I am currently a Postdoctoral Fellow in Lupu lab at OMRF.
I am interested in the motor system, especially the spinal cord, as well as in aging
and neurodegeneration. Currently, I primarily write computer simulations to investigate
spinal cord function, based on the electrophysiology data collected by the lab. I am also
interested in space biology, which brings together all my favorite research topics, such as
motor system function (and how the space environment affects it), development
(and how different would it be in space), neurodegeneration and aging (space is known to drive
accelerated aging, which can be leveraged for studying aging on Earth as well,
for maturing organoids faster, and so much more!).
Research summary
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As a Research Trainee at OMRF in the Fulbright's Visiting Research Graduate Training Program (now BioLab), I investigated the role of Eco1 in yeast meiosis. This work became my master's thesis in Biotechnology at WBBiB UJ. A related study on its human orthologs, Esco1 and Esco2, was published in PNAS.
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My doctoral work focused on preventing age-related alpha-motor neuron (MN) loss. The full dissertation entitled "Preventing age-related alpha-motor neuron loss" is available here.
- Because spinal cord aging is understudied, I began by characterizing age-related changes in the mouse spinal cord (Chapters 1 and 2; published here). Among the main changes contributing to MN loss are upregulation of matrix metalloproteinases (MMPs), low-grade inflammation with astrocyte and microglia activation, and increased blood-spinal cord barrier permeability.
- The next chapters focused on preventing these changes using two approaches:
- A genetic approach (Chapter 3): knocking out MMP-9 and MMP-12 had differential, sex-specific effects on age-related alpha-MN loss and muscle mass decline.
- A pharmacological approach (Chapter 4): treatment with OKN-007 reduced age-related alpha-MN loss (published here) and improved muscle function in wildtype mice (published here; co-first author).
- I then showed that OKN-007 is also neuroprotective in an ALS mouse model, which exhibits accelerated alpha-MN loss. The treatment significantly slowed disease progression, although it did not delay disease onset (Chapter 5; published here; co-first author).
- Finally, and interestingly, troponins were among the proteins whose abundance increases with age in the spinal cord. Although not canonically associated with neural tissue, troponins have previously been found in neurons. In aged MNs, troponins I and T translocate to the nucleus, where they may compete with transcription factors for binding sites. Further research is needed to determine whether this age-related translocation is specific to troponins or reflects a more general age-related disruption of the nuclear envelope (Chapter 6).
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My work on neuronal aging and neurodegeneration also sparked an interest in neural development, since some developmental pathways could potentially be leveraged to tackle neurodegeneration. This led me to my first postdoctoral position at Georgia Tech, which resulted in multiple publications. During that time, I also became the lab's bioinformatician and began working with neuronal simulations. Thank you to the Stolfi lab for those fruitful years!
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My next postdoctoral position was fully computational and continued my path in neuronal simulation. In the Bagnall lab at WashU, I developed simulations of larval zebrafish spinal cord circuits based on electrophysiological data collected by the lab. Thank you to the Bagnall lab for this opportunity!