2020 SRF Summer Scholar Profile: Anson Zhou

My name is Anson Zhou and I am a rising sophomore studying biomedical engineering at Johns Hopkins University. At Hopkins, I work at the Institute for NanoBioTechnology (INBT) and the Translational Tissue Engineering Center (TTEC) under the mentorship of Dr. Hai-Quan Mao. I have worked on a number of projects designing biomaterials-based medical devices for regenerative applications. In particular, I have been working to address functional nerve recovery and neuroma formation in amputee patients. In many cases, after a limb is amputated, severed nerves continue to regenerate despite having no target to synapse on to. As a result, these nerves aggregate together and form painful tumors known as neuromas. I have been developing a nanofiber hydrogel composite-filled nerve conduit to address this issue. By using this device in conjunction with a promising procedure known as Targeted Muscle Reinnervation (TMR), we can not only prevent neuroma formation, but also create the proper conditions for adoption of advanced and intuitive myoelectric prostheses.

This summer, I had the opportunity to work at the Sanford Consortium for Regenerative Medicine with Dr. Evan Snyder and Dr. Sandra Leibel. My project focused on developing a stem-cell derived model for Chronic Obstructive Pulmonary Disorder (COPD), one of the top five leading causes of death in developing countries. COPD primarily effects the elderly and smokers and is characterized by difficulty breathing and excessive mucus production in the airways.

In an attempt to better understand and treat medical conditions, in vitro disease models or “disease-in-a-dish” has become an increasingly popular approach in biomedical research. Here, tissue cultures are used to test potential therapies, model disease progression, and determine factors that contribute to disease development. For COPD, a number of disease models have been developed using primary cells, including human bronchial epithelial cells (HBECs) and pediatric asthmatic bronchial cells. In my project, I sought to develop a similar model but starting with human stem cells. Compared to primary cells, stem cells are more versatile for differentiation, are often immortalized, and do not require direct isolation from tissue. More importantly, we may be able to develop more substantial models using stem cells. Induced pluripotent stem cells (iPSCs) for example, is a type that begins as a differentiated somatic cell but is reverted back to a stem cell. Given its unique method of development, iPSCs can be sourced to contain genes that predispose an individual to develop COPD, opening opportunities for the development of a more complex and comprehensive disease model.

To test the potential of creating a COPD phenotype in a stem cell-based culture, I focused on inducing goblet cell hyperplasia (GCH), the condition that increases the proportion of mucus-secreting goblet cells and consequently leads to the aforementioned excessive mucus production in COPD. The stem cells were cultured in an air-liquid interface (ALI) to simulate the lung airway where GCH is most evident, and were treated with IL-13, a protein known to induce goblet cell differentiation and is overexpressed in COPD lung tissue. Through the use of immunofluorescent staining, I was able to identify and subsequently quantify the proportion of goblet cells after IL-13 treatment in order to determine whether GCH was induced in the culture.

2020 SRF Summer Scholar Profile: Aly Ung

I’m Aly Ung, a rising senior bioengineering major at UCLA. Prior to joining the SRF Summer Scholar Program, I worked primarily on liver-on-a-chip research, specifically the modeling of Non-Alcoholic Fatty Liver disease progression through an organ on a chip system and the assessment of the influence of mesenchymal stem cells on metastasis and tumor growth in Dr. Ali Khademhosseini’s lab under the supervision of Dr. Junmin Lee. During my time in SRF Summer Scholars Program, I had the privilege to work under Dr. Amutha Boominathan’s supervision to tackle the recovery of OxPhos gene functions in mitochondrial disorders as part of a larger effort of SRF to tackle age-related diseases/disorders.

Impacting approximately 7.5 out of every 100,000 individuals, mitochondrial disorders have been shown to have a diverse pathology portfolio which range in age from pediatric to adult onset diseases and affects essentially every organ system in the body– predominantly, the nervous, cardiovascular, and skeletal muscle tissues. The mitochondria is the only organelle (internal structures of a cell) that houses its own set of genetic material outside of the nucleus. Due to the lack of DNA repair mechanisms, the mitochondria is roughly 100x more vulnerable to mutations than the nucleus—resulting in the large array of clinical issues mentioned above. The most severe clinical issues are largely attributed to the mutations in genes that encode for important proteins within the energy making pathway—the OxPhos relay. My project is part of a larger effort to recover the functions of these important mitochondrial genes with sequences that are not mutated. My project aims to improve current gene insertions methods by allowing for a more controlled, site-specific insertion into the targeted genetic region by employing a method called GAPTrap. Additionally, I helped develop a qualitative assessment that will allow visualization of the mRNA (genetic blueprint of proteins) distribution across the cell and standardized a quantitative method that will help assess the metabolic performance of the cells by cell viability under certain conditions.

