A study led by USC on rats that consumed a high-fat, sugary diet suggests that a diet filled with junk food during adolescence may have long-lasting effects on the brain’s memory function. According to Scott Kanoski, a professor at USC Dornsife College of Biological Sciences, the research indicates that memory impairments persist in rats that were raised on a junk food diet. This study, along with previous research, highlights the potential long-term consequences of consuming a diet high in junk food.
According to a recent study in the journal Brain, Behavior, and Immunity, the effects of a poor diet in adolescence can have lasting impacts into adulthood. Lead author Anna Hayes and researcher Terry Davidson found that simply putting adolescents on a healthier diet can mitigate these long-term effects.
Prior research has indicated a connection between poor diet and Alzheimer’s disease. Individuals with Alzheimer’s tend to have lower levels of a key neurotransmitter in the brain called acetylcholine, which is crucial for memory, learning, attention, arousal, and involuntary muscle movement. This study aimed to further explore this link and its potential long-term consequences.The team wanted to understand how a high-fat, high-sugar diet might affect the brain, especially in younger individuals during the important adolescent developmental stage. By observing the impact of the diet on the rats’ acetylcholine levels and conducting memory tests, they hoped to gain insight into the connection between diet and memory. Specifically, the researchers studied a group of rats on a fatty, sugary diet and compared their acetylcholine levels to those of a control group of rats, while also testing their memory through specific tasks. The team focused on analyzing the brain responses of the rats to gain a better understanding of the relationship between diet and memory.The researchers examined the brains of the rats after death to look for any abnormalities in their acetylcholine levels. The memory test consisted of allowing the rats to explore new objects in different locations. Several days later, the rats were brought back to the same scene, which was almost identical except for the addition of a new object. The rats that were on the junk food diet displayed signs of not being able to remember which object they had seen before and where it was located, while the control group showed familiarity. “Acetylcholine signaling is a mechanism to help them encode and remember those events, analogous to ‘episodic memory’ in humans that allows us to remember specific past events.””The signal that helps us remember events from our past does not seem to be happening in animals that were raised on a diet high in fat and sugar,” lead author Hayes stated.
Kanoski stressed the importance of adolescence as a critical period for brain development, stating that some negative effects may be more difficult to reverse if they occur during childhood rather than adulthood.
Despite this, there is still potential for intervention, according to Kanoski, who mentioned that further studies are being conducted to explore this possibility.The researchers investigated if memory loss in rats fed a junk food diet could be reversed using drugs that increase acetylcholine release. They tested two drugs, PNU-282987 and carbachol, and discovered that when these treatments were administered directly to the hippocampus, the area of the brain responsible for memory and affected by Alzheimer’s disease, the rats’ memory was restored. However, without this specialized medical intervention, further research is needed to understand how memory problems caused by a junk food diet during adolescence can be reversed. The research team comprised Kanoski, Hayes, and other USC Dornsife members.The study was conducted by Logan Tierno Lauer, Alicia E. Kao, Molly E. Klug, Linda Tsan, Jessica J. Rea, Keshav S. Subramanian, Cindy Gu, Arun Ahuja, Kristen N. Donohue, and Léa Décarie-Spain; Natalie Tanios of Keck School of Medicine of USC; and Anthony A. Fodor and Shan Sun of University of North Carolina-Charlotte.
Funding for this research was provided by the National Institute of Diabetes and Digestive and Kidney Diseases grant DK123423 (SEK, AF), National Institute of Diabetes and Digestive and Kidney Diseases grant DK104897 (SEK), and the Postdoctoral Ruth L. Kirschstein National Research Service Award from the National Institute on Aging F32AG077932.(AMRH), National Science Foundation Graduate Research Fellowships (separate awards to LT and KSS), Quebec Research Funds postdoctoral fellowship 315201 (LDS) and the Alzheimer’s Association Research Fellowship to Promote Diversity AARFD-22-972811 (LDS).
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