To support JAX’s dual mission of discovery and education, we continually strive to provide cutting-edge, unique, and highly relevant training opportunities designed to prepare all JAX trainees for successful scientific careers.
Our NIA T32–funded Training Program in Precision Genetics of Aging and Dementia (PGAD) provides high-quality graduate and postdoctoral training to prepare trainees for careers as independent investigators in universities, research institutions and the biomedical industry. It brings together more than 16 highly productive and well-funded faculty mentors at the JAX Mammalian Genetics campus in Bar Harbor, ME and the JAX Genomic Medicine Campus in Farmington, CT who provide a uniquely interdisciplinary, integrated and comprehensive training environment. Research foci within the context of aging and age-related disease include mammalian genetics, hematology, vascular biology, immunology, nephrology, neurology, behavior, microbiome, systems genetics, and bioinformatics.
The T32 provides two slots for postdoctoral fellows and two predoctoral students. JAX participates in collaborative Ph.D. training programs with the Tufts School of Medicine, the University of Maine, and the University of Connecticut that have grown to critical mass.
We have also developed a T32 network for Aging (with the University of Arizona) and Alzheimer’s disease (with Indiana University and the University of Kentucky).
For more details on JAX training programs see…
| Postdoctoral Appointments | Mentor | Research Project | Fellowship/other support |
|---|---|---|---|
| Tamar Abel | Greg Carter | I am interested in better understanding the contributions of lipid biology to Alzheimer's disease (AD). Altered lipid profiles have been associated with AD. Additionally, many late-onset AD (LOAD) risk alleles are in genes involved in the process of lipid metabolism, including the most significant LOAD risk allele, APOE4. There is a reported genetic interaction between the AD risk gene APOE and cholesterol ester transfer protein (CETP). Furthermore, mice lack functional CETP which is critical to the balance of circulating lipoproteins; this imparts cardioprotective effects and may make mice resistant to AD. This project aims to determine molecular signatures in AD mediated by CETP with an emphasis on molecular pathways shared with APOE as a potential disease-altering mechanism. I am accomplishing this through the use of multi-omic datasets from both humans and mouse models. As part of this project, I am characterizing existing transgenic humanized CETP (hCETP) mouse models and working with the MODEL-AD consortium on a novel knock-in hCETP mouse. Computational strategies employed to analyze these datasets include trans-species analyses which have been designed to effectively compare mouse model data to relevant AD omic signatures from human cohorts. This study has significant relevance to public health since it will provide valuable insights into the role that lipids play in AD and may also pave the way for improved mouse models of AD. |
MODEL-AD (5U54AG054345-08) KOOB GRANT (1RF1AG079125-01) |
| John Bachman | Nadia Rosenthal | During postnatal muscle growth, muscle stem cells (satellite cells, SCs) divide and give rise to progenitors that fuse to developing muscle fibers. Fibro-adipogenic progenitors (FAPs) have been documented to play a role in dictating SC proliferative ability and ability to differentiate. To understand the role of FAPs in postnatal muscle development, I am currently breeding an inducible depletion model (PDGFRaCreER/+; Rosa26DTA/+) in which I will deplete FAPs at 4 weeks of age to assess the effects on SC proliferation, myofiber size, and myonuclear number. Additionally, I am investigating the role of IGF-1 signaling in dictating SC fate during postnatal development. | N/A |
| Predoctoral Appointments | Mentor | Research Project | Fellowships/other support |
| Jaycee Choi | Vivek Kumar | Since receiving T32 funding in Sept. 2023, Jaycee has continued work to quantify spatial learning and cognitive flexibility in aging and Alzheimer’s disease mouse models. Jaycee has made progress with analysis on reversal learning experiments of young adult C57BL/6J mice in a maze assay. Jaycee has also run aged C57BL/6J experiments at 15-months and 27-months to test age-related decline in spatial navigation and subsequent reversal learning of spatial navigation. Results show that young C57BL/6J mice learn to take perfect paths to the sugar pellet reward at a higher rate than another equivalently located node in the maze. | N/A |
| Emily Nickerson | Erik Bloss | The primary objective of Emily’s project is to identify the rules governing the transcellular spread of tau and to evaluate the intracellular consequences of the aggregation of the protein. | N/A |
| Postdoctoral Appointments | Mentor | Research Project | Fellowships/other support |
|---|---|---|---|
