A new study found markers of inflammation in the cerebrospinal fluid that protects the brain and spine from injury, linking these markers to symptoms like fatigue, depression and anxiety in patients with Parkinson's disease. Researchers say the findings may lead to new ways of treating the complex riddle of Parkinson's.
Lena Brundin, now an associate professor at the College of Human Medicine at Michigan State University, carried out the research as part of a team from Lund University in Sweden, Skåne University Hospital in Sweden and the Mayo Clinic College of Medicine in Jacksonville, Florida.
The team measured a number of inflammatory markers in fluid samples of patients with Parkinson's and in a control group without the disease.
Prof. Brundin told the press this week:
"The degree of neuroinflammation was significantly associated with more severe depression, fatigue, and cognitive impairment even after controlling for factors such as age, gender and disease duration."
A report on the study is available to read online in Brain, Behavior, and Immunity.
Parkinson's disease not limited to motor symptoms
There is currently no cure for Parkinson's disease, a chronic, progressive neurological disorder that results from loss of brain cells that produce dopamine, a chemical that helps brain cells communicate and control movement.
According to the Parkinson's Action Network, there are around 1 million Americans with Parkinson's disease, which the Centers for Disease Control and Prevention (CDC) place as the 14th leading cause of death in the US.
The primary symptoms of Parkinson's are trembling in hands, arms, legs, jaw and face, plus stiffness of limbs and trunk, coupled with slowness of movement, impaired balance, and other symptoms such as problems chewing, swallowing and speaking. As symptoms progress, patients experience difficulty walking, talking and carrying out simple tasks.
But in addition to these motor symptoms, patients with Parkinson's disease also experience depression, fatigue and cognitive impairment.
Brain inflammation link to Parkinson's not new
The idea that brain inflammation is somehow involved in Parkinson's disease is not new, and previous studies have already linked it to non-motor symptoms like depression, fatigue and cognitive impairment.
Previous research also suggests that inflammation in the brain could drive cell death, and drugs that target this process could offer new treatments to slow progression of the disease. For instance, a study published as far back as 2007 suggested that brain cell death in parkinsons may be reduced by blocking enzyme activity.
However, Prof. Brundin explains that many of these previous studies looking at inflammatory markers in the cerebrospinal fluid of Parkinson's patients have involved only small numbers of patients, often without comparing them to healthy controls.
The study investigated over 120 patients and controls
For their investigation, the team enrolled 87 Parkinson's patients between 2008 and 2012, together with 37 healthy controls.
All participants had routine blood tests and underwent physical exams.
The team tested for the following markers of inflammation: C-reactive protein (CRP), interleukin-6, tumor necrosis factor-alpha, eotaxin, interferon gamma-induced protein-10, monocyte chemotactic protein-1 (MCP-1) and macrophage inflammatory protein 1-beta.
The results showed that increased levels of inflammatory markers were significantly associated with more severe symptoms of depression, anxiety, fatigue, and cognition in the entire group of Parkinson's patients.
Also, after controlling for possible influencers such as duration of Parkinson's disease, age, gender, dementia and other factors, the team found high CRP levels were significantly tied to more severe symptoms of depression and fatigue, and high MCP-1 levels were significantly associated with more severe symptoms of depression.
Prof. Brundin says they hope new treatment options will emerge from studies like this that increase understanding of Parkinson's through finding links between inflammatory markers and non-motor symptoms.