Post of the Week: More Evidence Exercise May Be Good for PD
Posted 14 September 2009 - 06:55 AM
This study by the NPF center of excellence at USC provides us with more information supporting the potential positive role of exercise in PD. The investigators focused on AMPAR receptor--these help brain transmission. The abstract of the article is posted below for your reference.
J Neurosci Res. 2009 Sep 10. [Epub ahead of print] Links
Altered AMPA receptor expression with treadmill exercise in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned mouse model of basal ganglia injury.Vanleeuwen JE, Petzinger GM, Walsh JP, Akopian GK, Vuckovic M, Jakowec MW.
Department of Neurology, The George and MaryLou Boone Center for Parkinson's Disease Research, University of Southern California, Los Angeles, California.
Dopamine depletion leads to impaired motor performance and increased glutamatergic-mediated hyperexcitability of medium spiny neurons in the basal ganglia. Intensive treadmill exercise improves motor performance in both saline treatment and the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease. In the present study, we investigated the effect of high-intensity treadmill exercise on changes in alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) subunit expression, because these receptor channels confer the majority of fast excitatory neurotransmission in the brain, and their subunit composition provides a key mechanism for regulating synaptic strength and synaptic neuroplasticity and is important in modulating glutamatergic neurotransmission. Within the dorsolateral striatum of MPTP mice, treadmill exercise increased GluR2 subunit expression, with no significant effect on GluR1. Furthermore, neurophysiological studies demonstrated a reduction in the size of excitatory postsynaptic currents (EPSCs) in striatal medium spiny neurons (as determined by the input-output relationship), reduced amplitude of spontaneous EPSCs, and a loss of polyamine-sensitive inward rectification, all supportive of an increase in heteromeric AMPAR channels containing the GluR2 subunit. Phosphorylation of GluR2 at serine 880 in both saline-treated and MPTP mice suggests that exercise may also influence AMPAR trafficking and thus synaptic strength within the striatum. Finally, treadmill exercise also altered flip isoforms of GluR2 and GluR1 mRNA transcripts. These findings suggest a role for AMPARs in mediating the beneficial effects of exercise and support the idea that adaptive changes in GluR2 subunit expression may be important in modulating experience-dependent neuroplasticity of the injured basal ganglia.
Author of the Amazon Bestseller Parkinson's Treatment: 10 Secrets to a Happier Life
National Medical Director | NPF
UF Center for Movement Disorders & Neurorestoration
Read More about Dr. Okun at: http://movementdisor...hael-s-okun-md/
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Posted 14 September 2009 - 04:14 PM
For instance does it spark more dopamine to be made or does it come from something other than dopamine.
I know I feel better perhaps more noticeable one time versus another when I either use the treadmill or take a good walk and is the length of time a factor.
Thank you for all the help you do give us, it is much appreciated.
Posted 18 September 2009 - 11:59 PM
I think that is the take home message. This is one reason why I am such an advocate of daily exercise for all my PD patients.
Posted 18 October 2009 - 04:45 PM
Posted 19 October 2009 - 01:39 PM
Most research on the benefits of exercise is testing moderately vigorous exercise daily or almost daily for at least 45 minutes.
So as long as you don't lose your concentration, or trip and break your bones, or cause signifIcant harm to your tendons, ligaments, or heart (remember, as we age, our body is less forgiving to the same rigorous exercise we were able to get away with several years ago. It does not always have to be because of PD), I think it should be okay and helpful.
Posted 31 January 2010 - 03:56 AM
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