2020 SRF Summer Scholar Profile: Murial Ross

My name is Murial Ross, and I am a rising senior at Santa Clara University majoring in Bioengineering with a Biomolecular focus. At my university, I am working in Dr. Prashanth Asuri’s laboratory to explore the impact of hydrogel stiffness on human stem cells. There are many different types of hydrogels, each made up of a polymer that forms a gel that can retain water, similar to a sponge. Hydrogels are commonly used for wearable devices, like contact lenses, or provide 3D scaffolds for cells to grow. Researchers are exploring how altering properties of hydrogels, like stiffness, can impact toxicity of compounds to stem cells. By replicating stiffnesses of tissues, one could accurately gauge toxicity of a compound to that tissue type. Due to the online academic format in spring 2020, I have been remotely researching journal articles and writing segments for a review in the scientific journal Polymers on the use of nanoparticle-reinforced hydrogels in biomedical applications. The incorporation of nanoparticles, like clay or metal, can greatly improve and add new properties to hydrogels, enabling their use in applications like wound healing or drug delivery. This summer, I have been working in Dr. Evan Snyder’s laboratory at the Sanford Consortium for Regenerative Medicine through the SRF Summer Scholars Program. Dr. Snyder is the current Director of the Center of Stem Cells and Regenerative Medicine at Sanford Burnham Prebys Medical Discovery Institute. The laboratory focuses on stem cell research in the brain and lungs to provide insights on developmental biology, maintenance of optimal internal conditions in a healthy adult and recovery from injury. In response to the COVID-19 pandemic, the laboratory has created and infected organoids to explore the virus’s impact on the body in addition to testing drugs against COVID-19.  

My internship project focused on the impact of COVID-19 infection on the secretion of surfactant protein B (SP-B) in the brain. Surfactant is a mixture of lipids and proteins, used by the lungs to reduce surface tension to prevent lung collapse and to provide anti-inflammatory properties. Surfactant in the brain was recently discovered in 2013 by Stefan Schob and collaborators at the University Hospital Leipzig in Germany although its role in disease is still unknown. Based on Schob et al. ‘s research, SP-B is secreted in the choroid plexus of the brain, where cerebrospinal fluid (CSF) is produced, potentially explaining its presence in the CSF. CSF serves as a shock absorber to protect the brain, in addition to circulating nutrients and removing cellular waste products from the brain. Schob et al. believes SP-B has similar anti-inflammatory properties in the brain as it does in the lungs. In a clinical study, they demonstrated that the concentration of SP-B changes in response to neural inflammation due to infections or cerebral infarction, defined by an area of necrotic tissue due to a blockage or narrowing of the arteries that supplies blood and oxygen to the brain. In addition, they know surfactant decreases surface tension of bodily fluids, indicating a disturbance in SP-B could disrupt CSF flow and could cause neurological diseases. 

As more patients contract COVID-19, doctors have noticed some patients develop neurological symptoms ranging in severity from loss of smell and taste to encephalitis or acute cerebrovascular disease in the form of ischemic stroke or cerebral hemorrhage, both a type of brain bleeds. Many of the severe neurological symptoms are caused by neural inflammation or disrupt CSF flow. I hypothesize SP-B is upregulated in response to COVID-19 infection to counterbalance the detrimental effects of the immune system. A clinical study in Wuhan, China determined that 36% of patients presented with neurologic symptoms. Those that had severe COVID-19 infections were significantly older and were more likely to have more severe neurological symptoms. SP-B could play a role in the severity of COVID-19 related neurological symptoms. May et al. demonstrated that elderly patients produced significantly less CSF than younger patients. Since CSF production is decreased in elderly patients, I hypothesize that the SP-B secretion is also decreased in older patients, but further study would be needed. The severity of COVID-19 neurological symptoms in older patients could be linked with the decrease in SP-B, limiting the body’s natural anti-inflammatory response and regulation of CSF flow, therefore increasing the severity of symptoms. 

