Intrinsic and Extrinsic Motives Support Adults' Regular Physical Activity Maintenance.

Motives for physical activity were compared between adults who either successfully or unsuccessfully maintained regular physical activity over the last 10 years. Adults age 28-45 (N=721) completed an online survey, reporting their current physical activity levels and self-determination theory (SDT) motives, as well as their physical activity levels at least 10 years prior. With participants' current and retrospective reports of their physical activity, four sample subgroups were created, including maintainers, improvers, decliners, and sedentary. ANOVA analyses were used to examine differences in motives between physical activity maintenance groups. Those who successfully maintained regular physical activity (maintainers) reported higher intrinsic and extrinsic motives compared to those who were not regularly active ( P <0.05). Interestingly, maintainers reported similar physical activity motives compared to those who reported increased physical activity over time. Among the current sample and consistent with theory, motives for physical activity significantly influenced participants' long-term maintenance of regular physical activity. Future interventions should consider these constructs to promote sustained physical activity.

SMN deficiency negatively impacts red pulp macrophages and spleen development in mouse models of spinal muscular atrophy.

Spinal muscular atrophy (SMA) is a progressive neurodegenerative disease that is the leading genetic cause of infantile death. It is caused by a severe deficiency of the ubiquitously expressed Survival Motor Neuron (SMN) protein. SMA is characterized by α-lower motor neuron loss and muscle atrophy, however, there is a growing list of tissues impacted by a SMN deficiency beyond motor neurons. The non-neuronal defects are observed in the most severe Type I SMA patients and most of the widely used SMA mouse models, however, as effective therapeutics are developed, it is unclear whether additional symptoms will be uncovered in longer lived patients. Recently, the immune system and inflammation has been identified as a contributor to neurodegenerative diseases such as ALS. To determine whether the immune system is comprised in SMA, we analyzed the spleen and immunological components in SMA mice. In this report, we identify: a significant reduction in spleen size in multiple SMA mouse models and a pathological reduction in red pulp and extramedullary hematopoiesis. Additionally, red pulp macrophages, a discrete subset of yolk sac-derived macrophages, were found to be altered in SMA spleens even in pre-symptomatic post-natal day 2 animals. These cells, which are involved in iron metabolism and the phagocytosis of erythrocytes and blood-borne pathogens are significantly reduced prior to the development of the neurodegenerative hallmarks of SMA, implying a differential role of SMN in myeloid cell ontogeny. Collectively, these results demonstrate that SMN deficiency impacts spleen development and suggests a potential role for immunological development in SMA.