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Biology subjects

McCracken, M. K.

Publications and source records attributed to McCracken, M. K..

2 recordsLinked to original sources

Altering sensory cues for spatial navigation does not impose a dual-task effect on gait and balance

Walking is an attentionally demanding process that draws from a limited pool of attentional resources. Dual-task assessments, where individuals perform a cognitive task while walking, often reveal changes in gait and balance due to competing attentional demands. As cognitive task difficulty increases, the attentional resources necessary to complete the task also increase, leading to greater interference with gait and balance. However, these interactions are typically examined using contrived lab-based tasks, leaving it unclear how the cognitive processes engaged during real-world movement impact walking. In the present study, we investigated whether increasing the attentional demand of spatial navigation, a cognitive process intrinsically linked to movement, interferes with gait and balance. Healthy adults completed an ambulatory virtual reality homing task in which they walked through a virtual environment and navigated to previously visited locations while wearing ankle and lumbar trackers. We increased the attentional demand of navigation by removing sensory cues during this homing phase: full cues, visual cues only, or self-motion cues only. Navigation performance declined as sensory cues were removed, but we observed no corresponding changes in their spatiotemporal gait and balance metrics. These results show that, in healthy adults, increasing the attentional demand of spatial navigation does not interfere with gait and balance during real-world movement. This finding suggests that locomotor control may be robust to navigation-related cognitive demands. Further research is needed to determine why navigation did not interfere with mobility and to clarify the relationship between these two interconnected processes.

physiology↗

Monomeric IgA antagonizes IgG-mediated enhancement of DENV infection

Dengue virus (DENV) is a prevalent human pathogen, infecting approximately 400 million individuals per year and causing symptomatic disease in approximately 100 million. A distinct feature of dengue is the increased risk for severe disease in some individuals with preexisting DENV-specific immunity. One proposed mechanism for this phenomenon is antibody-dependent enhancement (ADE), in which poorly-neutralizing IgG antibodies from a prior infection opsonize DENV to increase infection of Fc gamma receptor-bearing cells. While IgM and IgG are the most commonly studied DENV-reactive antibody isotypes, our group and others have described the induction of DENV-specific serum IgA responses during dengue. We hypothesized that monomeric IgA would be able to neutralize DENV without the possibility of ADE. To test this, we synthesized IgG and IgA versions of two different DENV-reactive monoclonal antibodies. We demonstrate that isotype-switching does not affect the antigen binding and neutralization properties of the two mAbs. We show that DENV-reactive IgG, but not IgA, mediates ADE in an Fc gamma receptor-positive K562 cells. Furthermore, we show that IgA potently antagonizes the ADE activity of IgG. These results suggest that levels of serum DENV-reactive IgA induced by DENV infection might regulate the overall ADE activity of DENV-immune plasma in vivo and warrants further study as a predictor of disease risk and/or therapeutic.

immunology↗