For my project, I generated two types of brain organoids and infected them with a COVID-19 pseudovirus to analyze COVID-19’s impact on SP-B secretion. The pseudovirus has the same spike protein as the SARS-CoV-2, allowing the pseudovirus to imitate SARS-CoV-2 infection without the dangers of handling the live SARS-CoV-2 virus. I hypothesize there will be an increase in SP-B secretion from infected organoids compared to non-infected organoids, emphasizing that SP-B plays an immunological role in the brain and could impact the severity of neurological symptoms in older patients with SP-B deficiencies.

2020 SRF Summer Scholar Profile: Kaitlin Pensabene

My name is Kaitlin Pensabene, and I am a senior at Villanova University studying biochemistry. At Villanova, I work with Dr. Aimee Eggler studying the effects of small molecule antioxidants on the Nrf2/ARE pathway. Specifically, I have been studying not only how  transcriptional but also how translational processes are attenuated by oxidative stress. In doing so, I am investigating the mechanism by which reactive oxygen species shut down global protein synthesis while selectively upregulating synthesis of cytoprotective enzymes to reverse the effects of oxidative stress in a timelier manner. While interning with Turn Biotechnologies this summer, I studied the epigenetic effects of aging on a variety of diseases. Dr. Jay Sarkar and his team at Turn Biotech are focused on creating therapeutics that reverse age-related phenotypes and their associated diseases with applications in the skin, joints, muscle, and potentially many more tissues.

The basis of Turn Biotechnologies’ Epigenetic Reprogramming of Aging (ERA) therapeutic is to turn back the clock of a cell’s epigenetic signature. Imagine a young cells epigenome as a record you just bought. When you bring it home and play it on your record player, the music sounds beautiful and the record works perfectly, not skipping a single track. The grooves in the record are each representative of a modification to the epigenetic signature, like methylation, acetylation, ubiquitination, or phosphorylation. Each individual modification alone does not give the listener a song. But, together every single one of the grooves produces a harmonious symphony of musical notes that form music, just like the sum total of all the epigenetic markings results in a perfectly functioning cell capable of responding appropriately to stimuli and carrying out complex processes necessary for life.

Now imagine you own that record for many years, playing it constantly. Eventually, the record will inevitably accumulate a few scratches, perhaps some dust and dirt, that interfere with the reading of the record on the record player. Those perfectly placed grooves no longer come together to form a beautiful song but instead end up eventually sounding uncoordinated and messy. With enough scratches and dents built up from normal wear and tear, the record will start to skip often, and the songs won’t make much sense to the listener anymore. This is analogous to the aged epigenome, which has inevitably acquired flaws as a result of normal aging processes. The resulting epigenome is not as harmonious as it once was, leading to overstimulation or suppression, inappropriate expression of certain pathways, and dysregulated cellular activities. Consequently, disease occurs along with phenotypic changes we associate with aged individuals, such as muscular decay, vision and hearing loss, cognitive decline, and metabolic dysfunction.

The inevitability of aging would lead one to conclude that such a scratched-up record was doomed to never play the same music it once did. However, if one possessed a cloth and cleaning solution that could wipe away all the dirt and imperfections on the record, it would seem that it is indeed possible to reverse these deleterious effects. ERA technology is able to do just that. By “cleaning up” the aged cell’s epigenome, ERA can restore the cell to a more youthful state capable of functioning at the same capacity it once did. The beauty of ERA technology is that there is no manipulation done on the genomic level; in other words, no permanent changes are made to the record. ERA simply allows the record to play the same music it always did, never wiping away its memory completely but instead helping it to remember how to play that music smoothly and flawlessly.

2020 SRF Summer Scholar Profile: Mikayla Stabile

Mikayla is a rising senior working towards her bachelor’s degree in molecular biology at Harvey Mudd College. She previously worked as an intern for two summers in the Blish Lab at the Stanford University School of Medicine, where she researched NK cell recognition of influenza surface proteins and conducted an HIV cloning project. As part of the SRF Summer Scholars Program, she worked at the SRF Research Center under the guidance of Dr. Amit Sharma. Dr. Sharma is focused on studying how aging and cellular senescence affects the immune system, specifically methods to strengthen and focus the immune response to better target senescent cells.

Cellular senescence occurs when cells are exposed to a form of genetic damage, causing them to enter a state of permanent proliferation arrest. Senescent cells are known to accumulate with age and have been found to be linked with many age-related diseases, including osteoarthritis, atherosclerosis, and cancer. Stopping this accumulation of senescent cells is currently being investigated as a potential therapy for preventing the development of age-related diseases. In particular, Dr. Sharma’s team focuses on enhancing natural killer (NK) cell targeting of senescent cells. NK cells are a type of lymphocyte in the immune system that play a critical role in killing infected and diseased cells. Mikayla’s project involved investigating the effect of specific soluble serum factors produced by senescent cells that are known to reduce NK functionality. She tried to determine whether blocking or removing these factors would increase NK-mediated killing of senescent cells. To test this, she co-cultured NK cells with senescent human fibroblast cells in media with specific soluble factors that have either been removed or blocked with a drug. Then, she measured the amount of killing that occurs using a number of cytotoxicity assays.

