James Parkinson, a physician in 19th-century London, is credited with being the first to detail the symptoms of a neurodegenerative disorder now called Parkinson’s disease. Symptoms of the disease, however, were described as far back as 5,000 BCE in ancient Indian medical writings, and 2500 years ago in Chinese medical texts.
According to the American Parkinson’s Disease Association, about 1.5 million people in the U.S. suffer from PD, about 1 to 2% of people over the age of 60 and 3 to 5% of people over age 85. Incidence of PD ranges from 8.6 to 19 per 100,000 people. About 50,000 new cases are diagnosed in the U.S. every year, a number expected to rise as the population in the U.S. ages. PD onset before age 40 is rare. The disease affects all races and ethnic groups.
What Is Parkinson’s disease?
Parkinson’s disease, a progressive neurodegenerative disorder that impacts movement, muscle control, balance, and other bodily functions, is part of a group of conditions known as motor systems disorders. The nervous system disorder affects movement and develops gradually, often beginning with a slight tremor in one hand. Second only to Alzheimer’s disease as the most prevalent neurodegenerative disorder, Parkinson’s takes first place as the most frequently diagnosed movement disorder.
What Are PD Symptoms?
PD symptoms vary according to the individual. Early signs, which can be mild and go practically unnoticed, may begin on one side of the body and remain worse on that side, even when symptoms have spread to both sides. Typical symptoms are asymmetric tremors when at rest, rigidity, and bradykinesia (slow movement).
A tremor usually begins in one limb, such as a hand or fingers. A pill-rolling tremor, in which patients rub the thumb and forefinger back and forth, often manifests. Muscle stiffness can happen in any part of the body, limiting range of motion and causing pain.
Parkinson’s disease may also reduce a person’s ability to move and slow the person’s movement, rendering tasks that were once easy now challenging. A Parkinson’s patient may take shorter steps, have trouble getting out of a chair, and drag his or her feet when walking. Stooped posture and balance issues often arise. There can also be less capacity for engaging in unconscious movements, such as blinking, smiling, or walking with arms that swing naturally by your sides. There can also be speech problems: a person with PD may talk softly or quickly, slur words, hesitate before talking, or speak in a monotone. The ability to write may also be impacted.
Additional complications may be treatable or minimized. These include:
- Cognitive problems
- Depression and emotional changes
- Loss of motivation
- Swallowing problems
- Sleep problems
- Sleep disorders
- Rapid eye movement sleep behavior disorder
- Bladder problems
- Blood pressure changes
- Smell dysfunction
- Loss of energy
- Sexual dysfunction
What Causes Parkinson’s Disease?
Parkinson’s disease is a result of neurons in the brain breaking down or dying. Loss of these neurons produces dopamine, a chemical messenger in the brain, that produces the symptoms of PD. When dopamine levels are reduced, there is abnormal brain activity. While the exact cause of PD is unknown, genetic mutations and environmental triggers such as herbicides and pesticides can play a role.
Changes occur in the brains of people with Parkinson’s disease. Lewy bodies, clumps of specific substances within brain cells, are microscopic markers of PD. While many substances are found within Lewy bodies, researchers believe an important one is the natural and widespread protein called alpha-synuclein (A-synuclein).
The three types of Parkinson’s disease are grouped according to the age at which they manifest. Adult-Onset Parkinson’s Disease, the most common type, has an average age of onset of 60, rising as people advance into their 70s and 80s. Young-Onset Parkinson’s Disease, occurring between 21 and 40, is rare in the U.S., about 5 to 10% of diagnosed cases. Juvenile Parkinson’s Disease, with the age of onset before 21, is extremely rare.
There is currently no cure for Parkinson’s disease, which always gets worse over time. Death is usually because of complications, including pneumonia or falling-related injuries.
Parkinson’s disease changes the quality of life for patients and their families, and education is imperative in order to make the most worthwhile treatment decisions. Some medications and surgical procedures may drastically improve symptoms. Some research has shown that caffeine, green tea, and aerobic exercise may help to reduce the risk of developing PD.
How Is PD Treated?
Treatment and dosage options for PD depend on symptoms, other health issues and medications used to treat them, metabolism, and age. Because most PD symptoms are the result of a lack of dopamine in the brain, many drugs attempt to replenish dopamine or mimic the action of dopamine. These dopaminergic medications attempt to reduce muscle rigidity, enhance speed and coordination of movement, and lessen tremors.