| Alaina Reagan | Gareth Howell | 1) The aging cohorts I established reached their target ages, and the resulting data is currently being assessed. 2) Generated a novel conditional knock-in model to examine the MTHFR variant in target cell populations. 3) Initiated and maintained collaborations with two groups at Indiana University in order to incorporate both animal and human in vivo brain imaging in my project. |
Received a 2-year fellowship from the BrightFocus Foundation Alzheimer’s Disease Research Program that providies support for this project. |
| Brittany Angarola | Olga Anczukow | Dr. Angarola’s research is aimed at uncovering the link between aging breast biology and the increased incidence of breast cancer in aged breast tissue. | During her Ph.D. training, Dr. Angarola was supported by an NIH T32 (5T32GM007223-38), a Gruber fellowship, and the NSF graduate research fellowship. She is currently supported by the NIA-funded T32 Training Program in Precision Genetics of Aging, Alzheimer's Disease and Related Dementias (PGAD). |
| Jennifer SanMiguel | Jennifer Trowbridge | Dr. SanMiguel aims to 1) understand the cellular and molecular changes that occur in hematopoietic stem and progenitor cells that lead to hematological disorders and 2) use genetic mouse models of the complement gene, CR1, to dissect long vs short isoforms on their ability to influence altered inflammation and development of AD pathology from the periphery. | Dr. SanMiguel was supported by an NRSA F31 fellowship during her PhD training and a previous T32 through NICHD during the beginning of her postdoc. |
| Michael Maclean | Gareth Howell | Dr. Maclean hypothesizes that microglia contribute to the development of diabetic retinopathy and have unique transcriptional programs not found in otherwise healthy tissues. To test this hypothesis, his proposal includes two aims: (1) examine microglial diversity in obese type II diabetic murine central nervous system (CNS) tissues and (2) examine microglial states over time in type I diabetic CNS tissues. | N/A |
| Cara Hardy | Ron Korstanje | Voiding function and behavior are impacted in individuals with Alzheimer’s Disease (AD).The primary focus of Dr. Hardy’s work has been optimizing the Void Spot Assay (VSA) and the associated image analysis to be used on the numerous AD-associated pathology models available through MODEL-AD (JAX). We have worked to develop a novel analysis tool that is significantly easier to use than available applications. This application is in the final phases of development and will be released open-source to the scientific community. | N/A |
| Predoctoral Appointments | Mentor | Research Project | Fellowships/other support |
| Teresa Easterbrooks | Ron Korstanje | Teresa aims to elucidate how senescence and senescence-targeting drugs (senolytics) function, particularly focused on a genetically diverse population, as preliminary data from Dr. Korstanje’s lab has shown that senescence varies with genetic background. | N/A |
| Sarah Heuer | Gareth Howell & Catherine Kaczorowski | Completed deriving 10-15 embryonic stem cells lines for 14 B6xBXD mouse strains, analysis of AD-BXD single nuclear RNAseq comparison glia populations from resilient and susceptible strains, expansion of Lag3-KO-5XFAD mouse colony for candidate validation. | N/A |
| Elli Hartig | Basile Tarchini | A group of five proteins; MYO15A, WHRN, GPSM2, GNAI, and EPS8, are together referred to as the stereocilia elongation complex (EC). The primary hypothesis of this proposed research is that EC proteins play an active role in the maintenance of mature hair cells | Elli submitted an F31 application to the NIH National Institute of Deafness and Other Communication Disorders (NIDCD). Her application was reviewed and received an impact score of 16 (percentile not available for NIDCD fellowships). The application was recommended for funding and is currently pending administrative review. The F31 award is projected to begin July 1, 2022. |
| Ryan Englander | Olga Anczukow | Ryan is leveraging advances in long-read RNA sequencing to interrogate tumor transcriptomes and understand how aging-related changes in alternative splicing may impact cancer risk and prognosis. He is focusing on lung adenocarcinoma (LUAD) and breast cancer, which are among the leading causes of cancer burden and mortality in the United States. | N/A |
| Brianna Gurdon | Catherine Kaczorowski | Brianna proposes to validate the relationship between Lrfn2 expression and cortical AD-related neurodegeneration by creating an Lrfn2 overexpression mouse model. Neurodegeneration, dendritic spine morphology, and memory performance will be measured to determine whether increased Lrfn2 expression could rescue some of the detrimental effects of AD. | N/A |
We use cookies to personalize our website and to analyze web traffic to improve the user experience. You may decline these cookies although certain areas of the site may not function without them. Please refer to our privacy policy for more information.