Icon arrays reduce concern over COVID-19 vaccine side effects: a randomized control study.

On April 13, 2021, the CDC announced that the administration of Johnson and Johnson's COVID-19 vaccine would be paused due to a rare blood clotting side effect in ~ 0.0001% of people given the vaccine. Most people who are hesitant to get a COVID-19 vaccine list potential side effects as their main concern (PEW, 2021); thus, it is likely that this announcement increased vaccine hesitancy among the American public. Two days after the CDC's announcement, we administered a survey to a group of 2,046 Americans to assess their changes in attitudes toward COVID-19 vaccines. The aim of this study was to investigate whether viewing icon arrays of side effect risk would prevent increases in COVID-19 vaccine hesitancy due to the announcement. We found that using icon arrays to illustrate the small chance of experiencing the blood clotting side effect significantly prevented increases in aversion toward the Johnson and Johnson vaccine as well as all other COVID-19 vaccines.

How well do ordinary Americans forecast the growth of COVID-19?

Across three experiments (N = 1565), we investigated how forecasts about the spread of COVID 19 are impacted by data trends, and whether patterns of misestimation predict adherence to social-distancing guidelines. We also investigated how mode of data presentation influences forecasting of future cases by showing participants data on the number of COVID-19 cases from a 5-week period in either graphical, tabular, or text-only form. We consistently found that people shown tables produced more accurate forecasts compared to people shown line-graphs of the same data; yet people shown line-graphs were more confident in their estimates. These findings suggest that graphs engender false-confidence in the accuracy of forecasts, that people's forecasts of future cases have important implications for their attitudes concerning social distancing, and that tables may be better than graphs for informing the public about the trajectory of COVID-19.

Dynamic Recovery: GABA Agonism Restores Neural Variability in Older, Poorer Performing Adults.

Aging is associated with cognitive impairment, but there are large individual differences in these declines. One neural measure that is lower in older adults and predicts these individual differences is moment-to-moment brain signal variability. Testing the assumption that GABA should heighten neural variability, we examined whether reduced brain signal variability in older, poorer performing adults could be boosted by increasing GABA pharmacologically. Brain signal variability was estimated using fMRI in 20 young and 24 older healthy human adults during placebo and GABA agonist sessions. As expected, older adults exhibited lower signal variability at placebo, and, crucially, GABA agonism boosted older adults' variability to the levels of young adults. Furthermore, poorer performing older adults experienced a greater increase in variability on drug, suggesting that those with more to gain benefit the most from GABA system potentiation. GABA may thus serve as a core neurochemical target in future work on aging- and cognition-related human brain dynamics.SIGNIFICANCE STATEMENT Prior research indicates that moment-to-moment brain signal variability is lower in older, poorer performing adults. We found that this reduced brain signal variability could be boosted through GABA agonism in older adults to the levels of young adults and that this boost was largest in the poorer performing older adults. These results provide the first evidence that brain signal variability can be restored by increasing GABAergic activity and suggest the promise of developing interventions targeting inhibitory systems to help slow cognitive declines in healthy aging.

GABA levels in ventral visual cortex decline with age and are associated with neural distinctiveness.

Age-related neural dedifferentiation-a decline in the distinctiveness of neural representations in the aging brain-has been associated with age-related declines in cognitive abilities. But why does neural distinctiveness decline with age? Based on prior work in nonhuman primates and more recent work in humans, we hypothesized that the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) declines with age and is associated with neural dedifferentiation in older adults. To test this hypothesis, we used magnetic resonance spectroscopy (MRS) to measure GABA and functional MRI (fMRI) to measure neural distinctiveness in the ventral visual cortex in a set of older and younger participants. Relative to younger adults, older adults exhibited lower GABA levels and less distinct activation patterns for faces and houses in the ventral visual cortex. Furthermore, individual differences in GABA within older adults positively predicted individual differences in neural distinctiveness. These results provide novel support for the view that age-related reductions of GABA contribute to age-related reductions in neural distinctiveness (i.e., neural dedifferentiation) in the human ventral visual cortex.

A multidimensional functional fitness score has a stronger association with type 2 diabetes than obesity parameters in cross sectional data.

