Parkinson’s disease is a neurodegenerative disease caused by progressive loss of dopamine-producing neurons in the brain. Symptoms are mild at first, but progress over time, leading to impaired movement as well as other neurocognitive and psychiatric symptoms like depression, dementia, bowel and bladder problems, and difficulty sleeping.
Parkinson's Disease falls under theBrain Healthcategory.
Parkinson’s disease is a brain disorder caused by the death of dopamine-generating neurons in particular regions of the brain, affecting multiple body functions. Symptoms are initially mild but worsen over time and include a progressive loss of motor control, causing tremors, impaired balance, and bradykinesia (slowness of movement). Parkinson’s also affects non-motor functions of the brain, which can affect mood, behavior, and cognition. The onset of disease symptoms occurs after age 60 in most people, but 5-10% of people with Parkinson’s may start to experience symptoms before age 50. Although men are around 1.5 times more likely to develop Parkinson’s, women tend to have a faster disease progression and higher mortality rates.
The effects of Parkinson’s disease on the brain cause both motor (i.e., movement-associated) and non-motor symptoms. The symptoms are subtle at first, but progressively worsen over time.
Common motor symptoms of Parkinson’s disease include the following:
- Tremors, which can occur in different parts of the body including the head, arms, legs, and jaw
- Bradykinesia (slowness of movement)
- Changes in gait
- Impaired balance and coordination
- Muscle stiffness
(These motor symptoms make patients prone to serious falls and injuries.)
People with Parkinson’s disease may experience any of the following non-motor symptoms:
Parkinson’s disease is diagnosed primarily by symptoms, medical history, and a physical exam. Family medical history will also be reviewed, since a first-degree relative with Parkinson's disease increases the chance of diagnosis. There are currently no available tests for Parkinson’s disease. However, biomarkers that may be able to diagnose the disease before symptoms appear could be on the horizon. To be diagnosed with Parkinson’s disease, an individual needs to have parkinsonism, which is defined as bradykinesia (slowness of movement) along with muscle rigidity, tremors at rest, or both. In cases where diagnosis of Parkinson’s isn’t conclusive based on a physical exam, an imaging technique may be used to identify neuronal changes in the brain that are specific for Parkinson’s disease.
Because Parkinson’s reduces dopamine levels in the brain through the death of dopamine-generating neurons, the main medical treatment strategies are centered on dopamine. A few of the most common dopamine-based treatments are levodopa, which nerve cells use as a precursor to make dopamine; monoamine oxidase-B (MAO-B) inhibitors, which increase dopamine levels by reducing its breakdown; and dopamine agonists, which mimic the effects of dopamine. Anticholinergic drugs are also used to help reduce tremors and muscle stiffness, and amantadine may be prescribed to suppress involuntary movements.
The mechanisms driving the loss of dopamine neurons in the brain of people with Parkinson’s disease are not well-understood. However, excess generation of reactive oxygen species (ROS), inflammation, and mitochondrial dysfunction are common themes in the pathology. Many of the supplements researched for their possible therapeutic effects in experimental models and in clinical trials affect one or more of these pathological mechanisms.
The following supplements have been studied in people with Parkinson’s disease:
The role of diet in Parkinson's disease has been studied extensively, with particular foods being associated with either increased or decreased risk. For example, dairy products have been associated with increased Parkinson's disease risk, while coffee or tea consumption have been associated with decreased risk. Another observational study suggested that increased intake of foods such as fresh fruits and vegetables, olive oil, wine, coconut oil, and non-fried fish were associated with reduced risk, while consuming foods such as beef, fried foods, soda, and dairy products were associated with increased risk.
Although the above research suggests that an overall healthier diet pattern may help to decrease Parkinson's disease risk, cohort studies examining the associations between healthy diet patterns and Parkinson's disease have been inconclusive. However, multiple studies have noted associations between reduced Parkinson's disease risk and adherence to a Mediterranean diet.
For people who fail to respond to conventional therapies, deep brain stimulation may be used, wherein electrodes are implanted in the brain and attached to a small battery in the chest. The electrical impulses delivered to the brain help to relieve many of the motor symptoms of Parkinson's disease, such as tremor, rigidity, and bradykinesia.
Since tremors are associated with dysfunctional neuron signaling in the thalamus region of the brain, treatments that target the thalamus are often used for people who have tremor-predominant Parkinson’s disease, a subtype associated with tremors but a lack of muscle rigidity or bradykinesia. MRI-guided focused ultrasound may be used to burn tissue in or around the thalamus, or less commonly, thalamotomy, which involves the surgical severing of nerve fibers in the thalamus.
Occupational therapy may also be prescribed as a treatment to promote improved quality of life and recover or maintain function for daily living or work.
Parkinson’s disease is caused by death of dopamine-producing neurons in the substantia nigra pars compacta (SNPC) region of the brain, an important control center for motor function. The neurons in the SNPC communicate with other regions of the brain to control movement by releasing the neurotransmitter dopamine. When dopamine levels are reduced, the biochemical imbalance creates the characteristic PD motor symptoms such as tremors, bradykinesia, and impaired balance and coordination.
Although neuronal death in the SNPC is responsible for the characteristic symptoms associated with motor function in PD, other areas of the brain are also affected that may contribute to non-motor symptoms.