Sietske N. Heyn, PhD
Sietske N. Heyn is a medical writer with a PhD in neuroscience. Dr. Heyn's education includes a BS with honors from the University of Oregon, and a doctoral degree in neuroscience from the University of California at Davis. After completing postdoctoral training at the University of California, San Francisco, and many years of working as a medical writer at the Stanford University Center for Down Syndrome Research, Dr. Heyn now runs her own medical writing business.
Melissa Conrad Stöppler, MD
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
- Parkinson's disease facts
- What is Parkinson's disease?
- What causes Parkinson's disease?
- What genes are linked to Parkinson's disease?
- Who is at risk for Parkinson's disease?
- What are the symptoms of Parkinson's disease?
- What other conditions resemble Parkinson's disease?
- How is Parkinson's disease diagnosed?
- What is the treatment for Parkinson's disease?
- How can people learn to cope with Parkinson's disease?
- Can Parkinson's disease be prevented?
- What is the prognosis of Parkinson's disease?
- Parkinson's Disease FAQs
- Find a local Neurologist in your town
Parkinson's disease facts
- Parkinson's disease is a neurodegenerative disorder which leads to progressive deterioration of motor function due to loss of dopamine-producing brain cells.
- Primary symptoms include
- impaired balance,
- and later on a shuffling gait.
- Some secondary symptoms include
- Most individuals with Parkinson's disease are diagnosed when they are 60 years old or older, but early-onset Parkinson's disease also occurs.
- With proper treatment, most individuals with Parkinson's disease can lead long, productive lives for many years after diagnosis.
What is Parkinson's disease?
Parkinson's disease is the second most common neurodegenerative disorder and the most common movement disorder. It is characterized by progressive loss of muscle control, which leads to trembling of the limbs and head while at rest, stiffness, slowness, and impaired balance. As symptoms worsen, it may become difficult to walk, talk, and complete simple tasks.
The progression of Parkinson's disease and the degree of impairment vary from individual to individual. Many people with Parkinson's disease live long productive lives, whereas others become disabled much more quickly. Premature death is usually due to complications such as falling-related injuries or pneumonia.
Most individuals who develop Parkinson's disease are 60 years of age or older. Since overall life expectancy is rising, the number of individuals with Parkinson's disease will increase in the future. Adult-onset Parkinson's disease is most common, but early-onset Parkinson's disease (onset between 21-40 years), and juvenile-onset Parkinson's disease (onset before age 21) also exist.
Descriptions of Parkinson's disease date back as far as 5000 BC. Around that time, an ancient Indian civilization called the disorder Kampavata and treated it with the seeds of a plant containing therapeutic levels of what is today known as levodopa. Parkinson's disease was named after the British doctor James Parkinson, who in 1817 first described the disorder in great detail as "shaking palsy."
What causes Parkinson's disease?
A substance called dopamine acts as a messenger between two brain areas - the substantia nigra and the corpus striatum - to produce smooth, controlled movements. Most of the movement-related symptoms of Parkinson's disease are caused by a lack of dopamine due to the loss of dopamine-producing cells in the substantia nigra. When the amount of dopamine is too low, communication between the substantia nigra and corpus striatum becomes ineffective, and movement becomes impaired; the greater the loss of dopamine, the worse the movement-related symptoms. Other cells in the brain also degenerate to some degree and may contribute to non-movement related symptoms of Parkinson's disease.
Although it is well known that lack of dopamine causes the motor symptoms of Parkinson's disease, it is not clear why the dopamine-producing brain cells deteriorate. Genetic and pathological studies have revealed that various dysfunctional cellular processes, inflammation, and stress can all contribute to cell damage. In addition, abnormal clumps called Lewy bodies, which contain the protein alpha-synuclein, are found in many brain cells of individuals with Parkinson's disease. The function of these clumps in regards to Parkinson's disease is not understood. In general, scientists suspect that dopamine loss is due to a combination of genetic and environmental factors.
What genes are linked to Parkinson's disease?
In most individuals, Parkinson's disease is idiopathic, which means that it arises sporadically with no known cause. However, some of individuals diagnosed with Parkinsons also have family members with the disease. By studying families with hereditary Parkinson's disease, scientists have identified several genes that are associated with the disorder. Studying these genes helps understand the cause of Parkinson's disease and may lead to new therapies. So far, five genes have been identified that are definitively associated with Parkinson's disease.
- SNCA (synuclein, alpha non A4 component of amyloid precursor): SNCA makes the protein alpha-synuclein. In brain cells of individuals with Parkinson's disease, this protein aggregates in clumps called Lewy bodies. Mutations in the SNCA gene are found in early-onset Parkinson's disease.
- PARK2 (Parkinson's disease autosomal recessive, juvenile 2): The PARK2 gene makes the protein parkin. Mutations of the PARK2 gene are mostly found in individuals with juvenile Parkinson's disease. Parkin normally helps cells break down and recycle proteins.
- PARK7 (Parkinson's disease autosomal recessive, early onset 7): PARK7 mutations are found in early-onset Parkinson's disease. The PARK7 gene makes the DJ-1 protein, which may protect cells from oxidative stress.
- PINK1 (PTEN-induced putative kinase 1): Mutations of this gene are found in early-onset Parkinson's disease. The exact function of the protein made by PINK1 is not known, but it may protect structures within the cell called mitochondria from stress.
- LRRK2 (leucine-rich repeat kinase 2): LRRK2 makes the protein dardarin. Mutations in the LRRK2 gene have been linked to late-onset Parkinson's disease.
Several other chromosome regions and the genes GBA (glucosidase beta acid), SNCAIP (synuclein alpha interacting protein), and UCHL1 (ubiquitin carboxyl-terminal esterase L1) may also be linked to Parkinson's disease.
Who is at risk for Parkinson's disease?
- Age is the largest risk factor for the development and progression of Parkinson's disease. Most people who develop Parkinson's disease are older than 60 years years of age.
- Men are affected about 1.5 to 2 times more often than women.
- A small number of individuals are at increased risk because of a family history of the disorder.
- Head trauma, illness, or exposure to environmental toxins such as pesticides and herbicides may be a risk factor.
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