Pandemic stress associated with higher inflammation in Parkinson’s
COVID-19 data offer insight into how stress and inflammation may interact
- Higher stress levels were associated with increased inflammation in people with Parkinson's disease.
- COVID-19 pandemic data showed higher levels of the inflammatory marker CRP in Parkinson’s patients who were more reactive to stress.
- The findings highlight stress as a potential factor worth further study in Parkinson’s disease, particularly in relation to inflammation.
Stress may be linked to higher levels of inflammation in people with Parkinson’s disease, according to a new analysis of data collected during the COVID-19 pandemic.
The findings were reported in the study, “The interplay between stress, inflammation and Parkinson’s disease: insights from the COVID-19 pandemic,” published in npj Parkinson’s Disease.
Parkinson’s is a chronic condition in which certain cells in the brain gradually become damaged and die. The underlying causes of Parkinson’s are not fully understood, but growing evidence suggests that increased inflammation in the brain may play a role in how the disease progresses.
Research has also shown that psychological stress is closely linked to chronic inflammation. Because inflammation is believed to contribute to Parkinson’s progression, this raises the possibility that higher stress could worsen inflammation and disease symptoms. However, studying the relationship is challenging, since stress varies widely from person to person and is difficult to measure objectively.
The COVID-19 pandemic as a real-world stress test
The COVID-19 pandemic, along with measures to limit the spread of the virus, created significant stress for many people living with Parkinson’s disease. Researchers viewed this worldwide, real-world stressor as an opportunity to explore how stress may influence inflammation in Parkinson’s disease.
“The pandemic led to increased stress levels in people with [Parkinson’s] due to social isolation, fear of infection, and disruptions in routine care,” the researchers wrote, adding that this situation provides “a naturalistic context to examine how stress and inflammation interact to influence” Parkinson’s disease biology.
For the analysis, the researchers examined data from 256 people who enrolled in a Parkinson’s study at a center in the Netherlands aimed at tracking long-term outcomes. All participants had completed at least one study visit prior to the pandemic and at least one during the pandemic.
“We investigated the association between stress-related symptoms, particularly depressive and anxiety symptoms, and inflammatory [blood protein] levels in individuals with [Parkinson’s],” the scientists wrote. “We then examined how individual stress-reactivity influenced changes in these inflammatory markers after the onset of the COVID-19 pandemic.”
Using standardized mental health questionnaires, the researchers grouped participants into those who experienced a marked worsening in mental health after the pandemic began (high stress-reactive), and those whose mental health remained relatively stable despite the stress (low stress-reactive).
Stress-reactive patients showed higher inflammation
The researchers found that levels of CRP, a well-established marker of inflammation, were similar between the two groups before the pandemic. During the pandemic, however, CRP levels were significantly higher in patients who were highly reactive to stress. The data also showed that patients with higher levels of CRP or another inflammatory protein called IL-6 tended to report more severe depressive symptoms.
“We found that CRP concentrations increased during the pandemic, but only in those individuals who consistently reported increased stress-reactivity over an extensive period of six months, and not in individuals who were more resilient to stress in that period,” the scientists wrote.
The researchers found that the rise in CRP could not be explained by COVID-19 infection itself. When the analysis was limited to patients with no history of infection, the same differences between stress-reactive and stress-resilient groups were observed. Still, the researchers cautioned that this type of analysis cannot establish cause-and-effect relationships, emphasizing that further studies are needed to better understand how stress and inflammation interact in Parkinson’s disease.
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