Question: What causes Parkinson's Disease ?
Answer: A Shortage of Dopamine Parkinson's disease occurs when nerve cells, or neurons, in an area of the brain that controls movement become impaired and/or die. Normally, these neurons produce an important brain chemical known as dopamine, but when the neurons die or become impaired, they produce less dopamine. This shortage of dopamine causes the movement problems of people with Parkinson's. Dopamine is a chemical messenger, or neurotransmitter. Dopamine is responsible for transmitting signals between the substantia nigra and multiple brain regions. The connection between the substantia nigra and the corpus striatum is critical to produce smooth, purposeful movement. Loss of dopamine in this circuit results in abnormal nerve-firing patterns within the brain that cause impaired movement. Loss of Norepinephrine People with Parkinson's also have loss of the nerve endings that produce the neurotransmitter norepinephrine. Norepinephrine, which is closely related to dopamine, is the main chemical messenger of the sympathetic nervous system. The sympathetic nervous system controls many automatic functions of the body, such as heart rate and blood pressure. The loss of norepinephrine might help explain several of the non-movement features of Parkinson's, such as fatigue, irregular blood pressure, decreased gastric motility or movement of food through the digestive tract, and postural hypotension. Postural hypotension is a sudden drop in blood pressure when a person stands up from a sitting or lying-down position. It may cause dizziness, lightheadedness, and in some cases, loss of balance or fainting. Lewy Bodies in Brain Cells Many brain cells of people with Parkinson's contain Lewy bodies. Lewy bodies are unusual deposits or clumps of the brain protein alpha-synuclein, along with other proteins, which are seen upon microscopic examination of the brain. Researchers do not yet know why Lewy bodies form or what role they play in the development of Parkinson's. The clumps may prevent the cell from functioning normally, or they may actually be helpful, perhaps by keeping harmful proteins "locked up" so the cells can function. Genetic Mutations Although some cases of Parkinson's appear to be hereditary, and a few can be traced to specific genetic mutations, most cases are sporadic. Sporadic means the disease occurs randomly and does not seem to run in families. Many researchers now believe that Parkinson's disease results from a combination of genetic and environmental factors. Scientists have identified several genetic mutations associated with Parkinson's including mutations in the alpha-synuclein gene. They think that many more genes may be linked to the disorder. Studying the genes responsible for inherited cases of Parkinson's can help researchers understand both inherited and sporadic cases. The same genes and proteins that are altered in inherited cases may also be altered in sporadic cases by environmental toxins or other factors. Researchers also hope that discovering genes will help identify new ways of treating Parkinson's. Environmental Toxins Although researchers increasingly recognize the importance of genetics in Parkinson's disease, most believe environmental exposures increase a person's risk of developing the disease. Even in inherited cases, exposure to toxins or other environmental factors may influence when symptoms of the disease appear or how the disease progresses. There are a number of toxins that can cause parkinsonian symptoms in humans. Researchers are pursuing the question of whether pesticides and other environmental factors not yet identified also may cause Parkinson's disease. Viruses are another possible environmental trigger for Parkinson's. Mitochondria and Free Radicals Research suggests that mitochondria may play a role in the development of Parkinson's disease. Mitochondria are the energy-producing components of the cell and are major sources of free radicals. Free radicals are molecules that damage membranes, proteins, DNA, and other parts of the cell. This damage is called oxidative stress. Changes to brain cells caused by oxidative stress, including free radical damage to DNA, proteins, and fats, have been found in people with Parkinson's. Clinical studies now underway test whether agents thought to improve energy metabolism and decrease oxidative stress slow the progression of Parkinson's disease. Recent evidence suggests that mutations in genes linked to Parkinsons disease result in mitochondrial dysfunction. Buildup of Harmful Proteins Other research suggests that the cell's protein disposal system may fail in people with Parkinson's, causing proteins like alpha-synuclein to build up to harmful levels and trigger premature cell death. Additional studies have found that clumps of protein that develop inside brain cells of people with Parkinson's may contribute to the death of nerve cells, or neurons. However, the exact role of the protein deposits remains unknown. These studies also found that inflammation, because of protein accumulation, toxins or other factors, may play a role in the disease. However, the exact role of the protein deposits remains unknown. Researchers are exploring the possibility of vaccine development to decrease or prevent the accumulation of alpha-synuclein. While mitochondrial dysfunction, oxidative stress, inflammation, and many other cellular processes may contribute to Parkinson's disease, scientists still do not know what causes cells that produce dopamine to die. Genes Linked to Parkinsons Researchers have discovered several genes that are linked to Parkinson's disease. The first to be identified was alpha-synuclein or SNCA . Studies have found that Lewy bodies from people with the sporadic form of Parkinson's contain clumps of alpha-synuclein protein. This discovery revealed a possible link between hereditary and sporadic forms of the disease. Other genes linked to Parkinson's include PARK2, PARK7, PINK1, and LRRK2. PARK2, PARK7, and PINK1 cause rare, early-onset forms of the disease. Mutations in the LRRK2 gene are common in specific populations, including in people with Parkinson's in North Africa. Researchers are continuing to study the normal functions and interactions of these genes in order to find clues about how Parkinson's develops. They also have identified a number of other genes and chromosome regions that may play a role in Parkinson's, but the nature of these links is not yet clear. Whole genome wide association studies, or GWAS, of thousands of people with Parkinson's disease are now underway to find gene variants that allow for an increased risk of developing Parkinson's but are not necessarily causes of this disorder by themselves. A recent international study found that two genes containing mutations known to cause rare hereditary forms of Parkinsons disease are also associated with the more common sporadic form of the disease. This finding came from a GWAS which looked at DNA samples of European people who had Parkinsons disease and from those who did not have the disorder.
Source: NIHSeniorHealth

