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Physical training prevents depressive symptoms and a decrease in brain-derived neurotrophic factor in Parkinson's

T Tuon1, S S Valvassori2, G C Dal Pont2

  • 1Laboratory of Exercise Biochemistry and Physiology, Graduate Program in Health Sciences, Health Sciences Unit, Universidade do Extremo Sul Catarinense, Criciúma, Santa Catarina 88806-000, Brazil.

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|September 30, 2014
PubMed
Summary
This summary is machine-generated.

Physical exercise, including treadmill running and strength training, effectively combats depressive-like behaviors in Parkinson's disease (PD) mouse models. Both exercise types restored key neurotrophic factors, brain-derived neurotrophic factor (BDNF) and its receptor TrkB, demonstrating neuroprotective effects.

Keywords:
6-HydroxydopamineDepressionNeurotrophinsParkinson's diseasePhysical exercise

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Area of Science:

  • Neuroscience
  • Exercise Physiology
  • Neuropharmacology

Background:

  • Depression is a common comorbidity in Parkinson's disease (PD).
  • Physical exercise is hypothesized to mitigate depressive symptoms and neurodegeneration, potentially via brain-derived neurotrophic factor (BDNF).
  • Different exercise modalities may yield distinct neurobiological effects.

Purpose of the Study:

  • To investigate the impact of treadmill running versus strength training on depressive-like behavior in a PD mouse model.
  • To assess the effects of these exercise types on pro-BDNF, BDNF, and TrkB levels in the striatum and hippocampus.
  • To evaluate the neuroprotective potential of exercise in the context of PD.

Main Methods:

  • C57BL/6 mice underwent 60 days of treadmill running or strength training.
  • Parkinson's disease was induced using 6-hydroxydopamine (6-OHDA) striatal administration.
  • Depressive-like behavior, rotational behavior, and levels of pro-BDNF, BDNF, and TrkB were measured.

Main Results:

  • 6-OHDA induced increased immobility and rotational behavior, indicative of PD and depressive-like symptoms.
  • PD model mice exhibited reduced levels of pro-BDNF, BDNF, and TrkB in the striatum and hippocampus.
  • Both exercise interventions successfully prevented depressive-like behavior and normalized BDNF and TrkB levels.

Conclusions:

  • Exercise training, both aerobic and strength-based, demonstrates efficacy in mitigating depressive-like behaviors in a PD mouse model.
  • Physical activity can restore neurotrophic factor signaling pathways, including BDNF and TrkB, in brain regions affected by PD.
  • Exercise serves as a potential neuroprotective strategy for Parkinson's disease, addressing both motor and non-motor symptoms.