Everyone on the planet experiences the process of aging and countless individuals have faced the negative effects of the age-related diseases that have been linked so closely with senescence. Investigating senescent cell accumulation will expand current knowledge on age-related diseases and has the potential to offer new insights into future therapies that prevent and treat such conditions.

2020 SRF Summer Scholar Profile: Rithika Senthilkumar

My name is Rithika Senthilkumar, and I am a rising junior at the University of Massachusetts Amherst. I study Biochemistry and Molecular Biology and have had the pleasure of working in Dr. Heather Richardson’s Neurobiology of Stress and Addiction Lab. Dr. Richardson’s research focuses on using rodent models to study the neural, behavioral, and hormonal factors contributing to stress and addiction vulnerability. Under the mentorship of Dr. Said Akli, I have been working in a research team to determine how alcohol impacts myelin (a protein-lipid insulation that covers the axons of neurons and allows electric impulses to be carried through the axons) in the prefrontal cortex of adolescent mice and the underlying mechanisms contributing to these developmental changes. This research aims to gain insight into the effects that adolescent binge drinking has on myelination and development in the adolescent brain, contributing knowledge to better understand and characterize alcohol abuse and other substance abuse disorders. This summer, I have been working at the Sanford Consortium for Regenerative Medicine in La Jolla, CA under the mentorship of Ruslan Nuryyev in Dr. Evan Snyder’s Lab. The Snyder Lab’s research is focused on using stem cell biology to study neurological development, model neurodegenerative disease, and discover injury and disease therapeutics. Due to the COVID-19 pandemic, the Snyder Lab’s focus has expanded to study SARS-CoV-2 infection.

My project at the Snyder Lab this summer involved developing an organoid model to study SARS-CoV-2 infection in the central nervous system. Organoids are essentially miniature organs in a dish. They are developed to structurally and functionally mimic an organ and are widely used as models to study development and disease. Especially when it comes to the brain and nervous system, organoids are a great tool because they allow for the study of various neurological and neurodegenerative diseases without presenting ethical or technical difficulties.

My project aimed to study SARS-CoV-2 infection using an organoid model of the brain’s cerebral cortex. Even though respiratory symptoms are the most common symptoms for COVID-19, neurological symptoms, including stroke, have been reported. An organoid model of the brain can be used to address some of the ever-evolving questions about how the SARS-CoV-2 virus affects the brain. The organoids that I developed also incorporated blood vessels, which have been known to be one of the key viral entry sites for SARS-CoV-2.

I differentiated embryonic stem cells into vascularized cerebral organoids, which were characterized for both their neuronal and vascular formation to verify that they were differentiated appropriately. To study the virus’s interaction with the organoids, a SARS-CoV-2 pseudovirus was transfected into the organoids. The pseudovirus includes only the spike protein (the protein on the outer surface that is responsible for viral entry) but not any other viral components. The analysis of these organoid samples determined what percentage of cells in the organoid was infected, which specific cell types are the most targeted, which cell types contain the ACE2 receptor (this receptor has been shown to be responsible for viral entry in other tissues), and whether the ACE2 receptor is necessary for viral entry into cells. Answers to these questions enables further investigation into how SARS-CoV-2 affects the central nervous system as well as the role of the ACE2 receptor in facilitating cellular entry.

2020 SRF Summer Scholar Profile: Matangi Kumar

My name is Matangi Kumar, and I am a rising senior at the University of California, Davis with a major in Genetics and Genomics and a minor in Psychology. At UC Davis, I am a part of Dr. Megan Dennis’s lab which focuses on studying human genetics, evolution, and disease genetics by identifying previously uncharacterized genes that have been duplicated in the human genome, better known as human specific segmental duplications. In this lab, I am working with my mentor, graduate student Aarthi Sekar on a project entitled “Characterizing Human Specific Segmental Duplications and its role in the Evolutionary Expansion of the Human Neocortex.” As part of the SRF Summer Scholars Program, I have been working in Dr. Evan Snyder’s lab at the Sanford Consortium for Regenerative Medicine with my mentors, Dr. Sandra Leibel and Rachael McVicar. The Snyder lab’s research focuses on stem cell biology to understand normal development and recovery from injury and diseases, especially those related to age-related diseases.

