(Natural News)—Got memory loss? How about your parents or grandparents? There’s hope in science-based therapy. In two groundbreaking and complementary studies, Timothy Jarome, associate professor in Virginia Tech’s College of Agriculture and Life Sciences and the School of Neuroscience, and his graduate students have demonstrated how gene-editing tools can target age-related molecular changes in the brain to restore memory performance in older subjects.
Conducted on rats—widely recognized as a reliable model for studying memory and aging—these studies provide new hope for understanding and potentially reversing memory decline, a key factor in conditions such as Alzheimer’s disease.
- Targeting molecular aging in the brain: Timothy Jarome and his graduate students used advanced gene-editing tools to study and reverse age-related memory decline in rats, identifying specific molecular processes that can be modified to improve memory function in older subjects.
- K63 polyubiquitination and memory improvement: In the first study, the team discovered that aging alters K63 polyubiquitination—a key protein-tagging process—in both the hippocampus and amygdala. By using CRISPR-dCas13 to adjust these molecular levels, they successfully enhanced memory performance in older rats.
- Reactivating the IGF2 gene: The second study revealed that the memory-supporting IGF2 gene becomes silenced with age due to DNA methylation. Using CRISPR-dCas9 to remove these chemical tags reactivated the gene, restoring memory in older rats and demonstrating that precise molecular interventions can rejuvenate brain function.
- Collaborative graduate-led breakthroughs: Both studies, led by graduate students Yeeun Bae and Shannon Kincaid, highlight the importance of collaborative, student-driven research and show that targeting multiple molecular systems—not just one—may be key to preventing or treating age-related memory loss and Alzheimer’s disease.
Reversing memory loss through gene editing: Virginia Tech researchers uncover molecular pathways behind aging and memory decline
“Memory loss affects more than a third of people over 70,” Jarome explained. “It’s a major risk factor for Alzheimer’s. By pinpointing specific molecular changes that drive this process, we can better understand what goes wrong in dementia and begin developing new strategies for treatment.”
Targeting memory loss in key brain regions
The first study, published in Neuroscience and led by Jarome and doctoral student Yeeun Bae, focused on a cellular process known as K63 polyubiquitination. This process functions as a molecular “tagging” system that tells proteins inside the brain how to behave—helping neurons communicate and form memories.
The researchers discovered that aging disrupts K63 polyubiquitination differently across brain regions. In the hippocampus, a center for forming and retrieving memories, levels of K63 polyubiquitination increase with age, potentially impairing normal signaling. Using a sophisticated CRISPR-dCas13 RNA-editing system, the team reduced these levels and observed improved memory in older rats.
Conversely, in the amygdala, which governs emotional memory, K63 polyubiquitination declines with age. Surprisingly, by lowering it even further, researchers were able to boost memory performance.
“Together, these findings show how vital K63 polyubiquitination is to the brain’s aging process,” said Jarome. “In both brain regions, tweaking this one molecular process had a powerful effect on restoring memory.”
Reactivating a gene that supports memory
The second study, published in Brain Research Bulletin and led by Jarome with doctoral student Shannon Kincaid, examined another critical component of memory: the IGF2 gene, a growth-factor gene essential for memory formation. Over time, as the brain ages, this gene becomes chemically silenced in the hippocampus, reducing its beneficial effects.
“IGF2 is one of a few genes that’s imprinted—it’s expressed from only one parent’s copy,” Jarome explained. “When that single copy shuts down with age, you lose its protective benefits for memory.”
The researchers found that this silencing occurs due to DNA methylation, a natural process where chemical tags accumulate on a gene and switch it off. Using CRISPR-dCas9, a precise gene-editing tool, the team removed these methylation tags and reactivated IGF2. The result: older rats regained significantly better memory function.
“When we turned the gene back on, the older animals performed much better,” Jarome said. “Interestingly, middle-aged animals without memory problems weren’t affected—showing that intervention timing is crucial. You have to act when decline begins.”
Understanding the complex nature of memory decline
Together, these studies reveal that memory loss is not caused by a single molecule or pathway but rather by a combination of molecular changes that occur as the brain ages. “We tend to look at one molecule at a time,” Jarome noted, “but the truth is that many systems are changing simultaneously. To understand memory decline—or diseases like Alzheimer’s—we need to look at the broader molecular landscape.”
Collaborative and graduate-led research
Both projects highlight the collaborative, student-driven nature of Jarome’s lab. Supported by partnerships with Rosalind Franklin University, Indiana University, and Penn State, the work was led primarily by graduate researchers. Bae directed the K63 polyubiquitination study, while Kincaid led the IGF2 project.
“These are excellent examples of graduate-led, interdisciplinary research,” Jarome said. “Our students play an active role in designing experiments, analyzing data, and shaping the scientific questions that drive our discoveries.”
Ultimately, Jarome believes the findings point toward a promising future. “Everyone experiences some memory decline as they age,” he said. “But when that decline becomes abnormal, the risk for Alzheimer’s rises. The exciting part is that we’re finding these molecular changes can be corrected. That gives us a real path forward toward treatments that may one day preserve memory and cognitive health in aging brains.”
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