Blood levels of selenium, associated protein may be Parkinson’s markers
Higher levels of the trace metal have been noted in patients' cerebrospinal fluid
Levels of the trace metal selenium and its associated proteins, called selenoproteins, are altered in the blood of adults with Parkinson’s disease, a study reported.
Two of these affected proteins, selenoprotein P (SelP) and selenoprotein S (SelS), were examined, and the researchers suggested that selenium and SelP levels could help to diagnose Parkinson’s or identify those at risk.
“Our results suggest that [blood] levels of [selenium] and SelP could be a biomarker or risk factor for Parkinson’s,” the scientists wrote, noting that selenium and selenoproteins “play a crucial role in cellular regulation, [and] they have been linked to the onset of neurodegenerative processes.”
The study, “Selenium and selenoproteins role in Parkinson’s disease: Is there a link between selenoproteins and accumulated alpha-synuclein?” was published in the Journal of Trace Elements in Medicine and Biology.
Selenium may interact with alpha-synuclein to promote clumping
Parkinson’s is due to the progressive death of dopaminergic neurons, nerve cells responsible for making the signaling molecule dopamine, with abnormal clumps of the alpha-synuclein protein thought to contribute to their loss. Disease symptoms arise with the subsequent disruption in dopamine signaling.
Selenium (Se) is a trace metal, acquired via diet, that’s incorporated into selenoproteins. Studies have found selenium deposits in the brains of Parkinson’s patients and higher levels in their cerebrospinal fluid, which surrounds the brain and spinal cord. Selenium also may interact with alpha-synuclein, promoting protein clumping, the study noted.
To better understand the roles of selenium and selenoproteins in Parkinson’s, researchers in Iran tested blood samples from 30 adults (mean age, 67.23) with Parkinson’s. A group of 30 age- and sex-matched adults with no neurological disease were added as controls. The team measured levels of selenium, alpha-synuclein, and the selenoproteins SelP and SelS.
As expected, alpha-synuclein levels were markedly higher among patients compared with controls. At the same time, people with Parkinson’s had significantly higher levels of selenium and SelS and significantly lower levels of SelP than did controls.
A statistical analysis found that patients’ higher SelS and selenium levels correlated with elevated alpha-synuclein levels.
Because SelS is thought to help process and transport misfolded proteins, its association with alpha-synuclein suggests that SelS might be induced to prevent the transport — and eventual clearing — of misfolded alpha-synuclein from cells, the researchers wrote.
While selenium and SelP levels were not influenced by patients’ age, sex, or disease duration, higher SelS levels correlated with a younger age, and greater alpha-synuclein accumulation with older age.
Selenoprotein S, alpha-synuclein levels affected Parkinson’s severity
Increasing levels of SelS and alpha-synuclein significantly associated with worsening scores on the Unified Parkinson’s Disease Rating Scale (UPDRS), a standardized assessment to measure the severity of Parkinson’s symptoms. Blood levels of selenium and SelP also correlated with cognitive impairment and depression, two Parkinson’s nonmotor symptoms.
All patients were using disease treatments, and their selenium levels did not appear to be influenced by levodopa, the gold standard for treating Parkinson’s. Still, levodopa users had considerably higher levels of alpha-synuclein than nonusers, a finding the researchers found “interesting.”
Among other medications, SelS levels were only significantly lower in patients treated with Gocovri (amantadine), with a correlation seen between low SelS levels and Gocovri use.
“These findings imply that a change in the [blood] levels of Se and SelP may be a sign of Parkinson’s disease (PD) or at the least, a risk factor for the disease,” the researchers concluded. “Future perspectives could address how SelS can reduce the aggregation of alpha-synuclein.”
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