My project at the Snyder lab has been to generate a vascularized lung in vitro model from induced pluripotent patient-derived stem cells (iPSCs) to study the effects of surfactant protein B deficiency. An in vitro system uses a controlled environment under artificial conditions unlike an in vivo system that conducts experiments in living organisms. Surfactant Protein B (SPB) plays a critical role in healthy lung function by decreasing the surface tension and preventing the collapse of alveoli, the tiny air sacs of the lungs. SPB deficiency leads to alveoli collapse after exhalations and fluid in the lungs which lead to fatal implications. SPB deficiency is common in premature babies, where their lungs are not finished forming, but it is also present in the aging population because changes in surfactant production can change as people age. SPB deficiency is also implicated in the deadly disease, acute respiratory distress syndrome (ARDS). Current studies examining SPB deficiency have focused on epithelial-only models, which consist of only one cell type. However, to create a more accurate lung model, multiple cell lines such as endothelial or vascular cells need to be incorporated. Vasculature plays an important role in studying ARDS because changes to the endothelium can propagate inflammation. Because there have been very few studies looking at vascular integrity in SPB models, I am interested in developing an in vitro model to study SPB deficiency, specifically from iPSC lines, due to superior reproducibility compared to an in vivo model. This system also has the novel ability to develop patient-specific therapies because these iPSC cell lines can be developed from patients. While previous SPB-deficient and gene therapeutic models have been conducted in in vitro models, these models have not studied the relationship between epithelial alveolar type II cells and the endothelium. My project focuses on studying the integrity of endothelium in vascularized lung organoids derived from cells with functional SPB gene, cells that are SPB-deficient, and cells in which the SPB deficiency has been corrected to elucidate the need for pulmonary vasculature integrity in preventing the fatal progression of SPB deficiency.

2020 SRF Summer Scholar Profile: Gabrielle Klemme

My name is Gabby Klemme, and I am a senior majoring in biochemistry at Iowa State University. At Iowa State, I work in a biochemistry laboratory with Dr. Eric Underbakke, studying scaffolded signaling complexes. Specifically, my project focuses on creating a fluorescence dye that can be used to identify a Halo tag when coupled to it. A Halo tag is a protein that forms a complex when bound to a molecule, and the complex is then used to bind to another protein that is of interest. Through my Halo protein expression system, I re-engineered a gene construct to allow for ample purification, so that I may have a pure source of Halo tag for testing. This summer, I am working at the Sanford Consortium for Regenerative Medicine in Dr. Evan Snyder’s laboratory. With Dr. Snyder and my mentor, Rus Nuryyev, we are focused on studying the biology of stem cells and their roles in the tissues involved in maintaining the body’s stable internal state, developmental biology, and recovery from injury and disease. However, our current research focus has shifted to studying the relationship between stem cells and SARS-CoV-2 with my project looking at neural stem cells and their connection to the SARS-CoV-2 route of entry.

As more COVID-19 cases arise involving patients with neurological symptoms, such as headaches and disturbed consciousness, understanding the relationship between this virus and the central nervous system (CNS) has become vital. The virus responsible for COVID-19, named SARS-CoV-2, enters cells through the binding of the spike (S) protein on the virus to the angiotensin converting enzyme 2 (ACE2) receptor on the host cell. SARS-CoV-2 could cause severe neurological injury, further justifying the need for a better understanding of the virus and the different cell types and body systems it can affect. Thus, my project will look at the relationship between SARS-CoV-2 and cortical interneurons and will establish how the virus enters these neurons to cause infection. Cortical interneurons are a type of neuron found in the brain and are involved in regulating other types of neurons called excitatory neurons. Cortical interneurons regulate or inhibit the number of signals that are sent throughout the brain and nervous system. However, when they malfunction, they are not able to control the excitatory neurons causing overstimulation which is linked to neurological diseases, such as schizophrenia and epilepsy.

Since we are seeing neurological symptoms with COVID-19 infections, I proposed that neurons in the human body express the ACE2 receptor which binds to the S protein on SARS-CoV-2, allowing the virus to enter and infect the cells. To identify how SARS-CoV-2 enters neurons, I grew a cortical interneuron brain organoid, or a simplified brain grown in the laboratory, and later infected it with the virus. Finally, through the use of a confocal microscope, I visualized the neurons, virus, and ACE2 receptor to determine the appropriate SARS-CoV-2 route of entry into neurons. The most significant impact of this project is that the results will allow us to gain a better understanding of SARS-CoV-2 and how it can cause the neurological symptoms that are becoming more common. Furthermore, determining the route of entry SARS-CoV-2 takes into neurons can help develop therapeutics that target and prevent the virus from entering.