Question: What are the symptoms of Parkinson's Disease ?
Answer: Parkinson's disease does not affect everyone the same way. Symptoms of the disorder and the rate of progression differ among people with the disease. Sometimes people dismiss early symptoms of Parkinson's as the effects of normal aging. There are no medical tests to definitively diagnose the disease, so it can be difficult to diagnose accurately. Early Symptoms Early symptoms of Parkinson's disease are subtle and occur gradually. For example, affected people may feel mild tremors or have difficulty getting out of a chair. They may notice that they speak too softly or that their handwriting is slow and looks cramped or small. This very early period may last a long time before the more classic and obvious symptoms appear. Friends or family members may be the first to notice changes in someone with early Parkinson's. They may see that the person's face lacks expression and animation, a condition known as "masked face," or that the person does not move an arm or leg normally. They also may notice that the person seems stiff, unsteady, or unusually slow. As the Disease Progresses As the disease progresses, symptoms may begin to interfere with daily activities. The shaking or tremor may make it difficult to hold utensils steady or read a newspaper. Tremor is usually the symptom that causes people to seek medical help. People with Parkinson's often develop a so-called parkinsonian gait that includes a tendency to lean forward, small quick steps as if hurrying forward (called festination), and reduced swinging of the arms. They also may have trouble initiating or continuing movement, which is known as freezing. Symptoms often begin on one side of the body or even in one limb on one side of the body. As the disease progresses, it eventually affects both sides. However, the symptoms may still be more severe on one side than on the other. Four Primary Symptoms The four primary symptoms of Parkinson's are tremor, rigidity, slowness of movement (bradykinesia), and impaired balance (postural instability). - Tremor often begins in a hand, although sometimes a foot or the jaw is affected first. It is most obvious when the hand is at rest or when a person is under stress. It usually disappears during sleep or improves with a deliberate movement. - Rigidity, or a resistance to movement, affects most people with Parkinson's. It becomes obvious when another person tries to move the individual's arm, such as during a neurological examination. The arm will move only in ratchet-like or short, jerky movements known as "cogwheel" rigidity. - Bradykinesia, or the slowing down and loss of spontaneous and automatic movement, is particularly frustrating because it may make simple tasks somewhat difficult. Activities once performed quickly and easily, such as washing or dressing, may take several hours. - Postural instability, or impaired balance, causes people with Parkinson's to fall easily. They also may develop a stooped posture with a bowed head and droopy shoulders. Tremor often begins in a hand, although sometimes a foot or the jaw is affected first. It is most obvious when the hand is at rest or when a person is under stress. It usually disappears during sleep or improves with a deliberate movement. Rigidity, or a resistance to movement, affects most people with Parkinson's. It becomes obvious when another person tries to move the individual's arm, such as during a neurological examination. The arm will move only in ratchet-like or short, jerky movements known as "cogwheel" rigidity. Bradykinesia, or the slowing down and loss of spontaneous and automatic movement, is particularly frustrating because it may make simple tasks somewhat difficult. Activities once performed quickly and easily, such as washing or dressing, may take several hours. Postural instability, or impaired balance, causes people with Parkinson's to fall easily. They also may develop a stooped posture with a bowed head and droopy shoulders. Other Symptoms A number of other symptoms may accompany Parkinson's disease. Some are minor; others are not. Many can be treated with medication or physical therapy. No one can predict which symptoms will affect an individual person, and the intensity of the symptoms varies from person to person. Many people note that prior to experiencing motor problems of stiffness and tremor, they had symptoms of a sleep disorder, constipation, decreased ability to smell, and restless legs. Other symptoms include - depression - emotional changes - difficulty swallowing and chewing - speech changes - urinary problems or constipation - skin problems, sleep problems - dementia or other cognitive problems - orthostatic hypotension (a sudden drop in blood pressure when standing up from a sitting or lying down position) - muscle cramps and dystonia (twisting and repetitive movements) - pain - fatigue and loss of energy - sexual dysfunction. depression emotional changes difficulty swallowing and chewing speech changes urinary problems or constipation skin problems, sleep problems dementia or other cognitive problems orthostatic hypotension (a sudden drop in blood pressure when standing up from a sitting or lying down position) muscle cramps and dystonia (twisting and repetitive movements) pain fatigue and loss of energy sexual dysfunction. A number of disorders can cause symptoms similar to those of Parkinson's disease. People with Parkinson's-like symptoms that result from other causes are sometimes said to have parkinsonism. While these disorders initially may be misdiagnosed as Parkinson's, certain medical tests, as well as response to drug treatment, may help to distinguish them from Parkinson's. Diagnosis Can Be Difficult There are currently no blood, or laboratory tests to diagnose sporadic Parkinson's disease. Diagnosis is based on a person's medical history and a neurological examination, but the disease can be difficult to diagnose accurately. Early signs and symptoms of Parkinson's may sometimes be dismissed as the effects of normal aging. A doctor may need to observe the person for some time until it is clear that the symptoms are consistently present. Improvement after initiating medication is another important hallmark of Parkinson's disease. Doctors may sometimes request brain scans or laboratory tests to rule out other diseases. However, computed tomography (CT) and magnetic resonance imaging (MRI) brain scans of people with Parkinson's usually appear normal. Recently, the FDA (Food and Drug Administration) has approved an imaging technique called DaTscan, which may help to increase accuracy of the diagnosis of Parkinsons disease. Since many other diseases have similar features but require different treatments, it is very important to make an exact diagnosis as soon as possible to ensure proper treatment.
Source: NIHSeniorHealth

