Deep Brain Stimulation May Increase Levels of Inflammatory Factors in Parkinson’s, Study Suggests

Deep brain stimulation (DBS) may increase the levels of hepcidin — a hormone associated with iron accumulation and inflammation in the brain — in Parkinson’s disease patients, according to a small Polish study.

The study, “Higher serum levels of pro-hepcidin in patients with Parkinson’s disease treated with deep brain stimulation,” was published in the journal Neuroscience Letters.

As people age, iron accumulates in several brain regions and cells, including the microglia (the immune cells of the brain) and the astrocytes (cells that regulate nerve cell communication and survival ).

Increased iron accumulation, as well as brain inflammation, is associated with oxidative stress and cellular damage and is observed in several neurodegenerative disorders such as Parkinson’s and Alzheimer’s disease.

Hepcidin, an iron balance-regulatory hormone, suppresses ferroportin (FPN1) — the protein that transports iron out of cells — and leads to cellular iron accumulation.

Because inflammation can induce the production of hepcidin, this hormone may be a link between brain inflammation and iron-induced oxidative damage, both of which are involved in neurodegeneration in Parkinson’s patients.

Researchers in Poland evaluated the levels of pro-hepcidin — the precursor of hepcidin — in Parkinson’s patients treated only with medication, in those who, in addition to medication, also received DBS, and in healthy people (controls).

DBS — high-frequency stimulation in strategic brain areas through surgically implanted thin wires in the brain — is a treatment strategy for people with advanced Parkinson’s disease whose motor problems do not improve with medication.

Several studies have shown that DBS reduces motor symptoms as well as the necessary daily dose of medication, and improves patients’ quality of life.

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Blood samples were collected from 52 people with Parkinson’s disease (25 women and 27 men) with a mean age of 56, and 31 healthy individuals (15 women and 16 men) with no history of neurodegenerative disorders in the family and a mean age of 58.

Among Parkinson’s patients, 37 had been treated only with medication — levodopa (L-DOPA) and/or ropinirole (Requip) — and 15 with additional DBS (with a mean time from implantation of 28.4 months).

Parkinson’s patients had significantly higher levels of pro-hepcidin compared to healthy individuals, supporting the involvement of hepcidin in Parkinson’s disease.

Those treated with medication and deep brain stimulation showed the highest levels of pro-hepcidin. There was no association between hepcidin levels and the duration of DBS, patient’s age, duration of the disease, or medication dose.

Since DBS has been associated with the activation of microglia and astrocytes — which release inflammatory molecules — researchers hypothesized that the overproduction of pro-hepcidin in these patients may be related to DBS and its associated inflammation.

But considering the small group of patients treated with DBS, additional studies are needed to clarify this association and whether it affects the worsening of Parkinson’s disease.

“The results obtained should be interpreted very carefully but are an interesting observation that requires further research, including a larger group of patients,” the researchers wrote.