foundation, we have established human tau P30L mutant versus wildtype-expressing neurons as an in vitro model of disease to test whether restoration of lysosomal function can prevent or reverse the formation of toxic tau aggregates. We determined using this model that low-dose (0.1 microM) application of a pharmacological accelerator of autophagic flux, K604, decreases levels of phosphorylated tau and protects against neurite retraction associated with the P30L model, even following their formation. We now propose to use this model to test newly identified lysosomal rejuvenating factors recently identified by our laboratory as part of a compound library screen for such compounds. These could potentially serve as novel therapeutics for the treatment of Alzheimer’s and Parkinson’s disease.

Principal Investigator: Amutha Boominathan, PhD

SRF Research Center

Start Date: May or June

Mitochondria are the power plants of the cell and are also the only cellular organelle that possess their own DNA in mammals. In humans, mitochondrial DNA (mtDNA) codes for 13 important proteins, which all assemble into the oxidative phosphorylation relay. Mutations in mtDNA occur as a consequence of constant exposure to reactive oxygen species produced by the mitochondrial energy generation process as well as mistakes in mtDNA replication. These mutations accumulate over time due to inefficient repair mechanisms and compromise respiratory chain function. Inherited and acquired mutations in mtDNA result in impaired energy generation and are the cause for several pathologies such as Leber’s hereditary optic neuropathy (LHON), Myoclonic Epilepsy with Ragged Red Fibers (MERRF), Kearns-Sayre syndrome and Leigh syndrome.

 

At SENS Research Foundation, we are in the early stages of creating an exciting and innovative system to repair mitochondrial mutations. Using the allotopic approach, we have identified specific targeting elements/ sequences that can improve expression of these essential genes from the nuclear DNA and their transport to the correct location in mitochondria. The Summer Scholar selected will use a computational approach to design and test a library of constructs in model patient cell lines with specific mutations to mtDNA. The ability of re-engineered genes to rescue function will be evaluated through various techniques, such as protein gels, qPCR, and activity assays, with the potential of extending the studies to animal models.

Principal Investigator: Judith Campisi, PhD

Buck Institute for Research on Aging

Start Date: May or June

Senescence is a state where cells irreversibly arrest their growth against damage response. Accumulation of senescent cells (SnCs) with age contributes to age-associated phenotypes and diseases by altering the tissue microenvironment through secretion of cytokines, growth factors and metalloproteases, called the senescence-associated secretory phenotype (SASP). Our lab found that mitochondrial dysfunction induces a senescence state termed mitochondrial dysfunction-associated senescence (MiDAS), causing a distinct secretion profile and mitotic arrest. Progeroid mice that rapidly increase mtDNA mutations accumulated senescent cells in skin with a MiDAS SASP in vivo, which stimulated keratinocyte differentiation in cell culture. Recently, I established 3D skin organoid culture system to mimic human skin. The Summer Scholar will work on a project to characterize the differentiation of keratinocytes in 3D skin organoids formed by MiDAS fibroblasts compared to them formed by non-senescent fibroblasts. The scholar will further characterize keratinocyte differentiation and skin aging phenotype in the progeroid mouse model. The final goal of this study is to determine whether SASPs secreted from MiDAS cells play a key role in keratinocyte differentiation and imbalance in skin homeostasis, leading to skin aging.

Principal Investigator: Daniel Clemens, PhD

Underdog Pharmaceuticals

Start Date: May or June

SENS Research Foundation has spun out a project on atherosclerosis into a startup company called Underdog Pharmaceuticals. Underdog is engineering drugs that can bind and reverse the pathological effects of certain oxidized forms of cholesterol implicated in atherosclerosis and several other diseases of aging. The laboratory techniques involved include isolation of PBMCs and macrophages from human blood; flow cytometry to characterize macrophages in various states of differentiation, polarization, and disease; semi-automated (robotic liquid handler) biochemical binding and toxicity assays; ELISA; and other common molecular biology and biochemistry techniques. The choice of a specific project will depend on the skillset and preferences of the trainee. As an example, one project involves developing a new assay to accurately measure 7-keto cholesterol levels in tissue samples. Interested applicants do not need to know all the techniques required to run these assays but should be familiar with routine lab protocols and should not be uncomfortable working with human or animal blood and tissues.

Principal Investigator: Monica Colaiacovo, PhD

Harvard Medical School

Start Date: May or June

Cancer is a complex disease caused by uncontrolled cell proliferation and it is the second leading cause of death globally. There is a dire need for rapid and cost effective screening platforms that also provide a physiologically relevant background that include host immunity and a complex tumor microenvironment. We will implement a high-throughput screening strategy using the multicellular organism C. elegans to identify anticancer compounds. Many of the pathways that when deregulated lead to tumor formation are conserved between humans and C. elegans. We found that a constitutively active mutant in the FGFR3 (Fibroblast Growth Factor Receptor 3) ortholog old-2 in C. elegans causes late-onset germ cell tumors and sterility similar to the ovarian tumors and late-onset testicular tumors observed due to a constitutively activating mutation in FGFR3 in humans. Utilizing a strain carrying a fluorescent reporter to track mitotic germ cells/tumors, animal viability and fertility in the old-2 constitutively active mutant we will perform a high-throughput screen to identify compounds that suppress tumor formation and rescue fertility while also controlling for drug toxicity.