Question: What are the treatments for Parkinson's Disease ?
Answer: Deep Brain Stimulation Deep brain stimulation, or DBS, is a surgical procedure used to treat a variety of disabling disorders. It is most commonly used to treat the debilitating symptoms of Parkinsons disease. Deep brain stimulation uses an electrode surgically implanted into part of the brain. The electrodes are connected by a wire under the skin to a small electrical device called a pulse generator that is implanted in the chest. The pulse generator and electrodes painlessly stimulate the brain in a way that helps to stop many of the symptoms of Parkinson's such as tremor, bradykinesia, and rigidity. DBS is primarily used to stimulate one of three brain regions: the subthalamic nucleus, the globus pallidus, or the thalamus. Researchers are exploring optimal generator settings for DBS, whether DBS of other brain regions will also improve symptoms of Parkinsons disease, and also whether DBS may slow disease progression. Deep brain stimulation usually reduces the need for levodopa and related drugs, which in turn decreases dyskinesias and other side effects. It also helps to relieve on-off fluctuation of symptoms. People who respond well to treatment with levodopa tend to respond well to DBS. Unfortunately, older people who have only a partial response to levodopa may not improve with DBS. Complementary and Supportive Therapies A wide variety of complementary and supportive therapies may be used for Parkinson's disease. Among these therapies are standard physical, occupational, and speech therapies, which help with gait and voice disorders, tremors and rigidity, and decline in mental functions. Other supportive therapies include diet and exercise. Diet At this time there are no specific vitamins, minerals, or other nutrients that have any proven therapeutic value in Parkinson's disease. Some early reports have suggested that dietary supplements might protect against Parkinson's. Also, a preliminary clinical study of a supplement called coenzyme Q10 suggested that large doses of this substance might slow disease progression in people with early-stage Parkinson's. This supplement is now being tested in a large clinical trial. Other studies are being conducted to find out if caffeine, antioxidants, nicotine, and other dietary factors may help prevent or treat the disease. While there is currently no proof that any specific dietary factor is beneficial, a normal, healthy diet can promote overall well-being for people with Parkinson's disease, just as it would for anyone else. A high protein meal, however, may limit levodopa's effectiveness because for a time afterwards less levodopa passes through the blood-brain barrier. Exercise Exercise can help people with Parkinson's improve their mobility and flexibility. It can also improve their emotional well-being. Exercise may improve the brain's dopamine production or increase levels of beneficial compounds called neurotrophic factors in the brain. Other Therapies Other complementary therapies include massage therapy, yoga, tai chi, hypnosis, acupuncture, and the Alexander technique, which improves posture and muscle activity. There have been limited studies suggesting mild benefits from some of these therapies, but they do not slow Parkinson's disease and to date there is no convincing evidence that they help. However, this remains an active area of investigation.
Source: NIHSeniorHealth

