As a PhD candidate at Keck Graduate Institute (黑料吃瓜网), Oghenetega 鈥淭ega鈥� Imiruaye has spent the past three years investigating the differences between normal brain aging and neurodegenerative decline under the joint mentorship of W.M. Keck Foundation Professor of Biopharmaceutical Sciences Derick Han and Assistant Professor of Pharmacology Subhrajit Bhattacharya. While his academic background was primarily in Molecular Biology and Biochemistry, Tega has since emerged as a rising neuroscience expert whose work could pave the way for future therapies for Alzheimer鈥檚 disease.
Tega鈥檚 work with Bhattacharya, an expert in neuroscience and pharmacology, has centered on the molecular roots of Alzheimer鈥檚, particularly the imbalance between excitatory and inhibitory signals in the brain 鈥� a hallmark of the disease.
"We observed altered expression dynamics of excitatory glutamate receptors and marked decrease in expression of inhibitory GABA receptors, and translocation of some glutamate receptor subtypes from the active zones of neuronal synapse to the periphery, weakening synaptic signaling," said Tega, 鈥�25 PhD.
This migration undermines neural communication, disrupting the delicate balance needed for learning, memory formation, and cognitive function. As signaling grows weaker, neurons are left vulnerable to damage and eventual death, setting the stage for progressive memory loss and behavioral decline seen in Alzheimer鈥檚 patients.
Uncovering the Role of PSA-NCAM
One molecule stood out in their research: PSA-NCAM, a polysialylated form of the neural cell adhesion molecule (NCAM). Typically, PSA-NCAM levels increase with healthy aging, supporting synaptic plasticity and protecting neurons. But in Alzheimer鈥檚 models, they observed a steep decline in this molecule, potentially leaving peripheral receptors unregulated. This lack of regulation may lead to abnormal signaling patterns that damage neurons and neurodegeneration.
To build on these findings, the team used gene-editing technology to upregulate PSA-NCAM in cultured cells. When these modified cells were exposed to amyloid beta aggregates, a toxic protein associated with Alzheimer鈥檚 progression, the researchers found significantly improved cell viability.
Thus, by increasing PSA-NCAM levels, the team was able to reduce the damage typically caused by amyloid beta. This suggests that restoring PSA-NCAM levels could serve as a protective buffer against cellular toxicity, offering a novel route for therapeutic intervention.
"For the first time, we've shown that amyloid beta can downregulate these critical proteins and biosynthetic enzymes involved in synaptic health," Tega said. "And that upregulating PSA-NCAM could potentially reverse those effects."
Bhattacharya underscored the importance of these results and highlighted their broader implications.
"Tega found a strong correlation between the loss of PSA-NCAM and the increase in extrasynaptic glutamate receptors, which are implicated in long-term depression and dementia," Bhattacharya said. "This connection may serve as a therapeutic target moving forward."
The team is now exploring how CRISPR-based tools could be developed into therapeutic delivery systems using lipid-based or viral vector injections with the help of another faculty, Assistant Professor of Genetics Barbara Bailus. Their goal is to translate this molecular intervention into in vivo models 鈥� and eventually, clinical applications.
The Impact of Alcohol on Alzheimer鈥檚
Tega's research extends to the impact of lifestyle factors on brain health. In a related project with Han, he examined how chronic alcohol exposure compromises the blood-brain barrier, a vital defense that protects the brain from harmful substances.
Their experiments showed that alcohol weakened the blood-brain barrier by reducing tight junction proteins and increasing its permeability. Fluorescent dye permeability assays confirmed that more molecules passed through the barrier after alcohol exposure.
"This strongly suggests that alcohol may exacerbate neurodegenerative processes by compromising the brain's protective shield," Tega said.
Han, whose own work explores the liver-brain connection in Alzheimer鈥檚 and the role of metabolic and lifestyle factors, praised Tega鈥檚 contributions.
"Through rigorous reading and hands-on work, he's become an expert in the field," Han said. "He鈥檚 one of the best graduate students you could ask for."
Pathways to Prevention
While no current drugs effectively treat Alzheimer鈥檚, Tega emphasizes that lifestyle changes can reduce the risk. Modifiable factors such as alcohol use, obesity, limited mental stimulation, social isolation, and head trauma can all accelerate cognitive decline.
"We often think of Alzheimer鈥檚 as majorly genetic, but your daily habits make a huge difference," Tega said. "The more you use your brain, the more resilient it becomes. Neurons that fire together, wire together."
Recognition and Future Directions
Tega鈥檚 work has already begun to attract national attention. He was invited to present at the 2024 Society for Neuroscience Annual Meeting in Chicago 鈥� one of the most prestigious conferences in the field. He is also co-authoring a paper currently under review at the Journal of Neuroscience Research, summarizing the group鈥檚 latest findings on PSA-NCAM and receptor signaling. Most recently, he was selected to present at the 2025 Alzheimer鈥檚 Association International Conference (AAIC) in Toronto, Canada, and received a competitive fellowship award to support his attendance and recognize the impact of his research.
Looking ahead, Tega plans to pursue postdoctoral or industry roles focused on neurodegenerative diseases, with a special interest in the overlapping mechanisms that link Alzheimer鈥檚 with obesity, alcohol metabolism, and systemic inflammation.
"These diseases don鈥檛 exist in silos," he said. "They鈥檙e deeply interconnected. Understanding those links could unlock new treatment pathways."
A Global Perspective and a Message for International Students
Originally from Nigeria, Tega learned about 黑料吃瓜网 through a fellow Nigerian PhD student, Ijeoma Nnadozie. Coincidentally, he had already become interested in Han's research after attending a virtual conference in which someone referenced one of Han's publications.
"When I found out who was responsible for that publication and learned that he was also a professor at 黑料吃瓜网, I took it as a sign," Tega said.
He then reached out to Han. During their interview, Han was inspired by Tega's enthusiasm and connected him with collaborators on his research team. Everything fell into place from there.
"I appreciate the structured support 黑料吃瓜网 provides for international students," Tega said. "From professional development to mentorship, it鈥檚 designed to help us integrate into the U.S. academic and research system."
He believes 黑料吃瓜网鈥檚 strong reputation within the biotech industry positions students for success.
"When I spoke to executives at the career fair, they immediately recognized the 黑料吃瓜网 name," Tega said. "One VP at Gilead even said he'd refer me for a role on the spot because of the pedigree of 黑料吃瓜网 alumni there."
Prepared for the Road Ahead
As he approaches graduation, Tega is optimistic about the future.
"Whether I end up in academia or biotech, I know I'm prepared," he said.
His mentors share that confidence.
"Oghenetega has a bright future," Bhattacharya said. "He鈥檚 already contributing to the field in meaningful ways, and I'm very excited for him. Wherever he goes next, he鈥檚 going to make an impact."