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Megan Roy

Bio: Megan Roy is an academic researcher from American University. The author has contributed to research in topics: Cognitive skill & Cognition. The author has an hindex of 1, co-authored 1 publications receiving 49 citations.

Papers
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Journal ArticleDOI
TL;DR: Evidence is reviewed that consuming a WD is associated with the emergence of pathophysiologies in the hippocampus, an important brain substrate for learning, memory, and cognition, and how eating a WD could impair hippocampal function, producing cognitive deficits that promote increased WD intake and body weight gain.
Abstract: Over the past decade, a great deal of research has established the importance of cognitive processes in the control of energy intake and body weight. The present paper begins by identifying several of these cognitive processes. We then summarize evidence from human and nonhuman animal models, which shows how excess intake of obesity-promoting Western diet (WD) may have deleterious effects on these cognitive control processes. Findings that these effects may be manifested as early-life deficits in cognitive functioning and may also be associated with the emergence of serious late-life cognitive impairment are described. Consistent with these possibilities, we review evidence, obtained primarily from rodent models, that consuming a WD is associated with the emergence of pathophysiologies in the hippocampus, an important brain substrate for learning, memory, and cognition. The implications of this research for mechanism are discussed within the context of a "vicious-cycle model," which describes how eating a WD could impair hippocampal function, producing cognitive deficits that promote increased WD intake and body weight gain, which could contribute to further hippocampal dysfunction, cognitive decline, and excess eating and weight gain.

72 citations


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01 Jan 2018
TL;DR: The first large randomized controlled trials of multidomain lifestyle interventions to prevent cognitive impairment have been completed, and the results suggest that targeting interventions to individuals at risk of dementia is an effective strategy.
Abstract: Research into dementia prevention is of paramount importance if the dementia epidemic is to be halted. Observational studies have identified several potentially modifiable risk factors for dementia, including hypertension, dyslipidaemia and obesity at midlife, diabetes mellitus, smoking, physical inactivity, depression and low levels of education. Randomized clinical trials are needed that investigate whether interventions targeting these risk factors can reduce the risk of cognitive decline and dementia in elderly adults, but such trials are methodologically challenging. To date, most preventive interventions have been tested in small groups, have focused on a single lifestyle factor and have yielded negative or modest results. Given the multifactorial aetiology of dementia and late-onset Alzheimer disease, multidomain interventions that target several risk factors and mechanisms simultaneously might be necessary for an optimal preventive effect. In the past few years, three large multidomain trials (FINGER, MAPT and PreDIVA) have been completed. The FINGER trial showed that a multidomain lifestyle intervention can benefit cognition in elderly people with an elevated risk of dementia. The primary results from the other trials did not show a statistically significant benefit of preventive interventions, but additional analyses among participants at risk of dementia showed beneficial effects of intervention. Overall, results from these three trials suggest that targeting of preventive interventions to at-risk individuals is an effective strategy. This Review discusses the current knowledge of lifestyle-related risk factors and results from novel trials aiming to prevent cognitive decline and dementia. Global initiatives are presented, including the World Wide FINGERS network, which aims to harmonize studies on dementia prevention, generate high-quality scientific evidence and promote its implementation.

228 citations

Journal ArticleDOI
TL;DR: Sucralose may have effects on glucose metabolism, and this study complements findings previously reported in other trials, and further studies are needed to confirm the decrease in insulin sensitivity.

53 citations

Journal ArticleDOI
TL;DR: The current scientific evidence about the mechanisms and factors relating WD consumption with altered brain function and behavior are summarized, aiming to tackle and prevent this current pandemic.
Abstract: The Western diet (WD) pattern characterized by high daily intake of saturated fats and refined carbohydrates often leads to obesity and overweight, and it has been linked to cognitive impairment and emotional disorders in both animal models and humans. This dietary pattern alters the composition of gut microbiota, influencing brain function by different mechanisms involving the gut-brain axis. In addition, long-term exposure to highly palatable foods typical of WD could induce addictive-like eating behaviors and hypothalamic-pituitary-adrenal (HPA) axis dysregulation associated with chronic stress, anxiety, and depression. In turn, chronic stress modulates eating behavior, and it could have detrimental effects on different brain regions such as the hippocampus, hypothalamus, amygdala, and several cortical regions. Moreover, obesity and overweight induce neuroinflammation, causing neuronal dysfunction. In this review, we summarize the current scientific evidence about the mechanisms and factors relating WD consumption with altered brain function and behavior. Possible therapeutic interventions and limitations are also discussed, aiming to tackle and prevent this current pandemic.

47 citations

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TL;DR: It is proposed that the interaction of diet with the microbiome is at the core of most mechanisms by which gut microbes affect host brain function.

46 citations

Journal ArticleDOI
TL;DR: In this paper, the authors investigated whether the gut-derived hormone ghrelin acts in the ventral HPC (vHPC) to increase meal size through interactions with gut derived satiation signaling.

44 citations