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Special Populations

(43) COMMUNICATION ERROR: RELATIONSHIP BETWEEN NEURAL CELL ADHESION MOLECULE EXPRESSION AND MUSCLE ACTIVATION IN PARKINSON’S DISEASE

Thursday, July 11, 2024
2:00 PM – 3:30 PM East Coast USA Time
Location: Exhibit Hall
Abstract Details: PURPOSE: Parkinson’s disease (PD) is a neurodegenerative disorder that is characterized by motor and nonmotor symptoms. Motor symptoms often include bradykinesia, abnormal gait, resting tremor, and muscle rigidity. Neural cell adhesion molecule (NCAM) is expressed by muscle cells (myofibers) when there is disruption of the neuromuscular junction and the myofiber is denervated to signal a call for reinnervation by nearby motor neurons. If a myofiber fails to be reinnervated, it will undergo apoptosis; accumulated myofiber death will eventually influence muscle activation. However, the relationship between NCAM expression and muscle activation is unknown. Therefore, the purpose of this pilot study was to investigate the relationship between relative (rT1, rT2) NCAM expression and muscle activation in persons with PD.

Methods:  Bergstrom muscle biopsies of the vastus lateralis of the more-effected PD leg were collected from six persons with PD (F=4; 67±9 yrs). Immunofluorescence was used to analyze myosin heavy chain and NCAM expression. NCAM expression was quantified by manual counting. For muscle performance, torque was measured as p</span>articipants performed three maximal voluntary isometric contractions of the quadriceps femoris. Muscle activation was measured using surface electromyography (sEMG) of the vastus lateralis, and EMG and torque were collected at 2000 Hz. EMG signals were bandpass, zero phase, fourth order Butterworth filtered. Peak EMG amplitude (pEMG) was calculated as the highest 500 ms epoc from the EMG time curve normalized to the rate of EMG rise (RER). RER was calculated as the highest rate of change in EMG from the first derivative of the sEMG signal and normalized to pEMG (pRERn). Pearson correlation coefficients (r) were used to determine relationships between dependent variables. Significance was set at p< 0.05.

Results: rT1/NCAM+ (2.0 ± 1.4%) was negatively correlated with pRERn (1.04 ± 0.8 a.u.; r=-0.94, p</span>=0.005) and pEMG (r=-0.88, p=0.02). rT2/NCAM+ (3.2 ± 0.9%) was negatively correlated with peak torque (120 ± 54 Nm/s; r=-0.96, p=0.002). There we no significant correlations between any other variables. CONCLUSION: Our pilot data suggests that greater rT1/NCAM+ expression is associated with a slower rate (i.e., pRERn) and reduced amplitude (i.e., pEMG) of muscle activation. Increased denervation of T2 myofibers (i.e., greater T2/NCAM+) is associated with decreased peak torque, suggesting a contractile consequence of NCAM expression. Our data indicate that decreased innervation leads to a slower rate of muscle activation. Overall, higher NCAM expression may be indicative of compromised communication between the nervous system and skeletal muscle, leading to decreased muscle performance. PRACTICAL APPLICATIONS: Identifying disruptions in the communication between motor neurons and the myofibers they innervate may provide insight for the development of specific therapeutic exercise programs that can improve motor performance and quality of life for persons with PD. 

Acknowledgements: None