Instrumented measures of postural control in college dancers with and without chronic ankle instability.

OBJECTIVES: To determine whether collegiate dancers with chronic ankle instability (CAI) demonstrated impaired postural control during instrumented measures of single-leg static balance compared to dancers without CAI. DESIGN: Cross sectional design. SETTING: University dance studios. PARTICIPANTS: We included N = 39 dance majors from a large, public university. We stratified participants into CAI (n = 20, age = 20 ± 1.8, IdFAI = 17.3 ± 5.7, number of sprains = 1.9 ± 1.1) and Control groups (n = 19, age = 20 ± 1.2, IdFAI = 2.5 ± 3.0). MAIN OUTCOME MEASURES: Participants performed 3 x 10-s single-leg, static balance trials on a pressure mat in two different conditions, foot-flat eyes closed and demi-pointe eyes open. We measured six different time-to-boundary (TTB) measurements during each balance trial and calculated the average of the 3 trials for each condition. Participants also completed the Foot and Ankle Ability Measure (FAAM) sport and activities of daily living (ADL) questionnaires. RESULTS: The CAI group reported greater IdFAI and lower FAAM-ADL and FAAM-Sport scores compared to the control group. We observed no significant differences in TTB measurements between the CAI and control groups during either balance conditions. CONCLUSIONS: Instrumented measures of static postural control were not impaired in college dancers with CAI compared dancers without CAI.

Rescue of ATXN3 neuronal toxicity in Caenorhabditiselegans by chemical modification of endoplasmic reticulum stress.

Polyglutamine expansion diseases are a group of hereditary neurodegenerative disorders that develop when a CAG repeat in the causative genes is unstably expanded above a certain threshold. The expansion of trinucleotide CAG repeats causes hereditary adult-onset neurodegenerative disorders, such as Huntington's disease, dentatorubral-pallidoluysian atrophy, spinobulbar muscular atrophy and multiple forms of spinocerebellar ataxia (SCA). The most common dominantly inherited SCA is the type 3 (SCA3), also known as Machado-Joseph disease (MJD), which is an autosomal dominant, progressive neurological disorder. The gene causatively associated with MJD is ATXN3 Recent studies have shown that this gene modulates endoplasmic reticulum (ER) stress. We generated transgenic Caenorhabditiselegans strains expressing human ATXN3 genes in motoneurons, and animals expressing mutant ATXN3-CAG89 alleles showed decreased lifespan, impaired movement, and rates of neurodegeneration greater than wild-type ATXN3-CAG10 controls. We tested three neuroprotective compounds (Methylene Blue, guanabenz and salubrinal) believed to modulate ER stress and observed that these molecules rescued ATXN3-CAG89 phenotypes. Furthermore, these compounds required specific branches of the ER unfolded protein response (UPRER), reduced global ER and oxidative stress, and polyglutamine aggregation. We introduce new C. elegans models for MJD based on the expression of full-length ATXN3 in a limited number of neurons. Using these models, we discovered that chemical modulation of the UPRER reduced neurodegeneration and warrants investigation in mammalian models of MJD.