It is known that small and large numbers facilitate left/right respectively (the SNARC effect). Recently, it has been proposed that numerical magnitude is just one example of a range of quantities, which have a common cognitive/neural representation. To investigate this proposition, response congruency effects were explored for stimuli which differed according to their: (a) numerical size, (b) physical size, (c) luminance, (d) conceptual size and (e) auditory intensity. In a series of experiments, groups of undergraduate participants made two-alternative forced choice discriminations with their left or right hands. There were clear interactions between magnitude and responding hand whereby right hand responses were faster for stimuli with (a) large numbers, (b) large physical size, (c) low luminance, and (d) a reference to large objects. There was no congruency effect for the auditory stimuli. The data demonstrate that the response congruency effect observed for numbers also occurs for a variety of other non-numerical visual quantities. These results support models of general magnitude representation and suggest that the association between magnitude and the left/right sides of space may not be related to culture and/or directional reading habits.

Background/Objectives Vision-based speed of processing (VSOP) training is a promising cognitive intervention for older adults. However, it is unknown whether VSOP training can affect cognitive processing in individuals at high risk for dementia. Here, we examined cognitive and neural effects of VSOP training in older adults with amnestic mild cognitive impairment (aMCI) and contrasted those effects with an active control (mental leisure activities; MLA). Design A randomized single-blinded controlled pilot trial. Setting An academic medical center. Participants Twenty-one participants with aMCI. Intervention A 6-week computerized VSOP training. Measurements Multiple cognitive processing measures, instrumental activities of daily living (IADL), and two key resting state neural networks regulating cognitive processing: central executive network (CEN) and default mode network (DMN). Results We found that, compared to MLA control, VSOP training led to significant improvements in trained (processing speed and attention: F1,19 = 6.61, Partial η2 = 0.26, p = .019) and untrained cognitive domains (working memory: F1,19 = 7.33, Partial η2 = 0.28, p = .014; IADL: F1,19 = 5.16, Partial η2 = 0.21, p = .035), and protective maintenance in DMN (F1, 9 = 14.63, Partial η2 = 0.62, p = .004). Additionally, VSOP training, but not MLA, resulted in a significant improvement in CEN connectivity (Z = −2.37, p = .018). Conclusion We identified both target and transfer effects of VSOP training and revealed links between VSOP training and two key neural networks associated with aMCI. These findings highlight the potential of VSOP training to slow cognitive decline in aMCI. Further delineation of mechanisms underlying VSOP-induced plasticity is necessary to understand in what populations and conditions such training may be most effective.

The parasympathetic nervous system (PNS) is critical for adaptation to environment demands. PNS can reflect an individual's regulatory capacity of frontal brain regions and has been linked to cognitive capacity. Yet, the relationship of PNS function to cognitive decline and abnormal frontal function that characterize preclinical progression toward Alzheimer's disease (AD) is unclear. Here, we aimed to elucidate the relationship between PNS function and AD-associated neurodegeneration by testing two competing hypotheses involving frontal regions' activity (neurodegeneration vs. compensation). In 38 older human adults with amnestic mild cognitive impairment (aMCI) or normative cognition, we measured AD-associated neurodegeneration (AD signature cortical thickness; ADSCT), resting-state functional magnetic resonance imaging of frontal regions' spontaneous activation, and an electrocardiography measure of PNS (high frequency heart rate variability; HF-HRV). HF-HRV was assessed at rest and during a cognitive task protocol designed to capture HF-HRV reactivity. Higher HF-HRV at rest was significantly related to both more severe AD-associated neurodegeneration (lower ADSCT scores) and worse cognitive ability. Cognitive impairments were also related to greater suppression of HF-HRV reactivity. High activities of the anterior cingulate cortex significantly mediated relationships between ADSCT and both HF-HRV at rest and HF-HRV reactivity. Notably, these relationships were not affected by the clinical phenotype. We show that AD-associated neurodegeneration is associated with altered PNS regulation and that compensatory processes linked to frontal overactivation might be responsible for those alterations. This finding provides the first line of evidence in a new framework for understanding how early-stage AD-associated neurodegeneration affects autonomic regulation.