Question: what research (or clinical trials) is being done for Parkinson's Disease ?
Answer: In recent years, research on Parkinson's has advanced to the point that halting the progression of the disease, restoring lost function, and even preventing the disease are all considered realistic goals. While the goal of preventing Parkinson's disease may take years to achieve, researchers are making great progress in understanding and treating it. Genetics Research One of the most exciting areas of Parkinson's research is genetics. Studying the genes responsible for inherited cases can help researchers understand both inherited and sporadic cases of the disease. Identifying gene defects can also help researchers - understand how Parkinson's occurs - develop animal models that accurately mimic the death of nerve cells in humans - identify new approaches to drug therapy - improve diagnosis. understand how Parkinson's occurs develop animal models that accurately mimic the death of nerve cells in humans identify new approaches to drug therapy improve diagnosis. Researchers funded by the National Institute of Neurological Disorders and Stroke are gathering information and DNA samples from hundreds of families with members who have Parkinson's and are conducting large-scale studies to identify gene variants that are associated with increased risk of developing the disease. They are also comparing gene activity in Parkinson's with gene activity in similar diseases such as progressive supranuclear palsy. In addition to identifying new genes for Parkinson's disease, researchers are trying to learn about the function of genes known to be associated with the disease, and about how gene mutations cause disease. Effects of Environmental Toxins Scientists continue to study environmental toxins such as pesticides and herbicides that can cause Parkinson's symptoms in animals. They have found that exposing rodents to the pesticide rotenone and several other agricultural chemicals can cause cellular and behavioral changes that mimic those seen in Parkinson's. Role of Lewy Bodies Other studies focus on how Lewy bodies form and what role they play in Parkinson's disease. Some studies suggest that Lewy bodies are a byproduct of a breakdown that occurs within nerve cells, while others indicate that Lewy bodies are protective, helping neurons "lock away" abnormal molecules that might otherwise be harmful. Identifying Biomarkers Biomarkers for Parkinson's -- measurable characteristics that can reveal whether the disease is developing or progressing -- are another focus of research. Such biomarkers could help doctors detect the disease before symptoms appear and improve diagnosis of the disease. They also would show if medications and other types of therapy have a positive or negative effect on the course of the disease. The National Disorders of Neurological Disorders and Stroke has developed an initiative, the Parkinsons Disease Biomarkers Identification Network (PD-BIN), designed specifically to address these questions and to discover and validate biomarkers for Parkinsons disease. Transcranial Therapies Researchers are conducting many studies of new or improved therapies for Parkinson's disease. Studies are testing whether transcranial electrical polarization (TEP) or transcranial magnetic stimulation (TMS) can reduce the symptoms of the disease. In TEP, electrodes placed on the scalp are used to generate an electrical current that modifies signals in the brain's cortex. In TMS, an insulated coil of wire on the scalp is used to generate a brief electrical current. Drug Discovery A variety of new drug treatments for Parkinson's disease are in clinical trials. Several MAO-B inhibitors including selegiline, lazabemide, and rasagiline, are being tested to determine if they have neuroprotective effects in