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BIOMED PhD Thesis Defense

Title: 
Uncovering Etiological Roles in the Development of Alzheimer’s Disease (AD)

Speaker: 
Michiko Thwe, PhD Candidate
School of Biomedical Engineering, Science and Health Systems
Drexel University

Advisor:
Garth D. Ehrlich, PhD, FAAAS, FAAM
Professor 
Department of Microbiology and Immunology
Department of Otolaryngology-Head and Neck Surgery
College of Medicine
Drexel University 

Details:
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, neuroinflammation, amyloid-beta deposition, and tau pathology. Emerging evidence suggests that microbial dysbiosis and chronic host–pathogen interactions may contribute to AD pathogenesis, challenging the long-standing assumption that the human brain is sterile. This dissertation investigates the potential etiological role of microbial communities in Alzheimer’s disease through spatial microbiome profiling, comparative neurobiobank analyses, and strain-level genomic characterization of Cutibacterium acnes.

Using full-length 16S rRNA sequencing, postmortem brain tissues from Alzheimer’s disease and age-matched control cohorts were analyzed to evaluate microbial community composition and determine whether detected microbial signatures represented authentic tissue-associated microbiota or postmortem contamination. Spatial edge-versus-core analyses demonstrated substantial overlap between microbial profiles, supporting the conclusion that the observed bacterial communities were unlikely to arise solely from autopsy-related contamination. Comparative analyses across independent neurobiobanks revealed modest regional and institutional variation while identifying reproducible microbial community structures associated with AD brain tissue. Diversity and ordination analyses further demonstrated overlapping yet distinct microbial patterns related to diagnosis, anatomical location, and cohort origin.

To further investigate the potential contribution of Cutibacterium acnes to neurodegenerative disease, comparative genomics and pan-genome analyses were performed on deep tissue-derived isolates. Whole-genome sequencing demonstrated broad phylogenetic diversity and an open accessory genome enriched with genes associated with adhesion, biofilm formation, oxidative stress response, and virulence-associated functions. Deep tissue isolates were distributed across multiple phylogenetic lineages rather than a single tissue-associated clade, supporting the hypothesis that multiple C. acnes strains may possess the capacity for tissue persistence and inflammatory potential.

These findings contribute to the growing field of neurodegenerative microbiome research and support further investigation into microbial contributions to Alzheimer’s disease pathogenesis and related neuroinflammatory disorders.

BIOMED PhD Research Proposal 

Title: 
Primary Mitochondrial Disease Patient Treatment and Characterization

Speaker:
Kelsey Keith, PhD Candidate
School of Biomedical Engineering, Science and Health Systems
Drexel University

Advisors:
Marni J. Falk, MD
Executive Director
Mitochondrial Medicine Frontier Program
Distinguished Endowed Chair
Department of Pediatrics
Children's Hospital of Philadelphia (CHOP)
Professor, Division of Human Genetics
Department of Pediatrics
University of Pennsylvania Perelman School of Medicine

Ahmet Sacan, PhD
Teaching Professor
School of Biomedical Engineering, Science and Health Systems
Drexel University 

Details:
Primary mitochondrial diseases (PMD) are a heterogeneous group of rare, inherited disorders caused by mutations in mitochondrial or nuclear DNA that disrupt mitochondrial function. Although two therapies received FDA approval in 2025, treatment options for most patients remain limited, and the mechanisms underlying the marked genotype–phenotype variability in PMD are poorly understood. This proposal seeks to improve understanding of PMD pathophysiology and therapeutic strategies by integrating unbiased multiomics profiling, high-throughput drug screening, and mechanistic studies to identify novel disease pathways, therapeutic targets, and candidate treatments. We hypothesize that comprehensive molecular characterization combined with whole-organism screening approaches will uncover conserved and mutation-specific mechanisms that drive PMD and reveal actionable therapeutic opportunities.

To address this hypothesis, we will perform transcriptomic and metabolomic profiling across multiple zebrafish models of PMD to characterize disease heterogeneity and identify dysregulated metabolic pathways and druggable targets. In parallel, we will leverage high-throughput screening of 2,560 FDA-approved compounds in C. elegans PMD models using fluorescent reporters of mitochondrial stress and function to identify candidate therapeutics and uncover previously unrecognized treatment targets. Finally, we will investigate the mechanism of action of cycloheximide, a compound found to improve mitochondrial disease phenotypes despite concerns regarding toxicity, through aptamer-based proteomics to define the specific pathways responsible for its therapeutic effects and guide development of safer targeted alternatives.

The expected outcomes of this work include the identification of reproducible therapeutic candidates suitable for preclinical development or clinical translation, particularly among already FDA-approved compounds, as well as the discovery of novel molecular targets and mechanistic insights into PMD biology. Collectively, this research will advance both the fundamental understanding of mitochondrial disease and the development of effective targeted therapies for patients with PMD.

   Need help with your résumé? This is the perfect time to ask your questions.

Register on Handshake :  drexel.joinhandshake.com/edu/events/1924750

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https://drexel.joinhandshake.com/edu/events/1932338

BIOMED PhD Thesis Defense

Title: 
Examining CX3CR1 Inhibition Across Murine Models of Tubulointerstitial Disease

Speaker: 
Joshua Gale, PhD Candidate
School of Biomedical Engineering, Science and Health Systems
Drexel University

Advisors:
Maria P. Martinez-Cantarin, MD
Associate Professor
Division of Nephrology 
Medical Director, Kidney and Pancreas Transplantation 
Director, Diabetes Research in ESRD and Transplant
Sidney Kimmel Medical College
Thomas Jefferson University

Fred Allen, PhD
Teaching Professor 
Associate Dean for Undergraduate Education
School of Biomedical Engineering, Science and Health Systems
Drexel University

Details:
Chronic kidney disease (CKD) is characterized by a progressive decline in renal function that frequently results in irreversible tubulointerstitial fibrosis. While the clinical etiology of CKD is diverse, in many cases, structural changes are heavily driven by a sustained, macrophage-mediated inflammatory response. The CX3CL1/CX3CR1 signaling axis is a recognized and critical mediator of this targeted immune cell recruitment. To target the inflammatory cascade, this research investigates the efficacy of AD-0145, a novel small-molecule competitive antagonist targeting the CX3CR1 receptor on infiltrating immune cells, across acute (folic acid), and chronic (oxalate and adenine) murine models of tubulointerstitial disease.

Utilizing both prophylactic and delayed therapeutic dosing regimens, disease progression was tracked in vivo via transdermal glomerular filtration rate (GFR) devices, and inflammatory and fibrotic markers were recorded among others. In both acute and established disease states, systemic administration of AD-0145 successfully prevented the accumulation of F4/80+ macrophages. Crucially, flow cytometric analysis revealed that this receptor blockade significantly reduced both infiltrating and kidney resident macrophage populations. This reduction in renal macrophage burden significantly suppressed the secondary inflammatory cytokine cascade, halted downstream myofibroblast-associated markers, and limited interstitial Collagen III deposition, ultimately preserving renal function. Of major importance, this research also shows that inhibiting fractalkine’s only known receptor, CX3CR1 reduces crystal presence in the oxalate model of CKD, a novel finding that has not been reported in the literature.

Beyond evaluating pharmacological efficacy, critical assessment of these murine models revealed sex- and weight-dependent disparities in disease susceptibility.

Ultimately, this research provides the first pre-clinical proof-of-concept for small- molecule CX3CR1 antagonism as a viable anti-inflammatory and anti-fibrotic therapy.