Principal Investigator: Lisa Ellerby, PhD

Buck Institute for Research on Aging

Start Date: May or June

The Summer Scholar project will involve modeling disease and aging in human induced pluripotent stem models. The Ellerby laboratory has established a number of disease models of Huntington’s disease, Parkinson’s disease and aging. We have developed different methods to identify novel therapeutic targets for HD and aging. The Summer Scholar will generate models of disease and evaluate therapeutic targets to validate them for treatment of the disease.

Principal Investigator: Jennifer Garrison, PhD

Buck Institute for Research on Aging

Start Date: May or June

As animals age they exhibit correlated recognizable and predictable changes to their physiology. These changes occur nearly synchronously across multiple tissues. Alterations in neuromodulatory signaling that lead to disruption of homeostasis may be one mechanism by which these concerted changes occur during aging. We want to understand how neuromodulators influence behavior and aging. Our lab develops new methods to monitor and manipulate signaling in living animals and to identify the fundamental enzymes that regulate inter-tissue communication. The goal of this project will be to characterize the role of intermediate filaments during aging in a C. elegans model.

Principal Investigator: Pankaj Kapahi, PhD

Buck Institute for Research on Aging

Start Date: June

Human neurodegenerative diseases are characterized by progressive loss of neurons in the nervous system with aging being the major risk factor for disease onset.  Studies have revealed an involvement of a class of non-coding RNAs, known as microRNAs (miRNAs), in aging and neurodegenerative diseases.

MicroRNAs have been shown to influence neuronal survival and accumulation of toxic proteins that are associated with neurodegeneration and brain senescence. Evidence from animal models as well as in vitro studies has indicated that energy metabolism and nutrient-sensing pathways function as critical determinants of neuronal processes that may be required for brain repair or adult neurogenesis. Since, dietary factors can modulate expression levels of miRNAs, it is likely that miRNA pathways that are regulated by dietary interventions can be targeted for development of therapeutic strategies to prevent or delay neurodegenerative diseases. Dietary restriction (DR) is an evolutionarily conserved intervention that has been shown to extend healthy lifespan by eliciting cell protective effects in diverse tissues including brain. In this project, we will utilize a Drosophila neurodegenerative/Alzheimer’s disease model to provide mechanistic insights into the role of DR-modulated miRNAs and their downstream effectors in neurodegenerative disease pathogenesis as well as neuroprotection. We will utilize genetic, molecular and cell biology approaches to assess the efficacy of miRNAs in promoting brain health and preventing disease onset and progression.

Principal Investigator: Gordon Lithgow, PhD

Buck Institute for Research on Aging

Start Date: June

Dr. Lithgow’s lab is focused on understanding the role of aging in the origins of age-related chronic disease. Specifically, his lab has led the field in the identification of pharmacological interventions in aging. The Lithgow lab utilizes molecular genetics, biochemistry and a range of leading edge technologies, including proteomics and metabolomics. His team utilizes the microscopic worm, C. elegans, which ages rapidly but exhibits many characteristics of human aging.

 

This Summer Scholar project will use C. elegans and mammalian cell culture to explore how the mitochondrial unfolded protein response may initiate cell death cascades, such as necrosis, which has widespread implications for understanding aging and age-related diseases such as neurodegeneration and ischemia-reperfusion injury (stroke and heart attack). Prior experience with the nematode is desirable but not required. A strong interest in genetics and mitochondrial biology is also preferable.

Principal Investigator: Jay Sarkar, PhD

Turn Biotechnologies

Start Date: May or June

Turn Biotechnologies is a new rejuvenation therapeutics company spun out of Stanford University. The focus of the company is to develop epigenetic reprogramming technologies to reset aged cells back to a more youthful state. This represents a dramatic new form of anti-aging intervention, rather than just modulating a specific set of aging pathways these technologies remodel the entire gene expression landscape to a more youthful configuration. This approach has been shown to drive a more holistic reversion of aging phenotypes that is generalizable to a variety of different cells and tissues. Furthermore, these benefits extend to pathological states as well, and as such the company has developed these technologies for multiple age-related disease applications. Opportunities over the summer will provide a taste of these applications. An example project will be designing age reprogramming protocols to improve muscle stem cell therapy platforms. This will involve techniques like biopsy processing, cell sorting, cell transfection and transduction, live animal injection and imaging (may be done offsite), histology and analysis. Projects can evolve and positions can transition into a more full time basis.

