From: The effects of exercise on cognition in Parkinson’s disease: a systematic review
Study | Behavioral outcomes | Neurobiological outcomes | Major sources of risk of bias |
---|---|---|---|
Goes et al., 2013 [21] | Forced exercise following onset of experimental PD: | Changes in the striatum from forced exercise following onset of experimental PD: | Performance bias: sedentary control animals were not exposed to the swimming training program, the warm water or handled to be dried off following each session. |
• Decreased marker of depression (tail suspension) | • Decreased interleukin 1-beta levels (proinflammatory cytokines) | ||
• Improved motor coordination (decreased falls on Rotarod test) | • Attenuated inhibition of glutathione peroxidase activity, decreased glutathione reductase and glutathione S-transferase activity (all markers of oxidative stress) | ||
• Improved long-term memory, but not short-term memory in object recognition test | |||
• Increased dopamine, homovanillic acid, and 3,4-dihydroxyphenylacetic acid levels | |||
Gorton et al., 2010 [17] | Forced and voluntary exercise following onset of experimental PD: | Forced and voluntary exercise following onset of experimental PD: | Performance bias: each animal was only evaluated on one test. |
• Improved motor learning (Rotarod) | • Had no effect on levels of DA in the striatum and serotonin in the amygdala compared to saline controls | ||
• Reduced anxiety in elevated plus maze (passive avoidance task, authors linked to cognition/memory) | |||
• Forced and voluntary exercise increased DA in the striatum to similar levels following MPTP or saline administration | |||
• Had no effect on markers of depression, sucrose preference and tail suspension (MPTP lesion also had no effect) | |||
• Forced exercise increased 5HT in the nucleus accumbens in MPTP-treated mice compared to saline controls | |||
Tajiri et al., 2010 [18] | Exercise following onset of experimental PD: | Exercise following onset of experimental PD: | Information bias: exercise was started soon (24 hrs) after toxin administration, so the lesion may not represent a complete PD-like model. |
• Improved cylinder test, amphetamine-induced rotational test (authors linked to cognitive-related behavior) | • Preserved nigrostriatal dopamine neurons (increased tyrosine hydroxylase-positive fibers) | ||
• Increased migration of new-born neural stem/progenitor cells toward striatum | |||
• Up-regulated neurotrophic factors, BDNF and GDNF, in the striatum | |||
Aguiar et al., 2009 [19] | Forced and voluntary exercise before onset of experimental PD: | Neurobiological outcomes not assessed | Information bias: behavioral testing was soon (24 hrs) after the reserpine administration, so the lesion may not represent a complete PD-like model. |
• Improved motor deficits following a high dose of reserpine | |||
• Improved short-term social memory (tested through olfactory discrimination), with no deficit on motor or olfactory function from the low dose of reserpine | |||
Pothakos et al., 2009 [20] | Endurance exercise before and following onset of experimental chronic PD: | Endurance exercise before and after onset of experimental chronic PD: | Selection biases: there was not a group that received exercise and probenecid. There was also not a control group with only a saline injection. The effects of the control solution, probenecid, on cognition are not known. |
• Reversed balance and gait performance, restored regular movement | • Did not raise striatal DA (n = 6) | ||
• Did not reverse loss of tyrosine-hydroxylase fibers in substantia nigra (pars compacta) | |||
• Had no effect on learning (cued Morris water maze), amphetamine-stimulated locomotion or motor coordination | |||
Fisher et al., 2004 [16] | Exercise following onset of experimental PD: | Exercise following onset of experimental PD: | Information bias: the learning paradigm for behavioral results (learning to stay on the treadmill) relied substantially on motor capacity. |
• Improved velocity and endurance on treadmill | • Had no effect on tyrosine hydroxylase | ||
• Sensory feedback not needed over time for behavioral response (i.e., maintaining a forward position on treadmill), authors suggested indicative of learning | • Up-regulated dopamine D2 receptor mRNA expression | ||
• Down-regulated striatal DAT | |||
• Reversed increased nerve terminal glutamate in striatum (as a result of MPTP) |