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Exercise attenuates neuronal degeneration in Parkinson's disease rat model by regulating the level of adenosine 2A receptor

Parkinson's disease occurs due to loss of dopaminergic neurons, which alters the behavioural changes. The present study evaluates the effect of exercise on neurodegeneration against Parkinson's disease (PD) rat model and postulates its effect on novel molecular pathway. Rotenone was administered at 1 mg/kg s.c. every 48 h for 18 days for the in-duction of PD and exercise was given to rats for a period of 2 weeks after the confirmation of PD. Moreover, PD rats also received CGS 21680 (adenosine A2A receptor agonist, 0.5 mg/kg, i.p.) with exercise for a period of 2 weeks after confirmation of PD. The effect of exercise was assessed for motor and cognitive function in PD rats. The level of inflammatory cytokines and neurotransmitters was estimated in brain tissue of PD rats. Data of investigation reveal that exercise attenuates cognitive and motor function in PD rats, the exercise + CGS 21680 group shows reverse in the behavioural changes compared to exercise-treated PD rats. The level of inflammatory cytokines and neurochemical level ameliorated in the exercise-treated group compared to the PD group of rats, which is reversed in the exercise + CGS 21680 group. In conclusion, exercise protects neurodegeneration in PD rats by reducing aggregation of a-synuclein and activity of adenosine 2A receptor.

 

Comments:

This study appears to investigate the effects of exercise on Parkinson's disease (PD) in a rat model induced by rotenone, a compound known to induce PD-like symptoms by damaging dopaminergic neurons. The study design includes administering rotenone to induce PD-like symptoms, followed by a period of exercise intervention in the rats. Additionally, they administer an adenosine A2A receptor agonist (CGS 21680) along with exercise to evaluate its impact on PD symptoms.

Here's a breakdown of the study's findings:

1. **Rotenone-induced PD Model:** The rotenone administration caused behavioral changes indicative of Parkinson's disease in the rats. This includes motor and cognitive impairments.

2. **Effect of Exercise:** Exercise intervention post-PD induction showed positive effects by attenuating cognitive and motor dysfunction in PD rats. This suggests that exercise has a protective effect against neurodegeneration in this PD model.

3. **CGS 21680 (Adenosine A2A Receptor Agonist):** When administered along with exercise to PD rats, the CGS 21680 seems to reverse the positive effects of exercise. This reversal includes a return of behavioral changes and an increase in inflammatory cytokines and neurochemical levels, suggesting a potential role of adenosine A2A receptor activity in modulating the benefits of exercise on PD symptoms.

4. **Mechanism:** The study suggests that the protective effect of exercise on neurodegeneration in PD rats might be linked to reducing the aggregation of a-synuclein (associated with PD) and regulating the activity of adenosine 2A receptors.

In summary, the study indicates that exercise intervention post-PD induction in rats has beneficial effects in attenuating PD-related symptoms, possibly through mechanisms involving a reduction in a-synuclein aggregation and modulation of adenosine 2A receptor activity. However, the addition of the adenosine A2A receptor agonist alongside exercise appears to reverse these positive effects, indicating a complex interplay between exercise and this specific receptor's activity in the context of PD.

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