Neuroscience letters
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Neuroscience letters · Feb 2018
Sway regularity and sway activity in older adults' upright stance are differentially affected by dual task.
Age-related changes in postural control are attributed to visual, vestibular and proprioceptive dysfunctions, muscle weakness, and reduced availability of neural resources required for efficient balance control. Concurrent performance of complex cognitive tasks while standing or walking is expected to increase balance instability due to under-recruitment of brain resources and insufficient allocation of attention to the postural task. Both balance instability and attentional control of movements can, nonetheless, be determined from the center of pressure (CoP) measurements by examining the effects of dual-task on the amount of sway activity (as measured by CoP velocity - Vcop) and the statistical regularity of the CoP trajectory (the wavelet entropy of the signal - WEcop). ⋯ Furthermore, dual-task effects (% change in performance) on both sway characteristics were not significant (p > 0.1), suggesting that none of the attention demanding cognitive tasks used in the present study was sufficient to divert a critical amount of attentional resources from the postural task. Finally, performance of the mathematical counting (but not the word memorization) task was deteriorated from sitting to standing, however this effect was marginal (p = 0.075). Taken together, we proposed that while dual task could hinder balance control, postural stability may still be maintained by allocating more attentional resources to the postural task and reducing automatized control.
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Neuroscience letters · Feb 2018
Behavioral defects in a DCTN1G71A transgenic mouse model of Perry syndrome.
Perry syndrome is a rare neurodegenerative disease characterized by parkinsonism, depression/apathy, weight loss, and central hypoventilation. Our previously-conducted genome-wide association scan and subsequent studies identified nine mutations in DCTN1, the largest protein subunit of the dynactin complex, in patients with Perry syndrome. These included G71A in the microtubule-binding cytoskeleton-associated protein Gly-rich domain of p150Glued. ⋯ These behavioral defects parallel apathy-like symptoms and parkinsonism encountered in Perry syndrome. TDP-43 aggregates were not detected in the substantia nigra and cerebral cortex of the transgenic mice, although pathological aggregates of TDP-43 have been considered a major neuropathological feature of Perry syndrome. Our study reveals that a single mutation in the DCTN1 gene recapitulates symptoms of Perry syndrome patients, and provides evidence that DCTN1G71A transgenic mice represent a novel rodent model of Perry syndrome.