people with Parkinsons disease. The National Institute of Neurological Disorders and Stroke has launched a broad effort to find drugs to slow the progression of Parkinson's disease, called NET-PD or NIH Exploratory Trials in Parkinson's Disease. The first studies tested several compounds; one of these, creatine, is now being evaluated in a larger clinical trial. The NET-PD investigators are testing a highly purified form of creatine, a nutritional supplement, to find out if it slows the decline seen in people with Parkinson's. Creatine is a widely used dietary supplement thought to improve exercise performance. Cellular energy is stored in a chemical bond between creatine and a phosphate. More recently, NET-PD has initiated pilot studies to test pioglitazone, a drug that has been shown to stimulate mitochondrial function. Because mitochondrial function may be less active in Parkinsons disease, this drug may protect vulnerable dopamine neurons by boosting mitochondrial function. Cell Implantation Another potential approach to treating Parkinson's disease is to implant cells to replace those lost in the disease. Starting in the 1990s, researchers conducting a controlled clinical trial of fetal tissue implants tried to replace lost dopamine-producing nerve cells with healthy ones from fetal tissue in order to improve movement and the response to medications. While many of the implanted cells survived in the brain and produced dopamine, this therapy was associated with only modest functional improvements, mostly in patients under the age of 60. Some of the people who received the transplants developed disabling dyskinesias that could not be relieved by reducing anti-parkinsonian medications. Stem Cells Another type of cell therapy involves stem cells. Some stem cells derived from embryos can develop into any kind of cell in the body, while others, called progenitor cells, are less flexible. Researchers are developing methods to improve the number of dopamine-producing cells that can be grown from embryonic stem cells in culture. Other researchers are also exploring whether stem cells from adult brains might be useful in treating Parkinson's disease. Recent studies suggest that some adult cells from skin can be reprogrammed to an embryonic-like state, resulting in induced pluripotent stem cells (iPSC) that may someday be used for treatment of Parkinsons. In addition, development and characterization of cells from people with sporadic or inherited Parkinsons may reveal information about cellular mechanisms of disease and identify targets for drug development. Gene Therapy A number of early clinical trials are now underway to test whether gene therapy can improve Parkinson's disease. Genes which are found to improve cellular function in models of Parkinson's are inserted into modified viruses. The genetically engineered viruses are then injected into the brains of people with Parkinson's disease. Clinical studies have focused on the therapeutic potential of neurotrophic factors, including GDNF and neurturin, and enzymes that produce dopamine. These trials will test whether the viruses, by lending to the production of the protective gene product, improve symptoms of Parkinson's over time. The National Institute of Neurological Disorders and Stroke also supports the Morris K. Udall Centers of Excellence for Parkinson's Disease Research program . These Centers, located across the USA, study cellular mechanisms underlying Parkinsons disease, identify and characterize disease-associated genes, and discover and develop potential therapeutic targets. The Centers' multidisciplinary research environment allows scientists to take advantage of new discoveries in the basic, translational and clinical sciences that could lead to clinical advances for Parkinsons disease.
Source: NIHSeniorHealth

