Effect of Worry Level on Recall Memory for Odors in ApoE-ε4 Carriers and Non-Carriers.

OBJECTIVE: Increased levels of worry, age, and presence of the apolipoprotein-E (ApoE)-ε4 allele are associated with the risk of developing cognitive declines and Alzheimer's disease (AD). Odor memory performance has been shown to vary as a function of age and ApoE genotype, and odor memory tests are sensitive to preclinical AD. Worry is known to influence verbal memory; however, its effects on odor memory are unknown. This study aimed to assess the relationships between worry, age, and ε4 status on odor memory. METHOD: Worry was evaluated for young (n = 53) and older (n = 45) adults using the Penn State Worry Questionnaire. Odor memory was assessed using the California Odor Learning Test, an olfactory analogue to the California Verbal Learning Test. RESULTS: A significant main effect of worry on long-delay free recall was found, such that increasing worry was associated with better recall across age and ε4 status. A significant interaction effect between ε4 status and worry on both short-and long-delay cued recall was found, such that across age, higher worry was associated with increased cued recall scores among ε4-negative adults, and decreased scores among ε4-positive adults. CONCLUSIONS: Findings demonstrated that worry influences odor memory and exerts a particular effect on cued recall among ε4 carriers who are at a greater risk of developing AD. Worry is a modifiable predictor of cognitive decline and risk of dementia in aging. Future studies on the effects of treatments aimed at reducing worry (e.g., cognitive behavioral therapies for anxiety) on changes in cognitive functioning are warranted.

Age-Related Changes in Gustatory, Homeostatic, Reward, and Memory Processing of Sweet Taste in the Metabolic Syndrome: An fMRI Study.

Age affects the human taste system at peripheral and central levels. Metabolic syndrome is a constellation of risk factors (e.g., abdominal obesity and hypertension) that co-occur, increase with age, and heighten risk for cardiovascular disease, diabetes, and cognitive decline. Little is known about how age, metabolic syndrome, and hunger state interact to influence how the brain processes information about taste. We investigated brain activation during the hedonic evaluation of a pleasant, nutritive stimulus (sucrose) within regions critical for taste, homeostatic energy regulation, and reward, as a function of the interactions among age, metabolic syndrome, and hunger condition. We scanned young and elderly adults, half with risk factors associated with metabolic syndrome twice: Once fasted overnight and once after a preload. Functional magnetic resonance imaging data indicated significant effects of age as well as interactive effects with metabolic syndrome and hunger condition. Age-related differences in activation were dependent on the hunger state in regions critical for homoeostatic energy regulation and basic as well as higher order sensory processing and integration. The effects of age and metabolic syndrome on activation in the insula, orbital frontal cortex, caudate, and the hypothalamus may have particularly important implications for taste processing, energy regulation, and dietary choices.

Differential Effects of BMI on Brain Response to Odor in Olfactory, Reward and Memory Regions: Evidence from fMRI.

：Obesity has reached epidemic proportions, motivating research into the underlying mechanisms. Olfaction is a powerful mediator of food consumption, and obesity has been associated with altered olfactory sensitivity. The current study used an event-related functional magnetic resonance imaging (fMRI) to examine the central processing of odor in humans to gain insight into the effect of the body mass index (BMI) on the neural processes involved in rating the pleasantness of a food odor during a hunger state and in a satiety state. We hypothesized that, during the hedonic evaluation of food odor, BMI would be associated with differences in brain activation within olfactory and higher order processing areas important for perception, reward, and memory. We report novel findings of a dissociation between the relationship between BMI and activation in reward areas and in olfactory and odor memory areas, i.e., activation in reward areas decreased as BMI increased, whereas activation in primary olfactory and memory regions increased as BMI increased. A greater BMI is associated with decreased activation in the reward and frontal regions, supporting a blunted reward response in obesity. These findings have important potential implications for decision making, response inhibition, and reward-based behaviors that may play key roles as causal and maintenance factors in obesity. In contrast, a greater BMI is associated with an increased activation in the primary olfactory and memory areas, which was observed during a hunger state. These results raise the speculative hypothesis that high BMI may be associated with hyperactivation in the olfactory and memory areas, and that over time, the resulting excitotoxic effects may contribute to neurodegenerative changes in these areas.

Reduced brain response to a sweet taste in Hispanic young adults.

Hispanics have an increased risk for metabolic disorders, which evidence suggests may be due to interactions between lifespan biological, genetic, and lifestyle factors. Studies show the diet of many U.S. Hispanic groups have high sugar consumption, which has been shown to influence future preference for and consumption of high-sugar foods, and is associated with increased risk for insulin-related disorders and obesity. Taste is a primary determinant of food preference and selection. Differences in neural response to taste have been associated with obesity. Understanding brain response to sweet taste stimuli in healthy Hispanic adults is an important first step in characterizing the potential neural mechanisms for this behavior. We used fMRI to examine brain activation during the hedonic evaluation of sucrose as a function of ethnicity in Hispanic and non-Hispanic young adults. Taste stimuli were administered orally while subjects were scanned at 3T. Data were analyzed with AFNI via 3dROIstats and 3dMEMA, a mixed effects multi-level analysis of whole brain activation. The Hispanic group had significantly lower ROI activation in the left amygdala and significantly lower whole brain activation in regions critical for reward processing, and hedonic evaluation (e.g. frontal, orbitofrontal, and anterior cingulate cortices) than the non-Hispanic group. Differences in processing of sweet tastes have important clinical and public health implications, especially considering increased risk of metabolic syndrome and cognitive decline in Hispanic populations. Future research to better understanding relationships between health risk and brain function in Hispanic populations is warranted to better conceptualize and develop interventions for these populations.

Education level predicts retrospective metamemory accuracy in healthy aging and Alzheimer's disease.

The current study investigated the effect of education on retrospective metamemory accuracy in 143 healthy older adults and 143 early to moderate Alzheimer's disease (AD) patients, using retrospective measures of confidence in the accuracy of retrieval responses in an episodic odor recognition memory task. Relative confidence accuracy was computed as the difference between confidence judgments for correct and incorrect responses. In both AD patients and controls, individuals reporting 17 years of education or more had significantly more accurate levels of confidence than individuals with 12 years or less. Thus, education was a significant predictor of retrospective metamemory accuracy in healthy aging and AD.

Impaired odor identification in children with histories of heavy prenatal alcohol exposure.

Prenatal alcohol exposure can lead to behavioral and cognitive impairments across multiple domains. Many of the brain regions impacted by prenatal alcohol exposure are also linked with olfactory processing, and odor identification deficits have been documented in certain neurological disorders associated with these brain regions. As odor identification following prenatal alcohol exposure is not well studied, we compared odor identification in children with prenatal exposure to alcohol (AE) to typically developing controls (CON) (N = 16/group). It was hypothesized that children in the AE group would perform more poorly than children in the CON group on the San Diego Odor Identification Test, an identification test of 8 common household odorants. Children exposed to alcohol during prenatal development were significantly impaired in olfactory identification (M = 5.95, SE = 0.37) compared to typically developing controls (M = 7.24, SE = 0.37). These findings confirmed the hypothesis that prenatal exposure to alcohol is associated with odor identification deficits, and suggest that further research is warranted to identify the mechanisms underlying these deficits, the integrity of brain areas that are involved, and to determine whether olfactory performance might contribute to better identification of children at risk for behavioral and cognitive deficits.