Clinical Scenario: Joint instability is a common condition that often stems from inadequate muscle activation and results in precarious movement patterns. When clinicians attempt to mechanically treat the unstable joint rather than attending to the underlying cause of the instability, patient outcomes may suffer. The use of kinesiology tape (KT) on an unstable joint has been proposed to aid in improving lower-extremity neuromuscular control. Clinical Question: Does KT improve factors of neuromuscular control in an athletic population when compared with no-tape or nonelastic taping techniques? Summary of Key Findings: The current literature was searched, and 5 randomized controlled studies were selected comparing the effects of KT with no-tape or nonelastic taping techniques on lower-extremity neuromuscular control in an athletic population. Primary findings suggest KT is not more effective than no-tape or nonelastic tape conditions at improving lower-extremity neuromuscular control in a healthy population. Clinical Bottom Line: The current evidence suggests that KT is ineffective for improving neuromuscular control at the ankle compared with nonelastic tape or no-tape conditions. KT was also found to be ineffective at improving hip and knee kinematics in healthy runners and cyclists. However, preliminary research has demonstrated improved neuromuscular control in a population displaying excessive knee valgus during a drop jump landing, after the application of KT. Clinicians should be cautious of these conflicting results and apply the best available evidence to their evaluation of the patient’s status. Strength of Recommendation: There is grade B evidence that the use of KT on an athletic population does not improve biomechanical measures of ankle stability. There is inconclusive, grade B evidence that KT improves neuromuscular control at the knee in symptomatic populations.
Background
Alzheimer's disease (AD) is a chronic neurodegenerative disease that causes cognitive impairment. Neuroinflammation induced by activated microglia exacerbates AD. Regulatory T cells (Tregs) play roles in limiting neuroinflammation by converting microglial polarization. Therefore, adoptive regulatory T cell therapy is considered an attractive option for neurodegenerative disorders. However, the mechanism underlying Treg therapy via microglial modulation is not fully understood. In this study, we sought to determine whether adoptively transferred Tregs were effective when microglia were depleted by CSF-1R inhibition.
Methods
First, we inhibited microglial proliferation using GW2580, a CSF-1R inhibitor, when Tregs were transferred. Learning and memory were assessed using a passive avoidance test. The accumulation of Aβ and pTAU, a hallmark of AD, was measured using immunofluorescence. Microglial neuroinflammation was assessed using immunofluorescence and RT-PCR. To track adoptively transferred Tregs, Tregs from Thy1.1 mice were transferred to 3xTg-AD Thy1.2 mice and mouse tissues, including brains, were harvested after 3–112 days.
Results
We found that inhibition of microglial proliferation during Treg transfer did not alter the therapeutic effects of Tregs on cognitive deficits and the accumulation of Aβ and pTAU in 3xTg-AD mice. The expression of pro- and anti-inflammatory markers in the hippocampus of 3xTg mice showed that GW2580 did not affect the inhibition of neuroinflammation by Treg transfer. Additionally, adoptively transferred Tregs were commonly detected in the brain on day 7 after transfer and their levels decreased slowly over 100 days.
Conclusions
Together, these data suggest that adoptively transferred Tregs can survive longer than 100 days in the brain, suppressing microglial activation and thus alleviating AD pathology. The present study provides valuable evidence to support the prolonged efficacy of adoptive Treg therapy in AD.
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