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Apolipoprotein E (APOE) ε4 carriers and patients with amnestic mild cognitive impairment (MCI) have high risk of developing Alzheimer's disease (AD). The Scaffolding Theory of Aging and Cognition proposes that recruitment of additional frontal brain regions can protect cognition against aging. This thesis has yet to be fully tested in older adults at high risk for AD. In the present study, 75 older participants (mean age: 74 years) were included. Applying a voxel-wise approach, fractional amplitude of low-frequency fluctuations (fALFF) in resting-state functional neuroimaging data were analyzed as a function of APOEε4 status (carrier vs. noncarrier) and clinical status (healthy control [HC] vs. MCI) using a 2×2 analysis of covariance (ANCOVA). Measures of cognition and cerebrospinal fluid levels of amyloid-beta were also obtained. Three frontal regions were identified with significant interaction effects using ANCOVA (corrected p < .01): left-insula, left-inferior frontal gyrus (IFG), and right-precentral gyrus. The HC/APOEε4 carrier group had significantly higher fALFF in all three regions than other groups. In the entire sample, for two regions (left insula and left IFG), a significant positive relationship between β-amyloid and memory was only observed among individuals with low fALFF. Our results suggest higher activity in frontal regions may explain being cognitively normal among a subgroup of APOEε4 carriers and protect against the negative impact of AD-associated pathology on memory. This is an observation with potential implications for AD therapeutics.

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Memory deterioration is the earliest and most devastating cognitive deficit in normal aging and Alzheimer’s disease. Some older adults, known as “Supernormals”, maintain excellent memory. This study examined relationships between cerebral amyloid deposition and functional connectivity (FC) within the cingulate cortex (CC) and between CC and other regions involved in memory maintenance between Supernormals, healthy controls, and those at risk for Alzheimer’s disease (amnestic mild cognitive impairment). Supernormals had significantly stronger FC between anterior CC and R-hippocampus, middle CC (MCC) and L-superior temporal gyrus, and posterior CC and R-precuneus, while weaker FC between MCC and R-middle frontal gyrus and MCC and R-thalamus than other groups. All of these FC were significantly related to memory and global cognition in all participants. Supernormals had less amyloid deposition than other groups. Relationships between global cognition and FC were stronger among amyloid positive participants. Relationships between memory and FC remained regardless of amyloid level. This revealed how CC-related neural function participates in cognitive maintenance in the presence of amyloid deposition, potentially explaining excellent cognitive function among Supernormals.

Understanding the association between autonomic nervous system [ANS] function and brain morphology across the lifespan provides important insights into neurovisceral mechanisms underlying health and disease. Resting‐state ANS activity, indexed by measures of heart rate [HR] and its variability [HRV] has been associated with brain morphology, particularly cortical thickness [CT]. While findings have been mixed regarding the anatomical distribution and direction of the associations, these inconsistencies may be due to sex and age differences in HR/HRV and CT. Previous studies have been limited by small sample sizes, which impede the assessment of sex differences and aging effects on the association between ANS function and CT. To overcome these limitations, 20 groups worldwide contributed data collected under similar protocols of CT assessment and HR/HRV recording to be pooled in a mega‐analysis (N = 1,218 (50.5% female), mean age 36.7 years (range: 12–87)). Findings suggest a decline in HRV as well as CT with increasing age. CT, particularly in the orbitofrontal cortex, explained additional variance in HRV, beyond the effects of aging. This pattern of results may suggest that the decline in HRV with increasing age is related to a decline in orbitofrontal CT. These effects were independent of sex and specific to HRV; with no significant association between CT and HR. Greater CT across the adult lifespan may be vital for the maintenance of healthy cardiac regulation via the ANS—or greater cardiac vagal activity as indirectly reflected in HRV may slow brain atrophy. Findings reveal an important association between CT and cardiac parasympathetic activity with implications for healthy aging and longevity that should be studied further in longitudinal research.