Groundbreaking research from the University of Nevada, Las Vegas (UNLV) has unveiled new insights into how Type 2 diabetes may disrupt brain function in ways that resemble the early stages of Alzheimer’s disease. Central to this revelation is the anterior cingulate cortex (ACC), a vital but previously underexplored region of the brain that appears to play a key role in how elevated blood sugar affects memory and motivation. The study identifies a significant neurological link between diabetes and cognitive decline, offering a fresh perspective on a longstanding medical mystery.
Diabetes is widely recognised as a metabolic disorder that affects how the body regulates blood sugar and insulin. Among individuals with Type 2 diabetes—the most prevalent form of the disease—there is a notably higher risk of developing psychiatric and neurodegenerative conditions, including a 65% increased chance of Alzheimer’s disease. Despite this correlation, the precise biological mechanisms bridging these two conditions have remained poorly understood. The UNLV research team, led by psychology professor James Hyman, set out to investigate this link by examining the impact of diabetes on brain regions associated with cognition and emotional regulation.
The anterior cingulate cortex, or ACC, is a structure within the brain’s frontal lobe and is known to mediate various essential cognitive and emotional processes. These include motivation, decision-making, learning, and the processing of rewards, as well as goal-oriented behaviour and emotional regulation. Its function is particularly relevant in mood disorders such as depression, which frequently co-occur with chronic diseases like diabetes. Despite its central role in these processes, the ACC has not previously been a significant focus on research exploring the neurological impact of diabetes.
In this study, published in the Journal of Neuroscience as part of a special issue on the computational properties of the prefrontal cortex, researchers used rodent models to explore how diabetes might interfere with ACC function. They observed that rodents with diabetes demonstrated altered reward-related behaviour. While they showed heightened anticipation for rewards such as sweet treats, they did not pause to savour the reward once received. Instead, they rapidly moved on to seek the next pleasurable stimulus. This pattern of behaviour, researchers suggest, reflects a breakdown in how the brain processes and encodes reward experiences—an impairment that mirrors early symptoms of Alzheimer’s disease.
Further investigation revealed that high blood sugar and insulin resistance—hallmarks of Type 2 diabetes—may weaken the ACC’s ability to integrate information from other brain regions. In particular, the researchers focused on its connection with the hippocampus, a region critical for spatial and autobiographical memory. According to Hyman, the hippocampus informs the brain about its location, while the ACC interprets what the individual is doing and whether they are receiving a reward. In healthy brains, this combined input creates a coherent and memorable experience. However, in diabetic brains, this neural synchrony appears disrupted, impairing memory and motivation.
This research builds on earlier work by the same team, which had already suggested a link between diabetes and cognitive impairment. What makes this study especially significant is its identification of a specific brain circuit—the hippocampus-ACC pathway—that may be vulnerable in both diabetes and Alzheimer’s. This finding opens potential avenues for targeted therapies that could slow or mitigate the neurological consequences of Type 2 diabetes. It also reinforces the importance of maintaining metabolic health, particularly through diet and lifestyle interventions, to protect cognitive function over time.
With Type 2 diabetes affecting over 90% of the global diabetic population and approximately one in ten people worldwide living with the disease, the study’s findings carry broad implications. Not only does it underscore the cognitive risks posed by chronic hyperglycaemia, but it also suggests that early interventions aimed at preserving ACC and hippocampal function could serve as a buffer against long-term brain damage. The dampening of reward signals observed in diabetic models also corresponds with symptoms of anhedonia—the inability to experience pleasure—a key feature of both depression and Alzheimer’s, further reinforcing the relevance of these findings to mental health.
Looking ahead, Hyman and his team plan to continue exploring the relationship between the ACC and hippocampus, particularly in the context of neurodegeneration. He notes that Alzheimer’s disease can remain undiagnosed for decades due to the brain’s capacity for compensation, meaning individuals may appear cognitively normal even while their neural processing is subtly changing. “We saw evidence of this compensatory behaviour even in our study,” Hyman said. “Understanding how and when these changes begin could be crucial for developing earlier and more effective interventions in both diabetes and Alzheimer’s disease.”
More information: James Hyman et al, ACC reward location information is carried by hippocampal theta synchrony and suppressed in a Type 2 Diabetes model, JNeurosci. DOI: 10.1523/JNEUROSCI.1546-24.2025
Journal information: JNeurosci Provided by University of Nevada, Las Vegas
