Sumamry: A high-fat, sugary diet during adolescence may cause long-lasting memory impairments. The study found that rats raised on a junk food diet exhibited significant memory deficits that persisted into adulthood, despite switching to a healthier diet.
These effects were linked to disruptions in acetylcholine, a crucial neurotransmitter for memory and learning, highlighting the critical impact of diet on brain development. The research suggests that poor dietary habits in youth could have irreversible effects on cognitive functions.
Key Facts:
- Adolescent rats on a junk food diet showed reduced acetylcholine levels and struggled with memory tests designed to mimic human episodic memory.
- Memory impairments persisted even after the rats were switched to a healthy diet, indicating lasting impacts of early dietary choices.
- Potential reversibility of memory issues was tested using acetylcholine-inducing drugs, suggesting avenues for future research on dietary impact mitigation.
Source: USC
A new USC-led study on rats that feasted on a high-fat, sugary diet raises the possibility that a junk food-filled diet in teens may disrupt their brains’ memory ability for a long time.
“What we see not just in this paper, but in some of our other recent work, is that if these rats grew up on this junk food diet, then they have these memory impairments that don’t go away,” said Scott Kanoski, a professor of biological sciences at the USC Dornsife College of Letters, Arts and Sciences.
“If you just simply put them on a healthy diet, these effects unfortunately last well into adulthood.”
The study appears in the May issue of the journal Brain, Behavior, and Immunity.
In developing the study, Kanoski and lead author and postdoctoral research fellow Anna Hayes considered that prior research has shown a link between poor diet and Alzheimer’s disease.
People who suffer from Alzheimer’s disease tend to have lower levels of a neurotransmitter called acetylcholine in the brain that is essential for memory and functions such as learning, attention, arousal and involuntary muscle movement.
The team wondered what this could mean for younger people who may be on a similar fat-filled, sugary Western diet, particularly during adolescence when their brain is undergoing significant development.
By tracking the impact of the diet on the rats’ levels of acetylcholine, and running the rats through some memory testing, they could learn more about the important relationship between diet and memory.
The researchers tracked the acetylcholine levels of a group of rats on a fatty, sugary diet and in a control group of rats by analyzing their brain responses to certain tasks designed to test their memory. The team examined the rats’ brains post-mortem for signs of disrupted acetylcholine levels.
The memory test involved letting the rats explore new objects in different locations. Days later, the researchers reintroduced the rats to the scene that was nearly identical except for the addition of one new object.
Rats on the junk food diet showed signs they could not remember which object they had previously seen, and where, while those in 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 events from our past,” lead author Hayes explained.
“That signal appears to not be happening in the animals that grew up eating the fatty, sugary diet.”
Kanoski emphasized that adolescence is a very sensitive period for the brain when important changes are occurring in development.
“I don’t know how to say this without sounding like Cassandra and doom and gloom,” he said, “but unfortunately, some things that may be more easily reversible during adulthood are less reversible when they are occurring during childhood.”
There is at least some hope for intervention. Kanoski said that in another round of the study, the research team examined whether the memory damage in rats raised on the junk food diet could be reversed with medication that induces the release of acetylcholine.
They used two drugs, PNU-282987 and carbachol, and found that with those treatments given directly to the hippocampus, a brain region that controls memory and is disrupted in Alzheimer’s disease, the rats’ memory ability was restored.
But without that special medical intervention, Kanoski said more research is needed to know how memory problems from a junk food diet during adolescence can be reversed.
In addition to Kanoski and Hayes, the team included other USC Dornsife researchers 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; as well as Anthony A. Fodor, Shan Sun of University of North Carolina-Charlotte.
About this diet and memory research news
Author: Emily Gersema
Source: USC
Contact: Emily Gersema – USC
Image: The image is credited to Neuroscience News
Original Research: Open access.
“Western diet consumption impairs memory function via dysregulated hippocampus acetylcholine signaling” by Anna M.R. Hayes et al. Brain, Behavior, and Immunity
Abstract
Western diet consumption impairs memory function via dysregulated hippocampus acetylcholine signaling
Western diet (WD) consumption during early life developmental periods is associated with impaired memory function, particularly for hippocampus (HPC)-dependent processes.
We developed an early life WD rodent model associated with long-lasting HPC dysfunction to investigate the neurobiological mechanisms mediating these effects. Rats received either a cafeteria-style WD (ad libitum access to various high-fat/high-sugar foods; CAF) or standard healthy chow (CTL) during the juvenile and adolescent stages (postnatal days 26–56).
Behavioral and metabolic assessments were performed both before and after a healthy diet intervention period beginning at early adulthood.
Results revealed HPC-dependent contextual episodic memory impairments in CAF rats that persisted despite the healthy diet intervention. Given that dysregulated HPC acetylcholine (ACh) signaling is associated with memory impairments in humans and animal models, we examined protein markers of ACh tone in the dorsal HPC (HPCd) in CAF and CTL rats.
Results revealed significantly lower protein levels of vesicular ACh transporter in the HPCd of CAF vs. CTL rats, indicating chronically reduced ACh tone. Using intensity-based ACh sensing fluorescent reporter (iAChSnFr) in vivo fiber photometry targeting the HPCd, we next revealed that ACh release during object-contextual novelty recognition was highly predictive of memory performance and was disrupted in CAF vs. CTL rats.
Neuropharmacological results showed that alpha 7 nicotinic ACh receptor agonist infusion in the HPCd during training rescued memory deficits in CAF rats.
Overall, these findings reveal a functional connection linking early life WD intake with long-lasting dysregulation of HPC ACh signaling, thereby identifying an underlying mechanism for WD-associated memory impairments.
