Background: Falls among the elderly present significant physical, psychological, and economic challenges. Fall prevention strategies, such as balance and muscle strengthening exercises, are essential but often require long-term commitment. This study explores the potential of transcranial direct current stimulation (tDCS) as an adjunct to balance training to enhance physical performance in the elderly. Method: A randomized, double-blind, sham-controlled design was employed to compare balance training with active or sham tDCS. Participants underwent baseline assessments, followed by a six-week intervention period. The intervention protocol consisted of 2 mA, 20 min of anodal tDCS over the left primary motor cortex, three times weekly. Post-intervention assessments were conducted a few days after the intervention and follow-up at 4 weeks. Results: Following 18 sessions of anodal tDCS combined with balance exercise training, no significant group differences were observed for the Time Up and Go, One-Leg Standing, lower-limb strength, or the 6 min walk test (6MWT), although both the intervention and control groups demonstrated significant improvements over time. A significant group × time interaction was found only for the 6MWT, with participants in the intervention group exhibiting greater improvements in the 6MWT compared to controls. Conclusions: Anodal tDCS combined with balance exercise training selectively enhanced physical endurance but did not confer additional benefits for balance, gait, or leg strength in healthy older adults. These findings suggest that tDCS may serve as a promising adjunct to exercise for improving endurance-related outcomes in aging populations. Control of various variables for tDCS and exercise is necessary.
Long QT syndrome type 3 (LQTS3), caused by gain-of-function mutations in the SCN5A gene, encompasses a spectrum of clinical presentations, ranging from asymptomatic carriers to severe arrhythmic phenotypes, representing the “silent killer” and “brutal killer” dichotomy. The p.I239V mutation is associated with mild symptoms and minimal arrhythmic events, whereas the newly identified p.M1487K mutation is linked to life-threatening arrhythmic storms. This study aimed to explore the electrophysiological properties of these mutations and their responses to sodium channel blockers to advance precision medicine in LQTS3 management. Genetic analysis identified rare SCN5A mutations in two LQTS3 patients. Site-directed mutagenesis was used to construct mutant SCN5A plasmids, which were expressed in HEK293 cells. Electrophysiological properties were analyzed using patch-clamp techniques, and pharmacological responses to flecainide, mexiletine, and ranolazine were evaluated. Electrophysiological recordings correlated with clinical presentations. Both mutations showed increased window INa and faster recovery from inactivation. The p.I239V mutation lacked sustained INa, while p.M1487K exhibited significantly increased sustained INa (2.3 ± 2.15%, P < 0.0001). Mexiletine and ranolazine effectively reduced sustained INa by 76.15 ± 5.83, and 77.63 ± 9.41%, respectively, outperforming flecainide, aligning with clinical responses. This study highlights the role of sustained INa in LQTS3 severity and underscores the importance of mutation-specific treatments. By tailoring treatments to the electrophysiological characteristics of each mutation, precision medicine offers a promising approach to improving patient outcomes in LQTS3.