Table 3.
The effect and mechanism of exercise in PD animal.
| Mechanism | Result | Reference |
|---|---|---|
| Neurogenesis | 1. Many of the molecules that are increased by running, including serotonin, insulin-like growth factor, and BdNF, have been causally linked to running- enhanced neurogenesis. | 82–86 |
| 2. Proliferation of astrocytes and activation of microglia | ||
| 3. HIF 1-alpha expression: increasing fuel availability glucose transporters (GLUT-1 and GLUT-3) and glycolytic pathway enzymes and also promote neurogenesis, synaptogenesis, and angiogenesis | 87 | |
| 4. Physical exercise-induced changes in the hippocampus in vivo and confirms possibility of angiogenesis/neurogenesis underlying plasticity processes. | 14 | |
| Neuroplasticity | 1. Skill aerobic exercise (SAE) elevated expression of both presynaptic (Synaptophysin) and postsynaptic (PSD-95) proteins. | 53 |
| 2. Intensive treadmill running can reverse the loss of dendritic spines on striatal MSNs [50] Dendritic spine density in the B.G | ||
| 3. Exercise may alleviate brain inflammation-induced learning impairment: The long-lasting effect of exercise on LTP through enhancement of the expressions regarding BDNF, TrkB, and p-CREB. Treadmill exercise and wheel exercise exerted similar effects on these factors. | 88 | |
| 4. MPTP-exercise group increases expression of synaptophysin, PSD-95, TH, and dendritic spine in nigrostriatal dopaminergic neurons and fibers than MPTP treated group | 89 | |
| Neuroprotection | 1. Aerobic exercise regulates Rho/cofilin pathways to rescue synaptic loss | 90 |
| 2. Exercise activate the signaling pathways underlying brain protection. | 91 | |
| 3. Exercise increased availability of NTFs, which in turn can promote mitochondrial energy production, antioxidant defense, synaptogenesis, reduced inflammation, angiogenesis, and other processes that suppress apoptosis. | 92 | |
| 4. By promoting synaptic plasticity and neurogenesis in the hippocampus, BDNF mediates exercise induced improvements in cognitive function and neuroprotection | 93,94 | |
| Neurotransmission | 1. Enhacing DA transmission | 53 |
| i. Enhance vesicular release of dopamine, | ||
| ii. Increase of synaptic occupancy, and | ||
| iii. Decrease of dopamine clearance through reduced DAT expression. | ||
| 2. Effect of Glutamate transmission | ||
| i. Exercise alters the AMPA receptor subunit GluA2 expression, particularly localized to indirect DA-D2R containing MSNs | 95 | |
| ii. Exercise reduces synaptic excitability and postexcitatory synaptic potentials | ||
| iii. Exercise reduces the presynaptic storage of glutamate. | 96 | |
| iv. Reduces aberrant glutamatergic drive to restore cortico-striatal circuit function | ||
| Altering the BBB | Increases the availability of biomoleculesto enhance synapse formation and ameliorate the inflammation | 97 |
| Maintenance of cellular homeostasis | Physical exercise directly influences the responsiveness of CNS circuits involved in energy homeostasis. | 98,99 |
| Cerebral blood circulation | Aerobic exercise (AE) enhanced circulatory and respiratory efficiency that improves the body’s use of oxygen, and increase in the density of capillaries in the brain’s motor regions. | 100,101 |
| SAE resulted in greater increases in regional cerebral blood flow (rCBF) and prelimbic cortical activation |