A high-fat high-sugar diet-induced impairment in place-recognition memory is reversible and training-dependent

Westbrook, R. Frederick

doi:10.1016/j.appet.2016.12.010

Cited by 38 publications

(29 citation statements)

References 39 publications

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“…However, it is unclear whether this reflects a deterioration in performance in the controls or recovery in the WS-diet group. While this study cannot firmly conclude which possibility may be correct, we note that reversibility is observed in animal studies that use short-term Western-style dietary exposures [36]. Before turning to the interpretation of these data, two issues require consideration.…”

Section: Discussionmentioning

confidence: 78%

“…Participants then returned one week later following the end of the intervention phase (Day 8) and repeated the testing described for Day 1. They returned again approximately three weeks later for limited follow-up testing (Day 29), mainly to check if the consequences of the dietary intervention on HDLM were reversible-as suggested by recent animal data [36].…”

Section: Introductionmentioning

confidence: 99%

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Hippocampal-dependent appetitive control is impaired by experimental exposure to a Western-style diet

et al. 2020

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Animals fed a Western-style diet (WS-diet) demonstrate rapid impairments in hippocampal function and poorer appetitive control. We examined if this also occurs in humans. One-hundred and ten healthy lean adults were randomized to either a one-week WS-diet intervention or a habitual-diet control group. Measures of hippocampal-dependent learning and memory (HDLM) and of appetitive control were obtained pre- and post-intervention. HDLM was retested at three-week follow-up. Relative to controls, HDLM performance declined in the WS-diet group ( d = 0.43), but was not different at follow-up. Appetitive control also declined in the WS-diet group ( d = 0.47) and this was strongly correlated with HDLM decline ( d = 1.01). These findings demonstrate that a WS-diet can rapidly impair appetitive control in humans—an effect that could promote overeating in consumers of a WS-diet. The study also suggests a functional role for the hippocampus in appetitive control and provides new evidence for the adverse neurocognitive effects of a WS-diet.

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Section: Discussionmentioning

confidence: 78%

Section: Introductionmentioning

confidence: 99%

Hippocampal-dependent appetitive control is impaired by experimental exposure to a Western-style diet

et al. 2020

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“…52 Many of these studies, and others, have shown that high-fat diet-induced cognitive deteriorations are accompanied by elevated neuroinflammatory markers or responses in the hippocampus. 15,18,44,[48][49][50][51]53 However, the mechanisms by which these neuroinflammatory processes signal and/or affect the hippocampus are not entirely clear. There is growing evidence that high-fat diets may compromise the hippocampus by sensitizing the immune cells (most likely microglia) of this brain structure, thus priming the inflammatory response to subsequent challenging stimuli.…”

Section: Adult Consumption Of a High-fat Diet: A Vulnerability Factormentioning

confidence: 99%

“…46 Nonetheless, high-fat diet consumption has been demonstrated to impair hippocampus-dependent memory function in humans and rodents. For example, compared to rodents that consumed a control diet, those that consumed a high-fat and/or high-sugar diet exhibited robust impairments in various types of memory (e.g., spatial, contextual), as indicated by weaker performances in the Y-maze, 48 radial arm maze, 15 novel object recognition task, 15 novel place recognition task, 44,49 Morris water maze, 50 and contextual fear conditioning.…”

Section: Adult Consumption Of a High-fat Diet: A Vulnerability Factormentioning

confidence: 99%

Food for thought: how nutrition impacts cognition and emotion

et al. 2017

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More than one-third of American adults are obese and statistics are similar worldwide. Caloric intake and diet composition have large and lasting effects on cognition and emotion, especially during critical periods in development, but the neural mechanisms for these effects are not well understood. A clear understanding of the cognitive-emotional processes underpinning desires to over-consume foods can assist more effective prevention and treatments of obesity. This review addresses recent work linking dietary fat intake and omega-3 polyunsaturated fatty acid dietary imbalance with inflammation in developing, adult, and aged brains. Thus, early-life diet and exposure to stress can lead to cognitive dysfunction throughout life and there is potential for early nutritional interventions (e.g., with essential micronutrients) for preventing these deficits. Likewise, acute consumption of a high-fat diet primes the hippocampus to produce a potentiated neuroinflammatory response to a mild immune challenge, causing memory deficits. Low dietary intake of omega-3 polyunsaturated fatty acids can also contribute to depression through its effects on endocannabinoid and inflammatory pathways in specific brain regions leading to synaptic phagocytosis by microglia in the hippocampus, contributing to memory loss. However, encouragingly, consumption of fruits and vegetables high in polyphenolics can prevent and even reverse age-related cognitive deficits by lowering oxidative stress and inflammation. Understanding relationships between diet, cognition, and emotion is necessary to uncover mechanisms involved in and strategies to prevent or attenuate comorbid neurological conditions in obese individuals.

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“…In young adult rats a HFD of three to four months is necessary to cause overt inflammation-related cognitive deficits unless additional factors are present to compound these effects (Almeida-Suhett, Graham, Chen, & Deuster, 2017;Jeon et al, 2012;Pepping et al, 2013). Thus, in rodent models, a high sugar diet, neonatal or juvenile HFD, or HFD in conjunction with immune challenge can lead to memory deficits, but short-term HFD alone, in the young adult, does not (Beilharz, Maniam, & Morris, 2016;Boitard et al, 2014;De Luca et al, 2016;Sobesky et al, 2014;Sobesky et al, 2016;Tran & Westbrook, 2017).…”

Section: Introductionmentioning

confidence: 99%

High-fat diet worsens the impact of aging on microglial function and morphology in a region-specific manner

Spencer

Basri

Sominsky

et al. 2019

Neurobiology of Aging

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Hippocampal microglia are vulnerable to the effects of ageing, displaying a primed phenotype and hyper-responsiveness to various stimuli. We have previously shown that short-term high fat diet (HFD) significantly impairs hippocampal-and amygdala-based cognitive function in the aged without affecting it in the young. Here we assessed if morphological and functional changes in microglia might be responsible for this. We analysed hippocampus and amygdala from young and ageing rats that had been given three days HFD; a treatment sufficient to cause both hippocampaland amygdala-dependent cognitive and neuroinflammatory differences in the aged. Ageing led to the expected priming of hippocampal microglia in that it increased microglial numbers and reduced branching in this region. Ageing also increased microglial phagocytosis of microbeads in the hippocampus, but the only effect of HFD in this region was to increase the presence of enlarged synaptophysin boutons in the aged, indicative of neurodegeneration. In the amygdala, HFD exacerbated the effects of ageing on microglial priming (morphology) and markedly suppressed phagocytosis without notably affecting synaptophysin. These data reveal that, like the

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A high-fat high-sugar diet-induced impairment in place-recognition memory is reversible and training-dependent

Cited by 38 publications

References 39 publications

Hippocampal-dependent appetitive control is impaired by experimental exposure to a Western-style diet

Hippocampal-dependent appetitive control is impaired by experimental exposure to a Western-style diet

Food for thought: how nutrition impacts cognition and emotion

High-fat diet worsens the impact of aging on microglial function and morphology in a region-specific manner

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