Multiple studies have indicated that depression can greatly increase the probability of developing cancer and having a stroke, but a study published October 3 in Neurology reported that depression appears to increase the risk for Parkinson’s disease as well.
Of all the comorbid psychiatric diagnoses associated with Parkinson’s disease (PD), mood disorders are the most prevalent—showing up in approximately 40 percent of patients with PD, according to the Parkinson’s Disease Foundation. Many studies have shown mood disorders, such as depression, to be a consequence of PD, but recent studies have suggested that the onset of PD may be a consequence of depression.
“[I]t’s a long debate whether depression is a risk for PD, or merely a comorbidity or a prodromal symptom,” said Albert Yang, M.D., Ph.D., a professor of psychiatry at Taipei Veterans General Hospital in Taiwan, during an interview with Psychiatric News.
He explained that “studies have shown that depression precedes PD development… [but] such evidence has originated primarily from case-control studies that were limited by a small sample size and recall bias of the depression diagnosis.”
In an effort to determine a correlation between depression and PD onset, Yang and his colleagues analyzed medical records of 4,634 people with depression and 18,544 individuals who were free of depression for at least 10 years. Depression diagnosis codes were based on the ICD-9-CM. Diagnosis for PD was determined by neurologists.
The study results showed that people with depression were three times more likely to develop PD than were those without depression. Among the cohort with depression, participants over age 65 and individuals with more than a five-year history of treatment-resistant depression prior to PD diagnosis showed the greatest risk for PD onset.
“This study highlights the necessity of thinking about neurodegenerative disorders in certain depressive patients. Our study does not say that all depression leads to Parkinson’s disease, but identified that elderly depression and difficult-to-treat depression could need particular attention and possibly aggressive treatment for these patients,” said Yang.
When providing care to these populations, Yang suggested that “it may be beneficial to screen for any neurological disease, as depression may be a red flag.”
James Beck, Ph.D., vice president of Scientific Affairs at the Parkinson’s Disease Foundation, agreed.
“It would be worthwhile to screen for Parkinson’s disease,” Beck told Psychiatric News. “Many symptoms of depression are also symptoms seen in patients with Parkinson’s disease.” Because several studies have shown a strong interrelationship between depression and PD, Beck said that is highly possible that depression and PD could be consistent on a biological basis.
Few genetic association studies have focused on the correlation between PD and depression, according to Yang. He noted that genes studied to date include serotonergic genes and the thyrotrophic embryonic factor gene, but none of the studies have been replicated by a sufficient number studies and subjects.
“I am less optimistic in genetic association studies, although our group has also published many of them in aging, mood disorders, and schizophrenia.”
Yang acknowledged limitations in his current study, including lack of information on family history of PD, smoking, coffee drinking, and environmental factors such as exposure to pesticides—all factors that can influence PD development, he said.
He added that more population-based studies with longer-duration observations will be conducted, along with studies identifying the overlap of neuroimaging markers for depression and PD.
The study was funded by the Taipei Veterans General Hospital and the National Science Council. ■