The Effects of Instruction on Landing Strategies in Female College-Aged Dancers and Non-Dancers: A Pilot Study

Background Female athletic participation has increased over the past decade and with it the prevalence of knee injuries. Current research demonstrates an increased risk of anterior cruciate ligament (ACL) injury for female athletes. However, a number of studies have pointed out that ballet and modern dancers exhibit a lower incidence of ACL injuries despite the fact that they perform jumping and landing frequently. Objective The objective of this study was to examine how dance experience and instruction affect the lower extremity biomechanics during drop landings. Specifically, lower extremity joint alignment and muscle activation of gluteus maximus and gluteus medius were assessed. Design Quasi-experimental, cross-sectional Methods Thirteen active women, 5 dancers and 8 non-dancers, 18-22 years of age, were recruited to participate in this study. In the non-instructed (NI) condition, participants were shown a video demonstrating the drop landing movement in a leg turned out (externally rotated) position. The participants performed the drop landing based on their interpretation of the movement on the video. They were then shown the same video with additional verbal instructions (VI) on how to perform the landing, and asked to perform the same drop landing again. Surface electromyography (EMG) was used to measure muscle activation of the gluteus medius and gluteus maximus during the landings. Kinematics of the lower extremity joints during the deceleration phase of landing were acquired using a digital motion capture system. 2x2 repeated measures ANOVA’s were used to assess the effect of dance experience (dancers and non-dancers) and verbal instruction (NI and VI) on lower extremity biomechanics and gluteal muscle activation. Results The 2-way ANOVA revealed a significant group by condition interaction with right gluteus medius (p=0.003) and right glut maximus (p=0.009). Dancers showed a significant increase in gluteus medius (p=0.02) while non-dancers showed a significant decrease in gluteus medius (p=0.04) with verbal instruction. Both groups showed significant changes in knee valgus (p\u3c0.001), hip abduction (p=0.027), and hip internal rotation (p=0.031) with verbal instruction. No significant differences were found when comparing those kinematic variables between groups. Discussion and Conclusion Our results demonstrated that brief verbal instruction has an effect on landing kinematics in college aged women. For both dancer and non-dancers, decreased knee valgus, decreased hip internal rotation, and increased hip abduction were found after verbal instruction was given. In addition, dancers exhibited increased gluteal muscle activation with instruction whereas non-dancers showed a decrease in gluteal muscle activation with instruction. Our findings indicated that explicit movement instruction may result in diminished muscle activation in non-dancers. The heightened awareness of neuromuscular control from dance training may be related to the reduced knee injury risk

ΔFosB Regulates Gene Expression and Cognitive Dysfunction in a Mouse Model of Alzheimer\u27s Disease.

Alzheimer\u27s disease (AD) is characterized by cognitive decline and 5- to 10-fold increased seizure incidence. How seizures contribute to cognitive decline in AD or other disorders is unclear. We show that spontaneous seizures increase expression of ΔFosB, a highly stable Fos-family transcription factor, in the hippocampus of an AD mouse model. ΔFosB suppressed expression of the immediate early gene c-Fos, which is critical for plasticity and cognition, by binding its promoter and triggering histone deacetylation. Acute histone deacetylase (HDAC) inhibition or inhibition of ΔFosB activity restored c-Fos induction and improved cognition in AD mice. Administration of seizure-inducing agents to nontransgenic mice also resulted in ΔFosB-mediated suppression of c-Fos, suggesting that this mechanism is not confined to AD mice. These results explain observations that c-Fos expression increases after acute neuronal activity but decreases with chronic activity. Moreover, these results indicate a general mechanism by which seizures contribute to persistent cognitive deficits, even during seizure-free periods

Epigenetic suppression of hippocampal calbindin-D28k by ΔFosB drives seizure-related cognitive deficits.

The calcium-binding protein calbindin-D28k is critical for hippocampal function and cognition, but its expression is markedly decreased in various neurological disorders associated with epileptiform activity and seizures. In Alzheimer\u27s disease (AD) and epilepsy, both of which are accompanied by recurrent seizures, the severity of cognitive deficits reflects the degree of calbindin reduction in the hippocampal dentate gyrus (DG). However, despite the importance of calbindin in both neuronal physiology and pathology, the regulatory mechanisms that control its expression in the hippocampus are poorly understood. Here we report an epigenetic mechanism through which seizures chronically suppress hippocampal calbindin expression and impair cognition. We demonstrate that ΔFosB, a highly stable transcription factor, is induced in the hippocampus in mouse models of AD and seizures, in which it binds and triggers histone deacetylation at the promoter of the calbindin gene (Calb1) and downregulates Calb1 transcription. Notably, increasing DG calbindin levels, either by direct virus-mediated expression or inhibition of ΔFosB signaling, improves spatial memory in a mouse model of AD. Moreover, levels of ΔFosB and calbindin expression are inversely related in the DG of individuals with temporal lobe epilepsy (TLE) or AD and correlate with performance on the Mini-Mental State Examination (MMSE). We propose that chronic suppression of calbindin by ΔFosB is one mechanism through which intermittent seizures drive persistent cognitive deficits in conditions accompanied by recurrent seizures

ΔFosB Regulates Gene Expression and Cognitive Dysfunction in a Mouse Model of Alzheimer’s Disease

Alzheimer’s disease (AD) is characterized by cognitive decline and 5- to 10-fold increased seizure incidence. How seizures contribute to cognitive decline in AD or other disorders is unclear. We show that spontaneous seizures increase expression of ΔFosB, a highly stable Fos-family transcription factor, in the hippocampus of an AD mouse model. ΔFosB suppressed expression of the immediate early gene c-Fos, which is critical for plasticity and cognition, by binding its promoter and triggering histone deacetylation. Acute histone deacetylase (HDAC) inhibition or inhibition of ΔFosB activity restored c-Fos induction and improved cognition in AD mice. Administration of seizure-inducing agents to nontransgenic mice also resulted in ΔFosB-mediated suppression of c-Fos, suggesting that this mechanism is not confined to AD mice. These results explain observations that c-Fos expression increases after acute neuronal activity but decreases with chronic activity. Moreover, these results indicate a general mechanism by which seizures contribute to persistent cognitive deficits, even during seizure-free periods