Diabetes, particularly Type 2, may subtly alter the brain’s reward processing and memory systems, with effects resembling the early stages of Alzheimer’s disease, according to recent research. The study, led by James Hyman and his team from the University of Nevada, Las Vegas, explores how diabetes disrupts the communication between critical brain areas involved in emotion and cognition, particularly the hippocampus and the anterior cingulate cortex (ACC).
Type 2 diabetes has long been associated with an increased risk of neurodegenerative conditions, including Alzheimer’s disease, as well as psychiatric disorders such as mood disorders. However, the exact mechanisms linking these conditions have remained unclear. The researchers’ study, published in JNeurosci’s special collection on the computational properties of the prefrontal cortex, suggests that diabetes may interfere with the brain’s reward processing, a change that could have profound implications for understanding how the disease affects cognitive and emotional well-being.
In their experiment using a rat model, Hyman’s team focused on how diabetes impacted the rats’ behavior in a maze designed to test cognitive function and reward processing. While all rats pursued rewards, those with diabetes showed a diminished response to the locations where the rewards were found. The researchers noted that the rats with Type 2 diabetes exhibited weaker reward signals in the ACC, a brain region integral to emotion and decision-making. This weakened response was traced to reduced input from the hippocampus, the brain’s memory hub responsible for spatial navigation.
“The hippocampus informs the rat of its location in the maze, while the ACC signals the importance of that location based on the reward,” explains Hyman. “In diabetic rats, these signals don’t align, which prevents them from remembering the significance of rewarding locations.”
This disruption in the brain’s reward circuitry may explain the links between diabetes, mood disorders, and neurodegeneration. Hyman also suggests that the hippocampus-to-ACC communication could serve as a potential treatment target for diabetes-related cognitive decline, as well as mood disorders.
Furthermore, Hyman points out the striking similarity between the changes observed in diabetic rats and early Alzheimer’s disease. Alzheimer’s typically goes undiagnosed for many years, as the brain compensates for subtle cognitive decline. “Even though the diabetic rats behaved normally, their experience in the maze differed from that of healthy rats,” he says. “This could reflect the early cognitive changes that occur in Alzheimer’s before symptoms become apparent.”
The study underscores the need for further research into the neural changes caused by Type 2 diabetes, particularly how these changes might contribute to broader cognitive impairments and mental health disorders. By targeting specific brain regions, such as the ACC, new therapeutic strategies could emerge to help manage or even prevent some of the cognitive challenges associated with diabetes.
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