Parkinson's Disease

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    Bill Willis

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    Louie Neri, Graham Walker
    Last Updated: October 13, 2024

    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.

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    Parkinson's Disease falls under the Brain Health category.

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    5,241 participants in 14 trials and 5 meta-analyses

    What is Parkinson’s disease?

    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.[1] 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.[2][3][4]

    What are the main signs and symptoms of Parkinson’s disease?

    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.[1]

    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:

    • Depression
    • Fatigue and excessive daytime sleepiness
    • Anxiety
    • Cognitive decline[5] / Dementia
    • Constipation or urinary problems
    • Skin problems[6]

    What types of skin problems are associated with Parkinson’s disease?

    How is Parkinson’s disease diagnosed?

    Parkinson’s disease is diagnosed primarily by symptoms, medical history, and a physical exam.[4] Family medical history will also be reviewed, since a first-degree relative with Parkinson's disease increases the chance of diagnosis.[7] 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.[8] 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.[9] 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.[10]

    What are some of the main medical treatments 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.[1] 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.[11] Anticholinergic drugs are also used to help reduce tremors and muscle stiffness, and amantadine may be prescribed to suppress involuntary movements.[11]

    What are some of the main medical treatments for non-motor symptoms of Parkinson’s?

    Have any supplements been studied for Parkinson’s disease?

    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),[12][13] inflammation, and mitochondrial dysfunction are common themes in the pathology.[14] 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.[15][16]

    The following supplements have been studied in people with Parkinson’s disease:

    How could diet affect 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,[27] while coffee or tea consumption have been associated with decreased risk.[28][29] 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.[30]

    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.[31] However, multiple studies have noted associations between reduced Parkinson's disease risk and adherence to a Mediterranean diet.[32][31]

    Are there any other treatments for Parkinson’s disease?

    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.[11]

    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.[33]

    Are exercise interventions effective for treating Parkinson’s disease?

    What types of exercise interventions have been studied in people with Parkinson's disease?

    What causes Parkinson’s disease?

    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.[34] 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.[35]

    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[36] that may contribute to non-motor symptoms.[37]

    What causes skin problems in Parkinson’s disease?

    What causes neuron death in Parkinson’s Disease?

    Examine Database: Parkinson's Disease

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    Frequently asked questions

    What is Parkinson’s disease?

    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.[1] 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.[2][3][4]

    What are the main signs and symptoms of Parkinson’s disease?

    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.[1]

    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:

    • Depression
    • Fatigue and excessive daytime sleepiness
    • Anxiety
    • Cognitive decline[5] / Dementia
    • Constipation or urinary problems
    • Skin problems[6]
    What types of skin problems are associated with Parkinson’s disease?

    The following skin disorders may be experienced by people with Parkinson’s disease:[38]

    Seborrheic dermatitis (SD): SD is a chronic eczema-like condition that affects areas of the skin that tend to have more sebaceous (oil-producing) glands, such as the scalp, face, ears, and upper chest.[39] Other areas of skin where bends or folds are present, such as under the arms, breasts, or groin, may also be affected. Although SD is a common skin condition in the general population, it tends to occur with higher frequency in people with Parkinson’s disease.[40] Symptoms include increased dandruff and the formation of inflamed, scaly patches on areas of the skin that are affected. People with mild to moderate SD often respond well to antifungal medications or corticosteroids. However, some people with Parkinson’s disease may develop more severe forms of SD that may require treatment with more toxic, systemic antifungals, such as fluconazole or itraconazole.[41][40][42]

    Oily skin: People with Parkinson’s may also experience generally oily skin, without developing seborrheic dermatitis.

