The papers found in this section are some of the publications on our research. We have included a short descriptor and a pdf version of the manuscript. Please feel free to download any of interest. If you do download please let us know and say hello. All we ask is that if you use the paper in any manner you acknowledge the research group. A lot of work goes into each. It is our pleasure to make these available to the community. If you have any questions please do not hesitate to contact us directly or comment via the blog section on this web site. Enjoy.
Petzinger et al 2013 Exercise-enhanced neuroplasticity targeting motor and cognitive circuitry in Parkinson’s disease
This paper published in The Lancet is a review of our research up to that point. It develops and expands our interest in the role of cognition (thinking) on motor control. This supports a major hypothesis of our work; that deficits in cognition contribute to motor dysfunction underlying maladaptive neuroplasticity resulting in behavioral features seen in Parkinson's disease. Therefore a critical component of gaining benefit from exercise is by engaging in forms of physical activity that engage cognitive and motor circuitry. In other words, make exercise a learning modality.
Jakowec et al 2016 Engaging Cognitive Circuits to Promote Motor Recovery in Degenerative Disorders. Exercise as a Learning Modality
This paper published in Human Kinetics is a review, part of a presentation at a meeting in Krakow in 2016. It continues to explore our interest in the impact of cognition (thinking) on motor control. We also included a short historical account of neuroplasticity especially the concept of how experience and physical activity shape neuronal connections in the human brain. This review also includes an overview of findings in collaboration with Daniel Holschneider and Zhou Wang on changes in regions cerebral blood flow in rodents subjected to skilled exercise in comparison to aerobic exercise without skill. Findings indicated that skilled exercise engages circuits within the prefrontal cortex (PFC) demonstrating the importance of different forms of exercise and how they engage unique circuits within the brain to specifically target the cognitive-motor pathways.
Kintz et al 2017 Treadmill exercise modifies dopamine receptor expression in the prefrontal cortex of the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned mouse model of Parkinson’s disease
This paper published in NeuroReport is part of Natalie's Doctoral Thesis. MPTP-lesioned mice were subjected to 1 or 6 weeks of treadmill running and analysis carried out in dorsal striatum and PFC. In this report she shows that there are changes within the MPTP-lesioned mouse model with treadmill exercise in the pattern of expression of Dopamine D1 receptor (reduced expression) at both an early 1-week and late 6-week time point, Dopamine D2 receptor is increased early but reduced at the late time point, and dopamine D4 receptor is increased at both time points. In addition tyrosine hydroxylase protein and dopamine neurotransmitter are unaltered at both time points within the dorsolateral striatum but are elevated in the PFC at the late time point. These results suggest to us that there are differences in the expression of these proteins in comparison to our findings in the striatum under similar conditions.
Fisher et al 2004 Exercise-Induced Behavioral Recovery and Neuroplasticity in the 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine-Lesioned Mouse Basal Ganglia
This paper published in Journal of Neuroscience Research was the first publication on the effects of exercise on neuroplasticity in a rodent model of Parkinson's disease. Mice ran 5 days per week for 6 weeks for 1 hour achieving speeds up to 24 meters/minute. we also investigated any signs of stress by mice when subjected to intensive treadmill running. While there was elevated stress in the first couple of days this quickly dissipated and mice showed no evidence of shying away from the treadmill regimen. By 3 weeks those MPTP-lesioned mice that were initially slower on the treadmill were able to catch-up to normal mice and match their motor behaviors in terms of speed and duration. We then examined the restoration of the integrity of the basal ganglia since we speculated that exercise would accelerate the recovery of dopamine. We examined the channel responsible for dopamine uptake (the dopamine transporter DAT), the enzyme responsible for synthesizing dopamine (tyrosine hydroxylase TH), and levels of dopamine and its metabolites in tissues analyzed using HPLC. Contrary to our expectation we found that DAT and TH were down-regulated and expressed levels lower than those seen in MPTP-lesioned mice that did not exercise but were sedentary. When examining the degree of expression of the Dopamine D1 and D2 receptors mRNA transcripts using in situ hybridization histochemistry we did not see any change in the D1 receptor between MPTP-lesioned sedentary and exercise mice, but interestingly we did see elevated expression of the D2 receptor; a receptor that is important in cognitive and motor behaviors and that displays a remarkable degree of neuroplasticity in response to experience. And finally we observed changes in the distribution of the neurotransmitter glutamate in the basal ganglia raising the suspicion that glutamatergic neurotransmission is altered indicating that exercise may influence non-dopaminergic pathways as part of the system wide changes in neuronal circuits underlying the exercise-enhanced restoration of motor behavior we observed.