OBJECTIVES: We examine here the association of multidimensional functional fitness with type 2 diabetes mellitus (T2DM) as compared to anthropometric indices of obesity such as body mass index (BMI) and waist to hip ratio (WHR) in a sample of Indian population. RESEARCH DESIGN AND METHOD: We analysed retrospective data of 663 volunteer participants (285 males and 378 females between age 28 and 84), from an exercise clinic in which every participant was required to undergo a health related physical fitness (HRPF) assessment consisting of 15 different tasks examining 8 different aspects of functional fitness. RESULTS: The odds of being diabetic in the highest quartile of BMI were not significantly higher than that in the lowest quartile in either of the sexes. The odds of being a diabetic in the highest WHR quartile were significantly greater than the lowest quartile in females (OR = 4.54 (1.95, 10.61) as well as in males (OR = 3.81 (1.75, 8.3). In both sexes the odds of being a diabetic were significantly greater in the lowest quartile of HRPF score than the highest (males OR = 10.52 (4.21, 26.13); females OR = 10.50 (3.53, 31.35)). After removing confounding, the predictive power of HRPF was significantly greater than that of WHR. HRPF was negatively correlated with WHR, however for individuals that had contradicting HRPF and WHR based predictions, HRPF was the stronger predictor of T2DM. CONCLUSION: The association of multidimensional functional fitness score with type 2 diabetes was significantly stronger than obesity parameters in a cross sectional self-selected sample from an Indian city.

Network segregation varies with neural distinctiveness in sensorimotor cortex.

Normal aging is associated with declines in sensorimotor function. Previous studies have linked age-related behavioral declines to decreases in neural differentiation (i.e., dedifferentiation), including decreases in the distinctiveness of neural activation patterns and in the segregation of large-scale neural networks at rest. However, no studies to date have explored the relationship between these two neural measures and whether they explain the same aspects of behavior. To investigate these issues, we collected a battery of sensorimotor behavioral measures in older and younger adults and estimated (a) the distinctiveness of neural representations in sensorimotor cortex and (b) sensorimotor network segregation in the same participants. Consistent with prior findings, sensorimotor representations were less distinct and sensorimotor resting state networks were less segregated in older compared to younger adults. We also found that participants with the most distinct sensorimotor representations exhibited the most segregated sensorimotor networks. However, only sensorimotor network segregation was associated with individual differences in sensorimotor performance, particularly in older adults. These novel findings link network segregation to neural distinctiveness, but also suggest that network segregation may play a larger role in maintaining sensorimotor performance with age.

Foraging theory and the propensity to be obese: an alternative to thrift.

The evolutionary origin of obesity is classically believed to be genetic or developmentally induced thrift, as an adaptation to ancestral feast and famine conditions. However, recently the thrift family of hypotheses have attracted serious criticism necessitating alternative thinking. Optimization of foraging behaviour is an important aspect of behavioural evolution. For a species evolved for optimizing nutritional benefits against predation or other foraging risks, reduction in foraging risk below a threshold dramatically increases the steady-state body weight. In modern life where feeding is detached from foraging, the behavioural regulation mechanisms are likely to fail resulting into escalation of adiposity. At a proximate level the signalling pathways for foraging optimization involve fear induced signal molecules in the brain including Cocaine and Amphetamine Regulated Transcript (CART) interacting with adiposity signals such as leptin. While leptin promotes the expression of the fear peptides, the fear peptides promote anorectic action of leptin. This interaction promotes foraging drive and risk tolerance when the stored energy is low and suppresses hunger and foraging drive when the perceived risk is high. The ecological model of foraging optimization and the molecular model of interaction of these peptides converge in the outcome that the steady state adiposity is an inverse square root function of foraging risk. The foraging optimization model is independent of thrift or insurance hypotheses, but not mutually exclusive. We review existing evidence and suggest testable predictions of the model. Understanding obesity simultaneously at proximate and ultimate levels is likely to suggest effective means to curb the obesity epidemic.

Stochastic resonance model of synaesthesia.

In synaesthesia, stimulation of one sensory modality evokes additional experiences in another modality (e.g. sounds evoking colours). Along with these cross-sensory experiences, there are several cognitive and perceptual differences between synaesthetes and non-synaesthetes. For example, synaesthetes demonstrate enhanced imagery, increased cortical excitability and greater perceptual sensitivity in the concurrent modality. Previous models suggest that synaesthesia results from increased connectivity between corresponding sensory regions or disinhibited feedback from higher cortical areas. While these models explain how one sense can evoke qualitative experiences in another, they fail to predict the broader phenotype of differences observed in synaesthetes. Here, we propose a novel model of synaesthesia based on the principles of stochastic resonance. Specifically, we hypothesize that synaesthetes have greater neural noise in sensory regions, which allows pre-existing multisensory pathways to elicit supra-threshold activation (i.e. synaesthetic experiences). The strengths of this model are (a) it predicts the broader cognitive and perceptual differences in synaesthetes, (b) it provides a unified framework linking developmental and induced synaesthesias, and (c) it explains why synaesthetic associations are inconsistent at onset but stabilize over time. We review research consistent with this model and propose future studies to test its limits. This article is part of a discussion meeting issue 'Bridging senses: novel insights from synaesthesia'.

