Does active learning benefit spatial memory during navigation with restricted peripheral field?

Spatial learning of real-world environments is impaired with severely restricted peripheral field of view (FOV). In prior research, the effects of restricted FOV on spatial learning have been studied using passive learning paradigms – learners walk along pre-defined paths and are told the location of targets to be remembered. Our research has shown that mobility demands and environmental complexity may contribute to impaired spatial learning with restricted FOV through attentional mechanisms. Here, we examine the role of active navigation, both in locomotion and in target search. First, we compared effects of active versus passive locomotion (walking with a physical guide versus being pushed in a wheelchair) on a task of pointing to remembered targets in participants with simulated 10° FOV. We found similar performance between active and passive locomotion conditions in both simpler (Experiment 1) and more complex (Experiment 2) spatial learning tasks. Experiment 3 required active search for named targets to remember while navigating, using both a mild and a severe FOV restriction. We observed no difference in pointing accuracy between the two FOV restrictions but an increase in attentional demands with severely restricted FOV. Experiment 4 compared active and passive search with severe FOV restriction, within subjects. We found no difference in pointing accuracy, but observed an increase in cognitive load in active versus passive search. Taken together, in the context of navigating with restricted FOV, neither locomotion method nor level of active search affected spatial learning. However, the greater cognitive demands could have counteracted the potential advantage of the active learning conditions.

     

Glycosylated Hemoglobin Level,Race/Ethnicity,and Cognition in Midlife and Early Old Age

Empirical evidence linking racial/ethnic differences in glycosylated hemoglobin levels (HbA1c) to cognitive function in midlife and early old age is limited. We use biomarker data from the Health and Retirement Study (HRS, 2006–2014), on adults 50–64 years at baseline (57–73 years by 2014), and fit multinomial logistic regression models to assess the association between baseline HbA1c, cognitive function (using Langa–Weir classifications) and mortality across 8 years. Additionally, we test for modification effects by race/ethnicity. In age- and sex-adjusted models high HbA1c level was associated with lower baseline cognition and higher relative risk ratios (RRR; vs. normal cognition) for cognitive impairment no dementia (CIND; RRR = 2.3; 95%CI = [1.38;3.84]; p < .01), and dementia (RRR = 4.00; 95%CI = [1.76;9.10]; p < .01). Adjusting for sociodemographic, behavioral risk factors, and other health conditions explained the higher RRR for CIND and attenuated the RRR for dementia by approximately 30%. HbA1c levels were not linked to the slope of cognitive decline, and we found no evidence of modification effects for HbA1c by race/ethnicity. Targeting interventions for glycemic control in the critical midlife period can protect baseline cognition and buffer against downstream development of cognitive impairment. This can yield important public health benefits and reductions in burdens associated with cognitive impairment, particularly among race/ethnic minorities who are at higher risk for metabolic diseases.