Release date: 2017-05-08
Parkinson's disease is the second most common neurodegenerative disease after dementia. It affects more than 10 million people worldwide. In Australia alone, more than 70,000 people suffer from Parkinson's disease, every 340 people. One person is sick. Parkinson's disease mainly affects adults over the age of 55. About 20% of people will be diagnosed with Parkinson's disease under 50 years old, and 10% will be diagnosed with the disease under 40 years old.
It is estimated that Australia spends about 110 million Australian dollars a year on the treatment of Parkinson's disease, about twice the disease expenditure in 2005, and the researchers speculate that the prevalence of Parkinson's disease will double as of 2030, so look for Reliable therapy is the key to effective prevention and containment of Parkinson's disease.
2017 is the 200th year of Parkinson's disease discovery. 200 years ago (1817), the researcher James Parkinson first described the Parkinson's disease medically; the treatment of Parkinson's disease is in a radical state, the researchers Researcher James Parkinson advocates bloodletting or bleeding from the neck to treat the disease, followed by substances that induce skin blistering, and the application of small pieces of cork into the blisters to induce abscess release. Since then, research People began to explore slowly in the treatment of Parkinson's disease.
Early therapy
The mechanism of Parkinson's disease is the lack of a neuron that produces the neurotransmitter dopamine. Normally there are many nerve cells in the substantia nigra that produce the neurotransmitter dopamine; from the late 19th and early 20th centuries, researchers In-depth study of the substantia nigra in the brain. It was not until the 1960s that researchers discovered the key role of dopamine, and the drug therapy for Parkinson's disease made significant progress.
Previously, researchers developed a treatment for Parkinson's disease (blood-blood therapy). At the end of the 19th century, neurobiologist Jean-Martin Charcot from France proposed methods, including rest, reducing stress levels, and rhythmically by rocking the chair. damping. At the same time, the researcher Charcot also tested the Russian pulley and used this system to suspend the patient in midair to pull the spinal cord. Although this method has some improvement in the rigidity of the patient's body, due to the pressure generated by the patient's body and Side effects, so these methods are often quickly abandoned.
In the 1860s, the first drug therapy proposed by researcher Charcot and his student Ordenstein showed only modest benefits to patients, including hyoscyamine and other components from the plant belladonna. The researchers tested these substances because they noticed that Parkinson's patients usually drool, and these drugs can cause the body's saliva to dry up, while also slightly improving the individual's motor symptoms, such as tremors, muscle stiffness And sluggishness.
Researchers are not fully aware of the efficacy of these pharmaceutical preparations, and today they can effectively block the receptor of the neurotransmitter acetylcholine, which balances dopamine in the body (similar to the function of the seesaw) and reduces the excess of acetylcholine. Activity can help increase the level of dopamine in the body. Currently, purine and other anticholinergic drugs are the main treatments for patients with Parkinson's disease for the next 100 years.
Other early drug therapies for Parkinson's disease include ergot derivatives, which are fungi that affect rye. Now researchers know that ergot derivatives can mimic the effects of dopamine in the brain, and many modern Parkinson's disease drugs that mimic dopamine. They are all based on this drug development.
gold standard
A study in the 1950s found revolutionary changes in the treatment of Parkinson's disease. The researchers discovered that dopamine is mainly located in the striatum structure in the brain. This region can pass a long nerve cell. I want to be in contact with the brain's substantia nigra, and release dopamine into the striatum structure. In the 1960s, researchers Herbert Ehringer and Oleh Hornykiewicz found that dopamine is in a missing (removed) state in the brains of patients with Parkinson's disease.
Dopamine itself does not cross the blood-brain barrier (the blood-brain barrier blocks pathogens and other macromolecules from entering the brain through the bloodstream), which means that dopamine is not a drug therapy because it does not enter the brain. In 1961, the drug Levodopa showed a beneficial effect in the first clinical trial. Levodopa is a dopamine precursor that can be transported across the blood-brain barrier into the brain and converted to dopamine. The researchers found that levodopa significantly improved the function of the motor system in most patients with Parkinson's disease, and it also promotes normal exercise in patients with early Parkinson's disease.