The medications have reported side effects. They can be severe—abnormal heart rhythm, aggressive behavior, altered mental status, blood pressure drop upon standing, depression, difficult or painful urination, mood changes, severe nausea, and severe vomiting. Others tend to be less severe—confusion, constipation, anxiety, nervousness, nightmares, and twitching.
What Is Amino Acid Therapy for Parkinson’s?
L-dopa is an amino acid and hormone that is synthesized in the body from the amino acid tyrosine. It is used as a drug to treat Parkinson’s disease, but treatment with l-dopa (l-3, 4-dihydroxyphenylalanine) has been reported to have side effects.
In a case study, research focused on the interactions and applications of the neurotransmitters serotonin and dopamine, and their amino acid precursors (meaning the amino acids that help make these neurotransmitters). The study determined that most side effects and problems seen during treatment of Parkinson’s disease with l-dopa are the result of mismanagement of the amino acid precursors and systems affected by l-dopa. When l-dopa is given alone, levels of the amino acids tyrosine, tryptophan, 5-hydroxytryptophan (5-HTP), the sulfur amino acids such as cysteine, and serotonin decrease.
According to the 2016 article appearing in the International Journal of General Medicine, side effects occur when only l-dopa is administered to patients. To minimize the side effects of l-dopa, which include nausea, involuntary movements, and psychiatric problems, inhibitors need to be used. In other words, the researchers created a balance between l-dopa and serotonin—a chemical messenger that is supposed to have an effect on mood, behavior, and sleeping patterns—by administering l-dopa alongside 5-HTP, tyrosine, cysteine, and cofactors. When there is no such balance, the effectiveness of the l-dopa is minimized, according to the study.
After four months the patient had improvement in the tremor in the upper and lower extremities and regained coordination in his left hand. He could use the computer keyboard and play the guitar. He had improvement in gait and balance, less depression and anxiety, and more willingness to go out in public.
Because of the side effects that often accompany therapy with L-dopa, an alternative is to take dietary supplements of the amino acid tyrosine, the immediate precursor of L-dopa. Since tyrosine has a very low solubility, it is preferable to raise the tyrosine level by consuming phenylalanine. Tyrosine is produced from the metabolism of phenylalanine, and phenylalanine is highly soluble and thus easy to consume. However, a cautionary note is appropriate. While phenylalanine supplementation may be helpful in lieu of L-dopa therapy, phenylalanine and/or tyrosine supplements should be avoided if taking L-dopa. The similarities in the molecules may inhibit the absorption of L-dopa from the gut, thereby limiting the effectiveness of the medication.
Another study published in January 2018 in PLOS evaluated the profile of amino acid concentrations against PD progression. Researchers explained that amino acids are crucial to the central nervous system, serving as neurotransmitters, neuromodulators, and regulators of energy metabolism. Changes in blood concentrations of amino acids in PD patients have been linked to the amount of damage to the nervous system. The researchers discovered significant differences in concentrations of the amino acids alanine, arginine, phenylalanine, and threonine. The specific amino acid profile could serve as a biochemical marker of PD progression.
In another study about amino acids and Parkinson’s, researchers discussed a naturally occurring human enzyme, cyclophilin 40 or CyP40, that appears to unravel protein aggregates that damage nerve cells and thus contribute to both Alzheimer’s disease and Parkinson’s disease. According to a study in PLOS Biology by researchers at the University of South Florida in Tampa, the findings may lead to a new therapeutic strategy for these diseases.
The researchers explained that proteins implicated in most nerve diseases form improperly and then become an insoluble clump called an amyloid. The clumping effect keeps neurons from functioning properly. Tau proteins usually stabilize activity in the central nervous system. When they become defective due to clumping, neurodegenerative diseases such as PD develop.
CyP40 could reduce the amount of aggregated tau, changing it into a more soluble form. Experimental expression of CyP40 preserved brain neurons and rescued cognitive deficits and disaggregated a protein associated with Parkinson’s disease. This was the first demonstration of a substance that can disaggregate an amyloid responsible for a neurodegenerative disease. CyP40 may bind to aggregated protein to unstack and separate the amino acid chain, or it may bind to the protein before it forms aggregates, preventing it from clumping.