ABSTRACT
Cellular health is reliant on proteostasis-the maintenance of protein levels regulated through multiple pathways modulating protein synthesis, degradation and clearance. Loss of proteostasis results in serious disease and is associated with aging. One proteinaceous structure underlying the nuclear envelope-the nuclear lamina-coordinates essential processes including DNA repair, genome organization and epigenetic and transcriptional regulation. Loss of proteostasis within the nuclear lamina results in the accumulation of proteins, disrupting these essential functions, either via direct interactions of protein aggregates within the lamina or by altering systems that maintain lamina structure. Here we discuss the links between proteostasis and disease of the nuclear lamina, as well as how manipulating specific proteostatic pathways involved in protein clearance could improve cellular health and prevent/reverse disease.
ABSTRACT
The authors investigated how the nervous system responds to dual task performance. Because dual tasking is associated with greater postural challenges, it was hypothesized that spinal excitability would be reduced when simultaneously performing 2 tasks. For this experiment, participants maintained a lying or standing posture with or without performing a concurrent cognitive task (i.e., reacting to an auditory tone). Spinal excitability was assessed by eliciting the soleus Hoffmann reflex (H-reflex). Results indicated that the H-reflex was 6.4 ± 2.3% smaller (p = .011) when dual compared to single tasking. The reduced H-reflex amplitude, indicating a depressed spinal excitability, when dual tasking is suggested to reflect a neural strategy that individuals adopt to maintain postural stability when cognitive resources are divided between 2 concurrent tasks.