Question: What is (are) Parkinson's Disease ?
Answer: Parkinson's disease is a brain disorder that leads to shaking, stiffness, and difficulty with walking, balance, and coordination. It currently affects about half a million people in the United States, although the numbers may be much higher. Parkinson's disease is both chronic, meaning it lasts for a long time, and progressive, meaning its symptoms grow worse over time. It is not contagious.
Source: NIHSeniorHealth

Question: Who is at risk for Parkinson's Disease? ?
Answer: About 60,000 Americans are diagnosed with Parkinson's disease each year. The disease strikes about 50 percent more men than women. The average age of onset is 60 years, and the risk of developing the disease increases with age. Parkinson's disease is also more common in developed countries, possibly because of increased exposure to pesticides or other environmental toxins.
Source: NIHSeniorHealth

Question: What causes Parkinson's Disease ?
Answer: Parkinson's disease occurs when nerve cells, or neurons, in an area of the brain that controls movement die or become impaired. Normally, these neurons produce an important brain chemical known as dopamine, but once the neurons become impaired, they produce less dopamine and eventually die. It is this shortage of dopamine that causes the movement problems of people with Parkinson's.
Source: NIHSeniorHealth

Question: What is (are) Parkinson's Disease ?
Answer: Dopamine is a brain chemical messenger, or neurotransmitter. It is responsible for transmitting signals between a brain region called the substantia nigra and multiple brain regions. The connection between the substantia nigra and the corpus striatum is critical to produce smooth, purposeful movement. Loss of dopamine results in abnormal nerve-firing patterns within the brain that cause impaired movement.
Source: NIHSeniorHealth

Question: What is (are) Parkinson's Disease ?
Answer: Lewy bodies are unusual deposits or clumps of the brain protein alpha-synuclein, along with other proteins, which are seen upon microscopic examination of the brain. Many brain cells of people with Parkinson's disease contain Lewy bodies. Researchers do not yet know why Lewy bodies form or what role they play in the development of Parkinson's disease. The clumps may prevent the cell from functioning normally, or they may actually be helpful, perhaps by keeping harmful proteins "locked up" so that the cells can function.
Source: NIHSeniorHealth

Question: How to diagnose Parkinson's Disease ?
Answer: There are currently no blood or laboratory tests to diagnose sporadic Parkinson's disease. Diagnosis is based on a person's medical history and a neurological examination, but the disease can be difficult to diagnose accurately. Doctors may sometimes request brain scans or laboratory tests in order to rule out other diseases. However, computed tomography (CT) and magnetic resonance imaging (MRI) brain scans of people with Parkinson's usually appear normal. Recently, the FDA (Food and Drug Administration) has approved an imaging technique called DaTscan, which may help to increase accuracy of the diagnosis of Parkinsons disease. Since many other diseases have similar features but require different treatments, it is very important to make an exact diagnosis as soon as possible to ensure proper treatment.
Source: NIHSeniorHealth

Question: What is (are) Parkinson's Disease ?
Answer: Carbidopa is a drug that is usually given along with levodopa. It delays the body's conversion of levodopa into dopamine until the levodopa reaches the brain. This prevents or reduces some of the side effects that often accompany levodopa therapy. Carbidopa also reduces the amount of levodopa needed.
Source: NIHSeniorHealth

