Omega-3 fish oil supplements preserved brain regions that control breathing and restored normal breathing rates in mice with Parkinson’s disease-like conditions, according to a new study published in the journal neuroscience.
Parkinson’s disease is a brain disease known for causing tremors, stiffness, and slowness of movement, symptoms caused by the gradual death of dopamine-producing brain cells. As the disease progresses, many patients develop respiratory problems, and the resulting pneumonia is the main cause of death. These breathing problems are thought to occur because the disease ultimately damages certain areas of the brainstem that control automatic functions such as breathing and heart rate.
Although these respiratory complications have serious consequences, the standard treatment for Parkinson’s disease (levodopa) has little effect on this aspect of the disease. Levodopa replenishes dopamine and aids movement, but it does not target the underlying processes of inflammation and cell damage that cause exacerbations unrelated to movement.
Therefore, researchers are seeking additional treatments that can address these gaps. Scientists turned to omega-3 fatty acids (an active ingredient in fish oil supplements) because of their well-known anti-inflammatory and antioxidant properties.
A team led by Taina O. Macedo from the University of São Paulo in Brazil used 52 mice to model the disease. The mice were divided into four groups: a healthy control group, a healthy group given omega-3s, a Parkinson’s disease model group, and a Parkinson’s disease model group treated with omega-3s.
To create the Parkinson’s disease model, researchers injected a chemical called 6-hydroxydopamine directly into the brain. Omega-3 supplementation began 5 days after injection and continued for 10 days. We deliberately chose the timing because by day 5 dopamine cell damage was already well established, but the respiratory regions of the brainstem had not yet fully deteriorated. Respiration was assessed using a specialized sealed chamber, and the brain tissue was then examined under a microscope to count surviving neurons and assess immune cell activity.
As expected, omega-3 supplements were unable to restore or prevent the loss of dopamine-producing brain cells. However, in mice treated with omega-3, the number of neurons surviving in the respiratory region of the brainstem remained at a level similar to that of healthy control mice. In the absence of omega-3, Parkinson’s disease model animals showed significant cell loss in these same regions.
The cellular environment was also markedly different. In Parkinson’s disease model mice that were not given omega-3, brain immune cells showed signs of a reactive inflammatory state in the brain’s respiratory regions. Levels of harmful reactive oxygen species, a marker of oxidative stress and cell damage, were also elevated. Omega-3 treatment reduced this oxidative stress and attenuated abnormal changes in immune cells in these areas.
Importantly, these cytoprotections translated into measurable functional benefits. Parkinson’s disease model mice breathe significantly more slowly than healthy mice at rest, at about 161 breaths per minute compared to 183 breaths in controls. However, Parkinson’s disease mice treated with omega-3s breathed at a rate of about 183 breaths per minute, making them statistically indistinguishable from healthy mice.
The researchers said in their paper that these protective effects “are likely due to the antioxidant and anti-inflammatory properties of omega-3 fatty acids,” and that this finding “strengthens the therapeutic potential of omega-3s in neurodegenerative conditions.”
This study has important limitations. Results in animals do not necessarily translate to humans, especially for complex diseases. Human clinical trials will be needed to draw conclusions about whether omega-3 supplements benefit people living with Parkinson’s disease.
The authors of the study, “Omega-3 supplementation prevents functional and neurorespiratory damage present in animal models of Parkinson’s disease,” are Taina O. Macedo, Lais M. Cabral, Nicole C. Miranda, Fulvio A. Scorza, Thiago S. Moreira, and Ana C. Takaakura.
