Temitope Adeoye

tadeoye{at}usf{dot}{edu}

Hey there, thanks for stopping by! 👋

I’m a Physicist and PhD candidate in Computational Neurobiology at the University of South Florida, working in Dr. Ghanim Ullah’s lab. My research essentially revolves around looking at a bit of biology and seeing how it can be reduced to variables and equations.

I currenlty lead projects across genomics and biophysics, where I specifically apply systems biology strategies to uncover the cell-type-specific mechanisms of synaptic dysfunction in Alzheimer’s disease and related dementias. These methods primarily involve:

Theoretical and computational tools/methods for problems in whole cell biophysics and
Bioinformatics, network biology, and statistical techniques for problems in single-cell genomics (scRNA-seq), epigenomics (scATAC-seq), and spatial transcriptomics.

I recently interned on the Computational Biology team at Cajal Neuroscience, where I developed Machine Learning pipelines for single-cell multi-omics data analysis to help guide the interpretation of experiments on in-house disease models for target prioritization in in-vivo/vitro screening platforms.

As a scientist, I’m broadly interested in all aspects of computational biology for complex brain diseases and aging, machine learning applications in single-cell biology and drug discovery, and development of bioinformatics methods and pipelines.

Outside of research, my favorite activities are playing soccer, running, reading, gaming, and spending time with friends and family.

Want to dive deeper? Check out my previous works here.

news

Feb 26, 2025	I’m happy to announnce that this summer I’ll be joining the Regeneron Genetics Center as a PhD intern with the Neuroscience and Ophthalmology Therapeutic Area Genetics team. I’ll be working on connecting GWAS hits to drug response mechanisms in Tahoe-100M perturbation study. This project will address a fundamental question in precision medicine regarding how germline genetic variants identified through population-level GWAS studies manifest their effects at the cellular level, and how the effects interact with pharmacological interventions. Super excited to work on this with Ernst Mayerhofer and Sahar Gelfman.
Sep 12, 2024	I gave a talk at the annual meeting of Synapses Under Stress (RU 2795), hosted by Prof. Jürgen Klingauf at the University of Münster, Germany. My talk was titled *Alzheimer’s Disease-associated Intracellular Calcium Dyshomeostasis Leads to Impaired Presynaptic Function*, and I shared key results from the initial phases of my thesis. This work focuses on the cellular level disruptions associated with Ca²⁺ signaling in Familial Alzheimer’s Disease (FAD), including the effects of disrupted Ca²⁺ signaling on neurotransmitter release and synaptic plasticity in an in-silico model of FAD, and how Aβ-mediated cation pore formation modulates presynaptic Ca²⁺ dynamics and the downstream effects on exocytosis in-silico.
Aug 26, 2024	I’m honored to be awarded the Trainee Professional Development Award (TPDA) by the Society for Neuroscience (SfN) for SfN24. This award is given to graduate students demonstrating scientific merit and excellence in research and will support my attendance at the annual SfN meeting in Chicago this year. I’ll be presenting a poster on our lab’s recent work at the Early Career Poster Session on Saturday, October 5 from 6:30 PM – 8:30 PM and at the Alzheimer’s Disease: Genetics poster session PSTR446 (board Number: C59) on Wednesday, October 9 fro 1:00 PM - 5:00 PM. If you’re attending SfN24, I’d be delighted to connect and discuss our work . This wouldn’t have been possible without the invaluable guidance and support of my PI, Prof. Ghanim Ullah, at the University of South Florida.

selected publications

Systematic Analysis of Biological Processes Reveals Gene Co-expression Modules Driving Pathway Dysregulation in Alzheimer’s Disease

Temitope Adeoye, Syed I. Shah, and Ghanim Ullah

Aging and disease, 2024

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Alzheimer’s disease (AD) manifests as a complex systems pathology with intricate interplay among various genes and biological processes. Traditional differential gene expression (DEG) analysis, while commonly employed to characterize AD-driven perturbations, does not sufficiently capture the full spectrum of underlying biological processes. Utilizing single-nucleus RNA-sequencing data from postmortem brain samples across key regions—middle temporal gyrus, superior frontal gyrus, and entorhinal cortex-we provide a comprehensive systematic analysis of disrupted processes in AD. We go beyond the DEG-centric analysis by integrating pathway activity analysis with weighted gene co-expression patterns to comprehensively map gene interconnectivity, identifying region- and cell-type-specific drivers of biological processes associated with AD. Our analysis reveals profound modular heterogeneity in neurons and glia as well as extensive AD-related functional disruptions. Co-expression networks highlighted the extended involvement of astrocytes and microglia in biological processes beyond neuroinflammation, such as calcium homeostasis, glutamate regulation, lipid metabolism, vesicle-mediated transport, and TOR signaling. We find limited representation of DEGs within dysregulated pathways across neurons and glial cells, suggesting that differential gene expression alone may not adequately represent the disease complexity. Further dissection of inferred gene modules revealed distinct dynamics of hub DEGs in neurons versus glia, suggesting that DEGs exert more impact on neurons compared to glial cells in driving modular dysregulations underlying perturbed biological processes. Interestingly, we observe an overall downregulation of astrocyte and microglia modules across all brain regions in AD, indicating a prevailing trend of functional repression in glial cells across these regions. Notable genes from the CALM and HSP90 families emerged as hub genes across neuronal modules in all brain regions, suggesting conserved roles as drivers of synaptic dysfunction in AD. Our findings demonstrate the importance of an integrated, systems-oriented approach combining pathway and network analysis to comprehensively understand the cell-type-specific roles of genes in AD-related biological processes.
Upregulated Ca2+ Release from the Endoplasmic Reticulum Leads to Impaired Presynaptic Function in Familial Alzheimer’s Disease

Temitope Adeoye, Syed I. Shah, Angelo Demuro, and 2 more authors

Cells, 2022

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Neurotransmitter release from presynaptic terminals is primarily regulated by rapid Ca2+ influx through membrane-resident voltage-gated Ca2+ channels (VGCCs). Moreover, accumulating evidence indicates that the endoplasmic reticulum (ER) is extensively present in axonal terminals of neurons and plays a modulatory role in synaptic transmission by regulating Ca2+ levels. Familial Alzheimer’s disease (FAD) is marked by enhanced Ca2+ release from the ER and downregulation of Ca2+ buffering proteins. However, the precise consequence of impaired Ca2+ signaling within the vicinity of VGCCs (active zone (AZ)) on exocytosis is poorly understood. Here, we perform in silico experiments of intracellular Ca2+ signaling and exocytosis in a detailed biophysical model of hippocampal synapses to investigate the effect of aberrant Ca2+ signaling on neurotransmitter release in FAD. Our model predicts that enhanced Ca2+ release from the ER increases the probability of neurotransmitter release in FAD. Moreover, over very short timescales (30–60 ms), the model exhibits activity-dependent and enhanced short-term plasticity in FAD, indicating neuronal hyperactivity—a hallmark of the disease. Similar to previous observations in AD animal models, our model reveals that during prolonged stimulation (~450 ms), pathological Ca2+ signaling increases depression and desynchronization with stimulus, causing affected synapses to operate unreliably. Overall, our work provides direct evidence in support of a crucial role played by altered Ca2+ homeostasis mediated by intracellular stores in FAD.