Question: What are the treatments for Parkinson's Disease ?
Answer: Yes. Other medications available to treat some symptoms and stages of Parkinson's disease include direct dopamine agonists, MAO-B inhibitors, COMT inhibitors, an anti-viral drug, and anticholinergics. Direct dopamine agonists are drugs that mimic the role of dopamine in the brain. They can be used in the early stages of the disease, or later on to give a more prolonged and steady dopaminergic effect in people who experience "wearing off" or "on-off" effects from taking the drug. Dopamine agonists are generally less effective than levodopa in controlling rigidity and bradykinesia. They can cause confusion in older adults. MAO-B inhibitors are another class of drugs that can reduce the symptoms of Parkinson's by causing dopamine to build up in surviving nerve cells. COMT inhibitors prolong the effects of levodopa by preventing the breakdown of dopamine. COMT inhibitors can usually make it possible to reduce a person's dose of levodopa. Amantadine, an old antiviral drug, can help reduce Parkinson's symptoms in the early stages of the disease, and again in later stages to treat dyskinesias. Anticholinergics can help reduce tremors and muscle rigidity.
Source: NIHSeniorHealth

Question: What are the symptoms of Parkinson's Disease ?
Answer: Doctors may prescribe a variety of medications to treat the non-motor symptoms of Parkinson's disease, such as depression and anxiety. Hallucinations, delusions, and other psychotic symptoms may be caused by some drugs prescribed for Parkinson's. Therefore, reducing or stopping those Parkinson's medications may make these symptoms of psychosis go away. A variety of treatment options, including medications, also are available to treat orthostatic hypotension, the sudden drop in blood pressure that occurs upon standing.
Source: NIHSeniorHealth

Question: What is (are) Parkinson's Disease ?
Answer: Deep brain stimulation, or DBS, is a surgical procedure used to treat a variety of disabling disorders. It is most commonly used to treat the debilitating symptoms of Parkinsons disease. Deep brain stimulation uses an electrode surgically implanted into part of the brain. The electrodes are connected under the skin to a small electrical device called a pulse generator, implanted in the chest. The generator and electrodes painlessly stimulate the brain to help stop many Parkinson's symptoms such as tremor, bradykinesia, and rigidity. DBS is primarily used to stimulate one of three brain regions: the subthalamic nucleus, the globus pallidus, or the thalamus. Researchers are exploring optimal generator settings for DBS, whether DBS of other brain regions will also improve symptoms of Parkinsons disease, and also whether DBS may slow disease progression. Deep brain stimulation usually reduces the need for levodopa and related drugs, which in turn decreases dyskinesias and other side effects. It also helps to relieve "on-off" fluctuation of symptoms. People who respond well to treatment with levodopa, even if only for a short period, tend to respond well to DBS.
Source: NIHSeniorHealth

Question: What is (are) Parkinson's Disease ?
Answer: The Parkinsons Disease Biomarkers Identification Network, or PD-BIN, is an initiative developed by the National Institute of Neurological Disorders and Stroke to discover and validate biomarkers for Parkinsons disease. Biomarkers are measurable characteristics that can reveal whether the disease is developing or progressing. Biomarkers could help doctors detect Parkinsons disease before symptoms appear and improve diagnosis of the disorder.
Source: NIHSeniorHealth

Question: What is (are) Parkinson's Disease ?
Answer: The National Institute of Neurological Disorders and Stroke (NINDS) has launched a broad effort called NIH Exploratory Trials in Parkinson's Disease, or NET-PD, to find drugs to slow the progression of Parkinson's disease. The first studies tested several compounds. One of these, a nutritional supplement called creatine, is now being evaluated in a larger clinical trial to find out if it slows the clinical decline seen in people with Parkinson's disease. For more information on NET-PD trials visit: http://parkinsontrial.ninds.org.
Source: NIHSeniorHealth