    Sweating disorders: The neurological pathology of Parkinson’s disease can also affect the part of the nervous system that regulates sweating, resulting in hyperhidrosis (excessive sweating), or hypohidrosis, a condition in which insufficient levels of sweat are produced (which can lead to hyperthermia).[6]

    Rosacea: Rosacea is a chronic skin condition that causes blushing and the formation of small, pus-filled bumps on the face. The affected areas of skin can feel hot and tender, with small blood vessels visible on the skin surface. People with rosacea may also experience itching, burning, or stinging in the areas that are affected. Rosacea may also be a risk factor for developing PD, with one large cohort study noting a 2-fold increased risk of PD in people with ocular rosacea.[43]

    Increased melanoma risk: People with Parkinson’s may be at increased risk of developing melanoma, a type of skin cancer.[44][45]

    Bullous pemphigoid (BP): BP is the most common autoimmune-mediated blistering skin disease. People with BP develop large, fluid-filled blisters, commonly on areas of the skin associated with creases or folds, such as the elbows and knees.[46] BP may occur with increased frequency in people with Parkinson’s disease or other neurological disorders. One large case-control study found that while BP occurred in around 1% of the general population, it occurred with 3% frequency in people with Parkinson’s.[47]

    How is Parkinson’s disease diagnosed?

    Parkinson’s disease is diagnosed primarily by symptoms, medical history, and a physical exam.[4] Family medical history will also be reviewed, since a first-degree relative with Parkinson's disease increases the chance of diagnosis.[7] 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.[8] 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.[9] 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.[10]

    What are some of the main medical treatments 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.[1] 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.[11] Anticholinergic drugs are also used to help reduce tremors and muscle stiffness, and amantadine may be prescribed to suppress involuntary movements.[11]

    What are some of the main medical treatments for non-motor symptoms of Parkinson’s?

    A drug called rivastigmine, a cholinesterase inhibitor, is used to treat dementia in people with Parkinson's disease (or Alzheimer's).[57] Other treatments for non-motor symptoms are similar to treatments used for the same symptoms in people without Parkinson's disease.[4] For example, selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants, and norepinephrine reuptake inhibitors are used to treat depression in people with Parkinson's disease.[4] Melatonin has shown some efficacy for treating daytime fatigue and excessive daytime sleepiness in people with Parkinson's disease through improving sleep quality.[58] Although modafinil is often prescribed for excessive daytime sleepiness, it failed to improve objective measures of sleepiness in people with Parkinson's disease in a randomized controlled trial.[59]

    Have any supplements been studied for Parkinson’s disease?

    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),[12][13] inflammation, and mitochondrial dysfunction are common themes in the pathology.[14] 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.[15][16]

    The following supplements have been studied in people with Parkinson’s disease:

    How could diet affect 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,[27] while coffee or tea consumption have been associated with decreased risk.[28][29] 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.[30]

    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.[31] However, multiple studies have noted associations between reduced Parkinson's disease risk and adherence to a Mediterranean diet.[32][31]

    Are there any other treatments for Parkinson’s disease?

    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.[11]

    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.[33]

    Are exercise interventions effective for treating Parkinson’s disease?

    No current pharmacological therapies have the ability to stop or delay progression of Parkinson's disease, but the ability of exercise interventions to accomplish this are currently under investigation. Preclinical studies have found that exercise can reduce the loss of dopamine-generating brain cells in animal models of Parkinson's disease.[60] A human randomized controlled trial demonstrated that exercise can have positive effects on the brain in people with Parkinson's disease as well, at least in part through increased dopamine release and by promoting neuroplasticity.[61]

    Exercise-induced improvements in motor function have also been found in trials of people with Parkinson's disease. A phase 2 randomized controlled trial compared the effects of high-intensity interval training (HIIT) or lower-intensity exercise on a treadmill in people recently diagnosed with Parkinson's disease to a control group that received standard care only. The HIIT exercise group had significantly less decline in motor function over a 6 month period compared to the the low-intensity exercise group and non-exercising standard care group.[62] Neither the standard care group nor the low-intensity exercise group showed improvements in disease progression, however.