2020 SRF Summer Scholar Profile: Atharwa Mankame

My name is Atharwa Mankame. I am a senior at the University of Texas at Austin. I am a biomedical engineering major, and I work in Dr. Laura Suggs’ Biomaterials and Therapeutics Laboratory. Under the guidance of my graduate student mentor, Jessica Widman, I study the use of nanoparticles for drug delivery in order to stimulate the polarization of immune cells. My research has investigated optimal nanoparticle shapes for intratumoral accumulation, and I am currently working on testing various coupling chemistries for delivering drugs in vivo. As a 2020 SRF Summer Scholar, I interned with Underdog Pharmaceuticals. Underdog Pharmaceuticals is working toward developing a disease modifying treatment for atherosclerosis using modified cyclodextrins. Underdog’s drug treatment seeks not only to treat heart disease but also to reverse the damage it causes and revert the inflamed blood vessels back to a functioning healthy state.  

Underdog Pharmaceuticals is a for-profit spinoff of SENS Research Foundation. Being a startup company, Underdog faces certain challenges that I was able to learn about and work with the Underdog team to address. My summer project had me work with Michael Kope, co-CEO of Underdog Pharmaceuticals. I researched venture capital firms that could serve as potential Series A investors. My research involved studying a firm’s finances, investment history, interest in our product, and creating a database of all potential investors to best guide our own investment strategy. As my project progressed, I also worked slide decks for our proposals including the deck for the California Life Science Institute FAST Advisory Program. Concurrently with the VC firm reports, I also created reports directly on previously successful companies within the rejuvenation, cardiovascular, and small-molecule therapeutics sphere. This project will aid the decision making of the Underdog Pharmaceuticals board as it seeks investors for Q1 2021 Series A investment by compiling data on the most appealing investors and identifying key timeline events of previous companies.

2020 SRF Summer Scholar Profile: Dennis Gong

My name is Dennis Gong. I am a Biomedical Engineering and Applied Math & Statistics major at Johns Hopkins University. At Johns Hopkins, I work in Dr. Jordan Green’s immunoengineering and drug delivery lab, working on improving the potency of artificial antigen presenting cells (aAPCs) to improve immune stimulation with graduate student Savannah Est Witte. This summer, I am working in Dr. Michael Snyder’s multi-omics focused lab with Dr. Lihua Jiang to study the proteomic signatures of aging. In general, the Snyder Lab works to develop and use a variety of approaches to analyze genomes (DNA), transcriptomes (RNA), proteomes (protein), and regulatory networks, applying these approaches to understand human variation and health. My particular project involved understanding upregulated and downregulated protein pathways in aging to develop organ-specific maps of aging regulatory networks.

Aging is a dominant risk factor for many diseases, including cancer, cardiovascular disease, and neurodegeneration, and is associated with a variety of molecular changes including telomere attrition, DNA damage, mitochondrial dysfunction, and immune impairment. While exploratory studies in model animals have demonstrated the possibility of health and life extension with various intervention strategies, a targeted investigation of the molecular signature of aging may provide new insights. High-throughput -omics datasets have provided a more comprehensive map of molecular changes and have shown that aging is distinct at molecular, cellular and tissue levels. My project provides a proteome level characterization of age-related molecular changes in order to identify age-associated proteins and relevant biological pathways.

The Genotype-Tissue Expression (GTEx) project has sequenced human tissue samples from 1000+ people and 56 organ types, with 12,000+ measured proteins. The GTEx cohort contains all age groups, and includes transcriptome, genome, and proteomic data. Using linear regression methods, associations between protein expression and age can be developed. The result of this correlation analysis will be a list of aging-associated proteins that can be cross-referenced with similar analyses of genomic and transcriptomic data to elucidate aging-related pathways and develop aging biomarkers. These biomarkers are essential for developing a quantitative clinical understanding of disease, which can be used to measure the efficacy of therapeutics in clinical trials and give clinicians a quantitative understanding of the ‘molecular age’ of their patients to inform risk of developing disease. Additional uses might include identifying appropriate trial groups to segment the patient population as well as developing therapeutic targets.

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