Today, the drug levodopa remains one of the most effective and widely used drugs for the treatment of Parkinson's disease. It is usually used in conjunction with enzyme inhibitors, such as carbidopa, which can block before entering the brain. Broken levodopa, which can promote more levodopa into the brain, of course, this also increases the level of dopamine production. But unfortunately, as dopamine neurons continue to die in the brains of Parkinson's patients, the efficacy of levodopa is getting lower and lower, which requires an increase in drug dosage, and prolonged drug use can cause significant side effects in patients. Among them, severe dyskinesia and wearing-off, the patient's body will become stiff and slow.
The end effect can be solved by slowly releasing levodopa-carbidopa, such as Sinemet-CR, which ensures long-term release of the drug, thereby enabling the left-handedness in the blood of the patient's body. Pakistan is maintained at a stable level, but due to the slow release of the drug, the benefits of the controlled release tablets may take longer to appear.
In 2015, the FDA approved a drug called Rytary that combines rapid release and long-acting release of levodopa beads to solve the above problem; however, the drug is not yet approved in Australia; In the case of Parkinson's disease, levodopa in combination with the latent release gel form of Duodopa may be placed directly into the small intestine through a surgically implanted small tube, currently Duodopa in 2008. Approved by the Australian Drug Administration and entered the Australian Drug Benefits Program in 2011.
However, this treatment is only suitable for the treatment of a part of progressive Parkinson's patients, and surgical implantation of the small tube will also bring additional risks to the patient, such as infection and bleeding, and will also lead to some potential over time. Blockage and tubule movement, etc.
Other therapies
In addition to the drug levodopa, there are currently other drug therapy options for treating Parkinson's disease (although none of them can completely block the progression of Parkinson's disease). Some Parkinson's patients will continue to respond to the therapy, but the patient will experience dyskinesia or the drug's end effect, and surgery will come in handy. The most common is deep brain stimulation (DBS), which, like a pacemaker, produces a continuous electrical stimulation pulse that is usually delivered to a specific area of ​​the brain. In 2001, the therapy was in Australia. Approved for the treatment of Parkinson's disease.
Deep brain stimulation can significantly improve the performance of a variety of motor symptoms in most patients, usually 30% to 50% of patients will reduce the daily dose of drugs after treatment. However, deep brain stimulation is not recommended for all Parkinson's patients, and patients must meet a stringent set of criteria before performing the therapy. In a small number of cases, surgery usually causes some complications, such as convulsions. , bleeding or infection.
How to prevent disease progression?
All current treatments for Parkinson focus on the patient's symptoms, just like Parkinson's disease discoverer James Parkinson, whose ultimate goal is to develop a therapy that can modify the progression of the disease. A range of potential therapies are currently being developed based on reducing brain inflammation and preventing dopamine neuronal cell death, with the goal of preventing the accumulation of alpha synuclein in the brain of patients. The cells gather to form a toxic structure called Lewy bodies.
The goal of other therapies is to provide a substance that can help stimulate cell growth, proliferation, and healing, and researchers hope to develop pharmaceutical agents that protect the function of dopamine neurons. Of course, there is only time to prove whether one of the therapies can modify Parkinson's disease, but since Parkinson's disease has been discovered for 200 years, future researchers are full of confidence and motivation for the development of the disease therapy.
Reference material
[1]Statistics on Parkinson's
[2]What is Parkinson's
[3]Projected number of people with Parkinson disease in the most populous nations, 2005 through 2030
[4]The History of Parkinson's Disease: Early Clinical Descriptions and Neurological Therapies
Cold Spring Harb Perspect Med doi: 10.1101/cshperspect.a008862
[5]An Essay on the Shaking Palsy
[6]Substantia nigra and Parkinson's disease: a brief history of their long and intimate relationship.
Can J Neurol Sci
[7] Four pioneers of L-dopa treatment: Arvid Carlsson, Oleh Hornykiewicz, George Cotzias, and Melvin Yahr.
Mov Disord doi: 10.1002/mds.26120
[8] Sinemet CR sustained-release tablets
[9]From blood letting to brain stimulation: 200 years of Parkinson's disease treatment
Source: Bio Valley (WeChat: BIOONNEWS)
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