    A meta-analysis of 18 randomized controlled trials on the effect of exercise interventions in people with Parkinson's disease also found significant improvements in measures of motor function for exercise interventions in people with Parkinson's, compared to non-exercising or recreational-activity-only control groups. However, there were no significant improvements in non-motor Parkinson’s symptoms.[63]

    Overall, the growing body of research on exercise and Parkinson’s disease suggests that exercise may significantly slow disease progression, but more research is needed to better understand the type of exercise and intensity level that may be optimal in different individuals. Parkinson's disease also tends to present as different clinical subtypes in different individuals,[64] and it isn’t currently clear which subtypes may benefit the most from exercise interventions. The overall positive body of evidence has prompted the creation of evidence-based fitness programs designed to improve physical function and delay[65] disease progression in people with Parkinson's.

    What types of exercise interventions have been studied in people with Parkinson's disease?

    The following types of exercise interventions have been shown efficacy in randomized controlled trials of people with Parkinson's disease:

    What causes Parkinson’s disease?

    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.[34] 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.[35]

    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[36] that may contribute to non-motor symptoms.[37]

    What causes skin problems in Parkinson’s disease?

    Seborrheic dermatitis (SD): The cause of SD in Parkinson’s isn’t clear, but a number of ideas have been proposed:[48]

    • Changes in the skin microbiome
    • Impaired immune response to Malassezia spp., a type of yeast found in skin lesions of people with SD.
    • Increased amount of fatty acids on the surface of the skin
    • Disrupted skin-neurotransmitter signaling
    • Impaired skin barrier function caused by genetic factors
    • Abnormal shedding of keratinocytes, the most common type of skin cell
    • Motor dysfunction: Some researchers have suggested that SD may be indirectly caused by the motor symptoms of Parkinson’s,[49] since muscle rigidity and the loss of facial muscle control also reduce skin mobility.[50] In support of this idea, people with moderate to severe levels of Parkinson’s motor symptoms tend to have worse symptoms of SD, or a 1.8-fold increased risk of developing SD if they haven’t developed it yet.[49] Moreover, treatment with levodopa decreases oil secretion and improves SD symptoms in people with Parkinson’s disease,[51] further suggesting that SD is related to motor symptoms.

    Sweating disorders: Hyperhidrosis (excessive sweating), or hypohidrosis (insufficient sweat production): Sweating disorders in Parkinson’s disease are caused by changes to the autonomic nervous system, which controls sweating.[52] However, sweating disorders can also be treatment-induced. Therapies that affect dopamine levels, such as levodopa, can cause excessive sweating as a side-effect. Hyperhidrosis can also result when dopamine-based therapies stop working, which can be ameliorated by increasing the dosage.[6][53] Other treatments that improve motor function, such as deep brain stimulation,[54] also tend to improve excessive sweating.

    Dopamine-affecting treatments for Parkinson’s disease, such as levodopa, can also have negative effects on the skin in certain individuals. Levodopa can cause skin rashes in certain people, although this has been linked to an allergic reaction to a compounding dye used in the drug preparation, rather than a reaction to levodopa itself.[55][56]

    What causes neuron death in Parkinson’s Disease?

    A small number of Parkinson’s disease cases are inherited and caused by mutations in specific genes.[70] However, the majority of Parkinson’s cases occur in people without any known family history, and the cause of disease onset isn’t clear. Observational studies have implicated possible exposure to toxic chemicals such as pesticides or heavy metals as a possible contributing factor, and many of these agents are able to cause Parkinson’s-like symptoms in animal models.[71]

    Although the cause of neuron death isn’t currently understood, the following pathological mechanisms have been implicated:[72][73][74]

    • Dysfunctional proteostasis, which is the regulation of proteins. In people with Parkinson’s, the protein alpha-synuclein tends to form toxic, insoluble aggregates that accumulate in brain cells, contributing to the pathology. Cellular processes such as autophagy, a process that helps to break down and clear out damaged, misfolded proteins are also disrupted.
    • Pathological changes in mitochondrial function and calcium regulation
    • Increased levels of oxidative stress and neuroinflammation

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