Effectiveness of an exercise program on postural control in frail older adults

Background: Exercise programs have proved to be helpful for frail older adults. This study aimed to investigate the effects of an exercise program with a focus on postural control exercises in frail older adults. Method: Twenty-six older adults (76.7 +/- 4.9 years) deemed clinically stable, chosen from the Falls Unit, University Hospital Mutua Terrassa, Barcelona, Spain, participated in this single-group study. Volunteers' postural control was evaluated using the Timed Up and Go test (TUG) and the Guralnik test battery, and their static and dynamic posturography were evaluated using the Synapsys Posturography System (R). These evaluations were performed before and after the intervention program, which included an educational session and two weekly 1-hour sessions over an 8-week period of stretching exercises, proprioception, balance, and motor coordination. Data were analyzed using the Student's t-test or the Wilcoxon test, with a significance level of 5%. Results: The TUG and Guralnik tests did not show significant differences. Concerning static posturography, there was improvement in the base of support (P = 0.006), anteroposterior displacement with eyes open (P = 0.02) and closed (P = 0.03), and the total amplitude of the center of pressure with eyes closed (P = 0.02). Regarding dynamic posturography, a decrease of the oscillation speed in the anteroposterior direction (P = 0.01) was observed in individuals with their eyes open. Conclusion: The program used in this study was safe and was able to promote some improvement in postural control, especially in the anteroposterior direction and in the base of support. However, it is noteworthy that further improvements could be obtained from a program of longer duration and greater frequency.

Mutations in ADAR1 cause Aicardi-Goutieres syndrome associated with a type I interferon signature

Adenosine deaminases acting on RNA (ADARs) catalyze the hydrolytic deamination of adenosine to inosine in double-stranded RNA (dsRNA) and thereby potentially alter the information content and structure of cellular RNAs. Notably, although the overwhelming majority of such editing events occur in transcripts derived from Alu repeat elements, the biological function of non-coding RNA editing remains uncertain. Here, we show that mutations in ADAR1 (also known as ADAR) cause the autoimmune disorder Aicardi-Goutieres syndrome (AGS). As in Adar1-null mice, the human disease state is associated with upregulation of interferon-stimulated genes, indicating a possible role for ADAR1 as a suppressor of type I interferon signaling. Considering recent insights derived from the study of other AGS-related proteins, we speculate that ADAR1 may limit the cytoplasmic accumulation of the dsRNA generated from genomic repetitive elements.