Diabetes doesn’t just affect blood sugar—it can also damage your memory and thinking skills. Scientists discovered that a protein called NCOA3 plays an important role in protecting your brain from these problems. When people have diabetes, this protective protein drops to low levels in the brain areas that control memory. In experiments with mice, researchers found that boosting this protein helped restore lost memory function. This discovery could eventually lead to new treatments that prevent memory loss in people with diabetes, one of the most common complications that doctors worry about.

The Quick Take

  • What they studied: Whether a brain protein called NCOA3 controls memory problems that happen in people with diabetes
  • Who participated: Laboratory mice that were given diabetes through special diet and injections; researchers also studied brain cells grown in dishes
  • Key finding: Mice with low NCOA3 protein had worse memory problems, but when scientists increased this protein in the memory center of the brain, the mice’s memory improved significantly
  • What it means for you: This research suggests that NCOA3 might be a target for future medicines to prevent memory loss in diabetes patients, though human studies are still needed to confirm these findings

The Research Details

Scientists used two main approaches to understand NCOA3’s role. First, they created mice with diabetes by feeding them a high-fat diet and giving them a chemical injection that damages the pancreas. Then they tested these diabetic mice using memory games—like recognizing new objects, finding their way through mazes, and remembering scary situations. They measured NCOA3 protein levels in different brain regions and looked at related proteins that help brain cells communicate.

Second, they used two genetic techniques: one that removed the NCOA3 gene from specific brain cells, and another that increased NCOA3 levels in the memory center. This allowed them to see what happens when there’s too little or too much of this protein. They also grew brain cells in laboratory dishes and exposed them to high sugar levels to mimic diabetes conditions.

This approach is important because it shows cause-and-effect relationships. By removing and adding the protein, researchers could prove that NCOA3 directly controls memory problems—not just that the two are connected. Testing in both whole animals and isolated cells helps confirm that the findings are real and not accidental.

This is original research published in a respected neuroscience journal. The study used multiple testing methods (behavioral tests, protein measurements, and cell cultures) which strengthens the findings. However, this research was done only in mice, so results may not directly apply to humans. The sample size of mice wasn’t specified in the abstract, which is a minor limitation. The findings are recent (2026) and represent cutting-edge science.

What the Results Show

The main discovery was that NCOA3 protein levels drop significantly in the brain regions responsible for memory (the cortex and hippocampus) when diabetes develops. When researchers removed the NCOA3 gene from brain cells, the diabetic mice performed much worse on memory tests—they couldn’t recognize new objects as well and had trouble navigating mazes.

The opposite happened when scientists increased NCOA3 levels specifically in the hippocampus (the brain’s memory center). These mice showed meaningful improvement in memory function, suggesting that boosting this protein could reverse some diabetes-related brain damage.

At the molecular level, low NCOA3 was linked to reduced levels of other important brain proteins that help cells communicate with each other. When brain cells were exposed to high sugar levels in the lab, NCOA3 and related proteins decreased, mimicking what happens in diabetes.

The research identified a chain of molecular events: NCOA3 controls a protein called AGO2, which in turn regulates a molecule called miR-138-5p. This chain appears to affect synaptic plasticity—the brain’s ability to form and strengthen connections between nerve cells. When NCOA3 was low, this entire communication chain was disrupted, explaining how diabetes damages memory at the cellular level.

Previous research showed that diabetes harms memory, but the exact mechanisms weren’t clear. This study fills that gap by identifying NCOA3 as a key player. The findings build on earlier work showing that brain inflammation and reduced cell communication contribute to diabetes-related cognitive problems, adding a specific molecular target that could be therapeutically useful.

This research was conducted entirely in mice and laboratory cells, so results may not directly translate to humans. The study didn’t examine whether NCOA3 changes occur in people with diabetes or whether boosting it would help human patients. The exact sample size of mice used wasn’t reported. Additionally, the research focused on one type of diabetes model and didn’t test whether findings apply to different diabetes types or stages.

The Bottom Line

Based on this research, NCOA3 appears to be a promising target for developing new diabetes treatments that could prevent memory loss. However, these findings are preliminary and based on animal studies. Current recommendations remain: manage blood sugar levels through diet, exercise, and medication as prescribed by your doctor, since this is proven to reduce all diabetes complications. Do not change your diabetes treatment based on this research alone.

People with diabetes who are concerned about memory problems should be aware of this research, as it may eventually lead to new treatment options. Healthcare providers researching diabetes complications should pay attention to NCOA3 as a potential therapeutic target. This research is less immediately relevant to people without diabetes, though it advances general understanding of how the brain works.

This is early-stage research. Even if NCOA3-targeting drugs are developed, it typically takes 5-10 years for laboratory discoveries to become available treatments. People with diabetes should not expect NCOA3-based therapies for several years at minimum.

Want to Apply This Research?

  • Track cognitive function weekly using simple memory tests: recall a 10-item grocery list after 5 minutes, complete a timed maze puzzle, or use the app’s memory game feature. Record scores to monitor trends over time.
  • Use the app to set reminders for blood sugar management activities (medication timing, meal planning, exercise) since controlling blood sugar remains the proven way to protect brain health. Log memory concerns or cognitive changes to discuss with your doctor.
  • Establish a baseline cognitive score using the app’s built-in tests, then track monthly. If you notice memory decline, share these records with your healthcare provider. Combine cognitive tracking with blood sugar monitoring to identify patterns between glucose control and mental clarity.

This research describes laboratory findings in mice and does not yet represent proven treatments for humans. If you have diabetes and are experiencing memory problems, consult your healthcare provider—do not attempt self-treatment based on this research. Current diabetes management through medication, diet, and exercise remains the evidence-based approach to preventing complications. This article is for educational purposes and should not replace professional medical advice.