Type 2 diabetes may rewire the brain in ways that mimic early Alzheimer’s disease — and UNLV researchers say the “why” may lie in a previously unexplored connection between high blood sugar levels and a key part of the brain called the anterior cingulate cortex (ACC).
Diabetes is a group of diseases characterized by an imbalance of blood sugar or insulin levels. Scientists have long known that Type 2 diabetes patients are more prone to psychiatric and neurodegenerative disorders. The risk of developing Alzheimer’s is 65% higher in diabetics. But the exact link between diabetes and neurodegenerative diseases has been poorly understood.
The UNLV research team went searching for answers.
Based on their findings, published this week in the Journal of Neuroscience’s Computational Properties of the Prefrontal Cortex Special Collection, it appears that diabetes weakens ACC function — suppressing reward perception and memory signals — and induces mild cognitive impairment similar to that observed during the brain’s progression towards Alzheimer’s disease.
“Diabetes may be altering the brain similarly to early stages of Alzheimer’s disease,” said lead researcher and UNLV psychology professor James Hyman. “Further research is needed but these findings have the potential to help researchers unlock clues to improved diagnostic or treatment strategies for the disease.”
The study builds on the UNLV team’s previous research into the link between diabetes and Alzheimer’s, and represents the first time scientists have looked for clues within the ACC. The ACC is associated with fundamental cognitive processes — ranging from motivation, decision making, and learning to goal-oriented behavior (such as tracking tasks and experiences over time), pleasure seeking, and reward processing. The ACC’s role in regulating emotions also makes it integral to brain patterns observed in patients experiencing mood disorders and depression.
To gain insight into the interplay between the ACC and high blood sugar levels, scientists observed brain activity and behavior in rodent models.
Researchers found that diabetics’ anticipation of a reward, such as a sweet treat, is heightened in comparison to healthy brains. Additionally, after receiving the reward, healthy-brained subjects pause to savor, while the diabetics quickly move on to the next reward.
According to scientists, hyperglycemic insulin levels appeared to impair the ACC’s information-processing ability surrounding rewards. The researchers pinpointed the weakened reward signal to a dampened input into the ACC from another key brain area for Alzheimer’s disease called the hippocampus, which is involved in spatial and autobiographical memory.
“We think the hippocampus tells the subject where it is location-wise, and the ACC tells the subject what it is doing and that it’s getting a reward,” Hyman said. “These things should come together and make the subject remember it was just in a special, rewarding location, but this doesn’t happen with the ones that have Type 2 diabetes.”
The research team called their findings significant, given the importance of diet and lifestyle interventions to manage diabetes. Globally, 1 in 10 people contend with the illness, and 90% of cases are Type 2 diabetes — which is linked to obesity and can lead to chronic damage to nerves, blood vessels, and surrounding tissues and organs.
What’s more, study authors said, the hippocampus-to-ACC projection may be worth exploring as a treatment target for mood disorders to which the ACC is already linked. Hyman said his team’s research reveals direct evidence of muted reward processing and behaviors that are consistent with anhedonia, or the inability to experience pleasure — a common symptom of depression and Type 2 diabetes.
Additionally, he said, the circuit between the ACC and hippocampus is integrally important during the early stages of Alzheimer’s pathology. His team plans to continue its investigation into the connection between the neurodegenerative disorder and weakened ACC function.
“Alzheimer’s disease goes undetected for decades because our brains are good at finding ways to compensate. Before diagnosis, people behave normally despite having changes in information processing. We even observed that in this study,” Hyman said.
About the study
“ACC reward location information is carried by hippocampal theta synchrony and suppressed in a Type 2 Diabetes model” was published March 24, 2025 in the Journal of Neuroscience’s Computational Properties of the Prefrontal Cortex Special Collection. In addition to Hyman, the following researchers with UNLV’s Department of Psychology, Interdisciplinary Program in Neuroscience, and Kirk Kerkorian School of Medicine’s Department of Brain Health contributed to the study: Guncha Bhasin, Emmanuel Flores, Lauren A. Crew, Ryan A. Wirt, Andrew A. Ortiz, and Jefferson W. Kinney.
