Parkinson’s disease affects about one million Americans and 10 million people worldwide. With 60,000 new cases annually, it’s second only to Alzheimer’s as the most frequently diagnosed neurodegenerative disease in the United States.
Board-certified neurologist Andrew Lerman, MD, of Gables Neurology in Miami, Florida, is well-known for developing highly effective, personalized care strategies for progressive neurological disorders such as dementia, multiple sclerosis, and Parkinson’s.
Dr. Lerman is also actively engaged in ongoing research and clinical trials that are focused on the origins as well as the development of cutting-edge treatments for these complex diseases. He explains how genetics may increase your risk of developing Parkinson’s.
Understanding Parkinson’s disease
Parkinson's is a neurodegenerative disease that causes nerve cells (neurons) in your brain to gradually break down (degenerate) and die. The neurons most affected by Parkinson’s are those that produce a chemical messenger (neurotransmitter) called dopamine.
Your brain uses dopamine to:
- Regulate your mood and emotions
- Establish sleep patterns
- Enhance memory and concentration
- Manage your appetite
- Process pain
Dopamine also plays a vital role in fine and gross motor control or voluntary muscle movement. Writing requires fine motor control. Larger movements such as waving your arms or walking require gross motor control.
Although we know that Parkinson’s is related to neurodegeneration and resulting declines in dopamine, it’s not clear what causes the neurons to break down.
Genetic links to Parkinson’s disease
Research results regarding a genetic link to Parkinson’s are mixed. Approximately 15% of people with Parkinson’s have a family history of the disease that may be linked to mutations identified in several genes.
These changes have varying effects. A PARK7 gene mutation, for instance, affects production of a protein that normally protects structures (mitochondria) within your cells from damage. Individuals with this mutation may be at higher risk of developing early-onset Parkinson’s.
In some cases, the genetic changes are inherited from just one parent (autosomal dominant). Others are related to gene mutations inherited from both parents (autosomal recessive) who may have never developed Parkinson’s symptoms but transferred the genetic variants to their offspring.
Much of today’s research focuses on how these changes cause Parkinson’s and why some people with similar mutations develop the disease and others don’t.
Most specialists believe Parkinson’s disease is likely connected to a combination of genetic (hereditary) and environmental factors such as exposure to certain chemicals or toxins, as well as injury related to multiple concussions or other head trauma.
Treating Parkinson’s disease
Because there’s no cure for Parkinson’s yet, treatments focus on preventing symptoms such as tremors, gait instability, or difficulty with concentration from interfering with your quality of life.
Dr. Lerman’s participation in current research programs and clinical trials ensures his patients receive the most effective and advanced treatments available for Parkinson’s.
Otherwise, every individual responds differently to Parkinson’s disease and effective care strategies require a comprehensive and customized approach that’s tailored to fit your needs.
Your plan may, for instance, include a medication that replenishes your dopamine levels or one that simulates dopamine’s effects on your brain activity. Because Parkinson’s is a progressive disorder, your medications may need adjustment over time.
Other treatments include physical therapy to improve muscle strength and flexibility or occupational therapy to help you manage daily activities. Healthy habits such as routine exercise and a nutritional diet are also vital in successfully managing Parkinson’s.
For an accurate diagnosis and highly effective treatment for Parkinson’s disease, schedule an evaluation with Dr. Lerman at Gables Neurology today by calling our office or requesting an appointment online.