Neural distinctiveness declines with age in auditory cortex and is associated with auditory GABA levels.

Neural activation patterns in the ventral visual cortex in response to different categories of visual stimuli (e.g., faces vs. houses) are less selective, or distinctive, in older adults than in younger adults, a phenomenon known as age-related neural dedifferentiation. In this study, we investigated whether neural dedifferentiation extends to the auditory cortex. Inspired by previous animal work, we also investigated whether individual differences in GABA are associated with individual differences in neural distinctiveness in humans. 20 healthy young adults (ages 18-29) and 23 healthy older adults (over 65) completed a functional magnetic resonance imaging (fMRI) scan, during which neural activity was estimated while they listened to music and foreign speech. GABA levels in the auditory, ventrovisual and sensorimotor cortex were estimated in the same individuals in a separate magnetic resonance spectroscopy (MRS) scan. Relative to the younger adults, the older adults exhibited both (1) less distinct activation patterns for music vs. speech stimuli and (2) lower GABA levels in the auditory cortex. Also, individual differences in auditory GABA levels (but not ventrovisual or sensorimotor GABA levels) were associated with individual differences in neural distinctiveness in the auditory cortex in the older adults. These results demonstrate that age-related neural dedifferentiation extends to the auditory cortex and suggest that declining GABA levels may play a role in neural dedifferentiation in older adults.

Michigan Neural Distinctiveness (MiND) study protocol: investigating the scope, causes, and consequences of age-related neural dedifferentiation.

BACKGROUND: Aging is often associated with behavioral impairments, but some people age more gracefully than others. Why? One factor that may play a role is individual differences in the distinctiveness of neural representations. Previous research has found that neural activation patterns in visual cortex in response to different visual stimuli are often more similar (i.e., less distinctive) in older vs. young participants, a phenomenon referred to as age-related neural dedifferentiation. Furthermore, older people whose neural representations are less distinctive tend to perform worse on a wide range of behavioral tasks. The Michigan Neural Distinctiveness (MiND) project aims to investigate the scope of neural dedifferentiation (e.g., does it also occur in auditory, motor, and somatosensory cortex?), one potential cause (age-related reductions in the inhibitory neurotransmitter gamma-aminobutyric acid (GABA)), and the behavioral consequences of neural dedifferentiation. This protocol paper describes the study rationale and methods being used in complete detail, but not the results (data collection is currently underway). METHODS: The MiND project consists of two studies: the main study and a drug study. In the main study, we are recruiting 60 young and 100 older adults to perform behavioral tasks that measure sensory and cognitive function. They also participate in functional MRI (fMRI), MR spectroscopy, and diffusion weighted imaging sessions, providing data on neural distinctiveness and GABA concentrations. In the drug study, we are recruiting 25 young and 25 older adults to compare neural distinctiveness, measured with fMRI, after participants take a placebo or a benzodiazepine (lorazepam) that should increase GABA activity. DISCUSSION: By collecting multimodal imaging measures along with extensive behavioral measures from the same subjects, we are linking individual differences in neurochemistry, neural representation, and behavioral performance, rather than focusing solely on group differences between young and old participants. Our findings have the potential to inform new interventions for age-related declines. TRIAL REGISTRATION: This study was retrospectively registered with the ISRCTN registry on March 4, 2019. The registration number is ISRCTN17266136 .

Sensorimotor network segregation declines with age and is linked to GABA and to sensorimotor performance.

Aging is typically associated with declines in sensorimotor performance. Previous studies have linked some age-related behavioral declines to reductions in network segregation. For example, compared to young adults, older adults typically exhibit weaker functional connectivity within the same functional network but stronger functional connectivity between different networks. Based on previous animal studies, we hypothesized that such reductions of network segregation are linked to age-related reductions in the brain's major inhibitory transmitter, gamma aminobutyric acid (GABA). To investigate this hypothesis, we conducted graph theoretical analyses of resting state functional MRI data to measure sensorimotor network segregation in both young and old adults. We also used magnetic resonance spectroscopy to measure GABA levels in the sensorimotor cortex and collected a battery of sensorimotor behavioral measures. We report four main findings. First, relative to young adults, old adults exhibit both less segregated sensorimotor brain networks and reduced sensorimotor GABA levels. Second, less segregated networks are associated with lower GABA levels. Third, less segregated networks and lower GABA levels are associated with worse sensorimotor performance. Fourth, network segregation mediates the relationship between GABA and performance. These findings link age-related differences in network segregation to age-related differences in GABA levels and sensorimotor performance. More broadly, they suggest a neurochemical substrate of age-related dedifferentiation at the level of large-scale brain networks.