Animal studies suggest early exposure to Western diet is associated with lasting memory impairment

In a recent study published in the journal brain, behavior, immunityResearchers developed a primary Western diet (WD) mouse model associated with long-term hippocampal (HPC) dysfunction to examine the neurobiological processes underlying these effects.

study: Western diet intake impairs memory function through dysregulation of hippocampal acetylcholine signaling

Western diets rich in processed foods, saturated fats, and simple carbohydrates are associated with poor memory performance, particularly in hippocampal-dependent functions. The neurobiological processes underlying the developmental Western diet that contribute to long-term hippocampal damage are still unknown. Alterations in HPC neuron function associated with WD have been found, including altered synaptic plasticity, decreased brain-derived neurotrophic factor (BDNF) levels, and increased neuroinflammatory markers. Disruption of acetylcholine (ACh) signaling may contribute to memory impairment associated with a long-term Western diet.

About research

In this study, researchers investigated the long-term effects of early childhood Western diet intake on episodic memory in the hippocampus and the mediating effects of abnormal hippocampal acetylcholine signaling on behavioral outcomes.

In this study, we investigated whether the gut microbiota is functionally related to WD-induced memory impairment in early childhood by making a dietary selection that simulates current human WD (some sugar We used a relevant Western dietary model that incorporated macronutrients (from many fatty food and drink replacements) and macronutrients. Due to changes in HPC ACh activity.

To describe the early Western diet model in rats, researchers employed a “junk food” cafeteria-style diet (CAF). During the juvenile and teenage years (26–56 days of age), rats were fed a cafeteria-style diet (high-fat and high-sugar foods ad libitum; CAF) or regular chow (CTL). The researchers conducted metabolic and behavioral assessments before and after a healthy eating intervention that began in early adulthood. They gave control rats (CTLs) the same amount of food and drink containers, but those containers were fed regular chow.

The researchers monitored their weight and food intake three times a week. They estimated the total kilocalorie intake from each CAF diet component by multiplying the weight of each rodent's food and drink by the energy density of that component. They calculated the kilocalorie consumption from each macronutrient in CAF-fed animals based on the kilocalorie intake of each CAF diet component and the composition of each macronutrient. In the first group, memory impairment persisted even after 30 days of a healthy diet, and subsequent cohorts were given a Western diet for up to 30 days (PN 56). Researchers evaluated protein indicators of acetylcholine tone in the dorsal HPC (HPCd) of CAF and CTL rats. They used Novel Object in Context (NOIC) to assess HPC-dependent contextual episodic memory and Novel Location Recognition (NLR) to assess spatial recognition memory.

Researchers investigated the role of ACh neurotransmission in the human brain (HBC) and its possible impact on memory performance. They investigated the abundance of proteins involved in ACh signaling in HPCs and conducted correlation studies between key microbial taxa and VAChT levels. They also investigated changes in acute ACh signaling dynamics during episodic memory challenge in CAF and CTL rats. After a 30-day healthy dietary intervention, they measured ACh signaling using fiber photometry in vivo. The researchers also investigated whether pharmacological treatment with ACh receptor agonists could reverse long-term memory impairment in CAF rodents.

result

This study found that early cortical water WD (cortical water WD) intake caused long-term abnormalities in hippocampus-dependent memory performance in CAF rodents, independent of healthy dietary intervention. Researchers observed significant differences in spatial recognition memory using NLR and NOIC. This indicates that in memory tests that did not involve the HPC, early Western diet intake did not lead to significant differences in recognition of novel items.

WD in early childhood did not affect motor activity indicators or anxiety. This suggests that chronic HPC-dependent memory impairment caused by WD is not affected by anxiety-like habits or changes in motor activity. The researchers also detected changes in the gut microbiome of CAF animals, with significant differences at the genus level between CAF animals and controls. However, these initial significant differences showed a reversal after the healthy diet intervention. Correlation studies between specific taxa and memory performance on his NOIC test after the first life Western diet access period remained significant after FDR adjustment. Bifidobacterium and Lactococcus Although abundance showed a negative association with memory ability assessed by NOIC, intestinal lactic acid bacteria A positive association was shown.

WD in early childhood causes a long-term reduction in chronic HPC ACh signaling tone. Immunoblot examination of dorsal HPC tissue obtained during the healthy dietary intervention period showed no changes in ChAT or AChE levels. However, CAF rats showed lower levels of her VAChT than her CTL rats. WD in early childhood alters acute ACh signaling patterns during memory tests, resulting in impaired performance in CAF rats.

This study found that early exposure to Western diet (WD) was associated with long-term episodic memory deficits mediated by changes in hippocampal acetylcholine (ACh) transmission. α7 nicotinic receptors are important mediators of WD-induced memory dysfunction. It is unlikely that the gut microbiota is involved in the long-term her HPC dysfunction associated with her WD in infancy. Further studies are needed to improve our understanding of the functional relationship between aberrant HPC ACh signaling and her WD-related memory impairment in women.