A new study by researchers at the University of Nevada, Las Vegas (UNLV) suggests that Type 2 diabetes may alter brain function in ways similar to early Alzheimer’s disease. The team has identified a potential link between high blood sugar levels and a critical area of the brain, the anterior cingulate cortex (ACC), which could help explain why individuals with diabetes are at an increased risk of developing Alzheimer’s.
Diabetes, particularly Type 2, is known to disrupt blood sugar and insulin regulation, and patients are more susceptible to neurodegenerative conditions. In fact, people with diabetes face a 65% higher risk of Alzheimer’s. However, the mechanisms behind this connection have remained unclear.
The UNLV study, published this week in the Journal of Neuroscience’s Computational Properties of the Prefrontal Cortex Special Collection, provides new insights into how diabetes might impair the ACC, a brain region involved in emotional regulation, motivation, decision-making, and memory. The researchers found that diabetes weakens the ACC’s ability to process reward signals and memory, leading to mild cognitive impairments akin to the early stages of Alzheimer’s disease.
“Diabetes might be altering the brain in ways that mirror the onset of Alzheimer’s disease,” said James Hyman, a psychology professor at UNLV and lead researcher. “Our findings could be crucial for developing improved diagnostic tools or treatment strategies for Alzheimer’s.”
This study builds upon previous UNLV research that explored the link between diabetes and Alzheimer’s, marking the first time scientists have investigated the role of the ACC in this context. The ACC is crucial for managing behaviors such as goal-directed actions, pleasure-seeking, and reward processing. It is also involved in emotional regulation, which makes it important for understanding mood disorders and depression.
To explore how high blood sugar affects the ACC, the team conducted experiments with rodent models, examining both brain activity and behavioral responses. They found that diabetic rodents had an exaggerated anticipation of rewards, such as food, compared to healthy rodents. However, after receiving the reward, the diabetic rodents quickly moved on to the next one, while healthy rodents paused to savor the moment.
The researchers discovered that elevated blood sugar and insulin levels disrupted the ACC’s ability to process reward-related information. This disruption was traced to reduced communication between the ACC and the hippocampus, another brain region critical for memory formation, particularly spatial and autobiographical memory.
“The hippocampus tells us where we are, and the ACC tells us what we are doing and whether we’re being rewarded. These signals should align to help us remember a rewarding experience, but this doesn’t happen in Type 2 diabetes,” Hyman explained.
The findings have significant implications, especially considering the global prevalence of Type 2 diabetes, with 1 in 10 people affected, 90% of whom have the condition. The study emphasizes the importance of managing diabetes through diet and lifestyle interventions to prevent long-term damage to brain function.
Furthermore, the research team highlighted that the hippocampus-ACC connection could offer a potential target for treating mood disorders, such as depression, that are linked to ACC dysfunction. Their study also found evidence of behaviors consistent with anhedonia, the inability to experience pleasure, a common symptom in both depression and diabetes.
The researchers plan to continue investigating the link between weakened ACC function and Alzheimer’s pathology, as the ACC-hippocampus circuit plays a vital role in the early stages of Alzheimer’s disease.
“Alzheimer’s often goes undetected for years because the brain compensates for changes in information processing. Even before a diagnosis, individuals may appear to function normally. We observed this phenomenon in our study as well,” Hyman added.
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