Principal Investigator: Khalid Shah, PhD

Harvard Medical School

Start Date: May or June

Cell-based therapies are emerging as a promising strategy to tackle cancer. We have developed tumor cell surface receptor targeted T cells and adult stem cells expressing novel bi-functional pro-apoptotic and immunomodulatory proteins and oncolytic viruses. Using different primary and metastatic tumor models that mimic clinical settings, we show that engineered stem cells expressing novel bi-functional proteins or loaded with oncolytic viruses target both the primary and the invasive tumor deposits and have profound anti-tumor effects. Recently, we have reverse engineered cancer cells using CRISPR/Cas9 technology and demonstrated self-tumor tropism and therapeutic potential of receptor self-targeted engineered cancer cells. These studies demonstrate the strength of employing engineered cells and real-time imaging of multiple events in preclinical-therapeutic tumor models and form the basis for developing novel cell based therapies for cancer.

Principal Investigator: Amit Sharma, PhD

SRF Research Center

Start Date: May or June

Senescent cells are characterized by an irreversible arrest of the cell cycle and secrete a unique milieu of pro-inflammatory cytokines, chemokines, and growth factors collectively referred to as the senescence-associated secretory phenotype (SASP) due to which these cells have been implicated in a large number of age-related diseases, and recent efforts to develop therapeutic interventions are centered around selectively eliminating senescent cells (senolytics). While these approaches present two possible avenues for reducing the impact of senescent cells, they still lack specificity for their intended target.

We are focusing on developing therapeutic interventions to selectively eliminate senescent cells by utilizing innate immune cells like Natural Killer (NK) cells. These innate immune cells have evolved mechanisms to selectively induce apoptosis in target cells based on the expression of ligands on the target cells.  In addition, recent publications suggest that (a) senescent cells have evolved mechanisms to escape NK cells or (b) NK cells lose their ability to eliminate senescent cells with aging. We will utilize approaches to isolate and enrich NK cells from human blood and investigate the mechanism by which they can selectively target and kill senescent cells. The main aim of the project is to test these hypotheses using in vitro and ex vivo cell co-culture experiments.

 

This approach will afford better understanding of mechanisms involved in NK cell interaction with senescent cells, which will be critical in designing targeted therapeutic approaches to age-related diseases caused by the accumulation of senescent cells.

Principal Investigator: Evan Snyder, MD, PhD

Sanford Consortium for Regenerative Medicine

Start Date: May or June

We believe the study of stem cell biology will provide insights into many areas: developmental biology, homeostasis in the normal adult, and recovery from injury. Indeed, past and current research has already produced data in these areas that would have been difficult or impossible via any other vehicle. We have engaged in a multidisciplinary approach, simultaneously exploring the basic biology of stem cells, their role throughout the lifetime of an individual, as well as their therapeutic potential. Taken together, these bodies of knowledge will glean the greatest benefit for scientists and, most importantly, for patients. All of our research to date has been performed in animal models with the ultimate goal of bringing them to clinical trials as soon as possible.

Possible research project options include:

  1. Model Parkinson’s Disease (PD) using human induced pluripotent stem cells (hiPSCs)
  2. Search for molecules that confer a resistance to age-related degeneration
  3. What directs the homing of neural stem cells to areas of pathology?

Principal Investigator: Michael Snyder, PhD

Stanford University

Start Date: May or June

The Genotype-Tissue Expression (GTEx) project funded by NIH common fund has sequenced thousands of human tissue samples from around 1000 people and 56 different types of organs. One of the main aims is to understand the association of genetic variations to phenotypes.  However, the massive data generated by GTEx not only can provide information to explain the variations but also can be used to study aging. The GTEx cohort contains all age groups, and the data provides molecular profiles from multi-omics. Most of the previous aging studies were done using animal models or with very limited clinic data. For a few large-scale studies, they are mainly based on genomic information in general. As part of the GTEx project, our lab has sequenced the proteome of multiple organs from many individuals.  Compared to genomics, proteomics is closer to phenotype and can provide direct evidence. Integrating proteomics information with other omics can provide a more comprehensive molecular profile for the study of aging at organ level. However, integrating information from multi-omics is a daunting task. It requires knowledge from both domains and also needs sophisticated mathematical models. We believe results from this study will greatly advance the understanding of aging.

– The 2020 SRF Summer Scholars Program application period will open on Tuesday, October 15, 2019. –

The application for the 2020 SRF Summer Scholars Program is now available.

Applications will be accepted until noon PST Wednesday, January 15, 2020 (12pm PST 1/15/20).
Please be sure to download the recommendation instructions and give your
recommender(s) ample time to submit your letter of recommendation by the deadline.

Other SRF Education Opportunities

SRF Postbacc Fellowship Program

Offering recent graduates the opportunity to conduct biomedical research to combat diseases of aging under the guidance of a scientific mentor, with the goal of preparing participants for a career in regenerative medicine research.

SRF Postbac Fellowship Program

Offering recent graduates the opportunity to conduct biomedical research to combat diseases of aging under the guidance of a scientific mentor, with the goal of preparing participants for a career in regenerative medicine research.

SRF Alliance

Funding PhD students at Oxford University in the field of healthcare translation to research international guidelines pertaining to digital health development and implementation, as well as healthcare regulation and standards world-wide.

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