Role of neurotransmitters in Parkinson’s disease

Role of neurotransmitters in Parkinson’s disease

Introduction

Neurological disorders and neurotoxins that cause harm in the basal ganglia and substantia nigra influence play a crucial role in causing neurological illnesses such as Parkinson disease. Parkinson disease is a progressive neurological disorder that affects the nervous system and impinges on body movements. It occurs because of death of dopamine-producing neurons within the substantia nigra. Shaking, muscle stiffness, slow movement, and impaired balance are symptoms of the neurological disorder. MPTP is an example of neurotoxins that have proved to be advantages in the studies concerning the disease. 1-methyl-4-phenyl -1, 2, 3, 6 tetrahydropyridine seems to destroy particular neurons that that are engaged in Parkinson’s disease (Cicchetti, Drouin-Ouelle, & Gross, 2009). MPTP has contributed to the implementation of the animal model for testing new treatment of the disease. Additionally, the neurotoxin has generated insights concerning the probable pathogeneses of the neurological disorder. MPTP is neurological toxin antecedent to MPP+ that result to permanent signs of Parkinson’s illness via destruction of dopaminergic neurons present in the substantia nigra, brain constituent. MPTP has generated a lot of interest among researchers to study the pathogenesis of the Parkinson’s disease due to its ability to target neurons that are involved in the neurological disorder (Cicchetti, Drouin-Ouelle, & Gross, 2009). This paper discusses the role of neurotransmitters in Parkinson’s disease and potential future and current treatments of this illness.

Role of neurotransmitters in Parkinson’s disease

According to Miller, James-Kracke, Sun, & Sun (2009), dopamine acts as a neurotransmitter in the brain, sending nerve signals to other cells. Substantia ganglia contains cell that are in charge of dopamine production. The dysfunction of dopamine system is the causality of Parkinson’s disease that causes tremor and stiffness. This implies that nerve impulses are not sent to body cells. The disorder is not fatal but with dropping levels of dopamine, it worsens disabling the movement of an individual. Parkinson’s disease has symptoms that are not easily recognized and manifest after the disease has caused adverse effects to the patient. Patients susceptible the disorder are administered with drugs that enable dopamine system to continue regenerating dopamine. In Parkinson’s disease, the administration of medicines causes production of dopamine, a neurotransmitter, which is responsible for transmission of signals (Jackson-Lewis & Smeyne, 2005).

Another neurotransmitter called norepinephrine an antecedent to the epinephrine hormone plays critical roles in Parkinson’s disease. It reduces stress due to its anti-stress chemical characteristics in the body and Parkinson’s disease is not an exception. As result chronic discharge of epinephrine into the bloodstream occurs. Epinephrine is an example of adrenaline hormone, which is normally released in emergencies, and Parkinson’s disease is an exemption. Epinephrine can reduce the amount of dopamine required to as precursor for norepinephrine hence helping in preservation of dopamine. This in turn reduces the depletion of dopamine reducing the chances of occurrence of Parkinson’s disease (Zhou, Huang, & Przedborski, 2008).

Epinephrine neurotransmitter has the capability to induce conversion of glucose from glycogen hence extending muscle action and help in achieving muscle control and improving of motor symptom. The management of acetylcholine activation and overstimulation of epinephrine have essential influences on motor control. The inhibition of acetylcholine and epinephrine will reduce and improve the motor symptoms of Parkinson’s disease.

Treatment of Parkinson disease

Parkinson’s disease has no recognized treatment to reverse the breakdown of nerve cells therefore; patients only relieve symptoms of the disease through medication. Surgery has been employed though in a few cases to treat symptoms of the disease. Parkinson’s disease patients have diverse treatment relying on the category of treatment a patient will need, but may also change during disease progression. Other factors that influence changes in treatment are age, work status, family, and living condition. Parkinson’s treatment might entail medication, surgery, and home treatment among others (Yokoyama, Kuroiwa, Yano, & Araki, 2008).

Home treatment

Home treatment is meant to aid patients adjust as the illness progresses and be self-reliant as much as possible. Initial phases of the disease have no major disruption on the patient’s life, but as it advance individual disabling sets in affecting the quality of life due to inability to continue working, offer parental duties, and take of home. Home treatment involves various aspects. The first aspect is modification of activities and home. Under this aspect, the patient needs to abridge daily activities and repositioning furniture to for offering support for movement within the house. The second aspect that the patient needs to adhere to is to eat healthy foods such as ample fruits, vegetables, cereals, grains, legumes, fish, poultry,  lean meat and low-fat dairy products.  Parkinson’s disease patients should have regular body exercise and physical therapy that are important in both initial and later stages of the illness. Symptoms such as tremor can be treated by putting weight on the hand to reinstate control. Voice and speech problems need to be addressed by speech-language pathologist. Eating problems and salivation is a symptom that can be managed by changing the diet. Family members and friends can provide social support to reduce levels of depression. Another sign refered to as dementia, which leads to memory loss and confusion can treated through administration of drugs.

Medication treatment

Medication is another form of treatment that is commonly employed to relieve symptoms of the Parkinson’s disease. However, the essential target of medication is to contain brain chemical, refered to as dopamine, which results to symptoms of the disorder. Drug administration is normally deployed when symptoms are on the verge of disabling a patient’s life. These drugs have a prescription on stipulated time to be taken. Miller, James-Kracke, Sun, & Sun ( 2009) affirm that medication treatment might vary basing on the symptoms, age, and response to certain drugs. Drugs have the capability to improve symptom and simultaneously present side effects to the patient. As such, it requires much time to employ the best combination of drugs for a specific patient. There are different choices of medicines namely levodopa and carbidopa, dopamine agonists, COMT inhibitors, MAO-B inhibitors, Amantadine and acetylcholine agents.

Levodopa and carbidopa medicine

This medicine works by its conversion to dopamine by the brain. Carbidopa is administered by levodopa to inhibit conversion of levodopa outside the brain. Several benefits are allied to the usage of levodopa and carbidopa. The combination enables provision of dopamine to the brain due to inhibited brain-exterior conversion. It also lessens the side effects that might result by high levels of dopamine outside the brain via decreasing the provision of unused dopamine outside the brain. High levels of dopamine outside the brain can result to nausea, vomiting, and low blood pressure. The combination of levodopa and carbidopa improves the effect of levodopa hence it manages symptoms (Yokoyama, Kuroiwa, Yano, & Araki, 2008).

Levodopa is used to manage symptoms of Parkinson and its usability is throughout the stages of the disease. It is the most effectual drug that mitigates symptoms of Parkinson’s disease. It decreases stiffness, slowness, and tremors and enhances muscle mobility. Muscle mobility can influence control, balance, and body movement. Levodopa has no effect on dementia, freezing, constipation, urinary problems and impotence. However, it does not hamper with disease progression, but enhances mobility and prevents relentless disability. The medicine has been observed to allow patients to be self-reliant for a longer time.

Side effects of levodopa are less imperative than the benefits and they include troubled breathing, hives, swelling of lips, face, tongue or throat, anxiety, agitation, confusion, hallucination, abnormal thinking, clumsiness, nausea or vomiting, worse tremor,  and twitching of lips, tongues, legs or face.

Dopamine agonists

This medicine arouses the nerve receptors in the brain that would usually be stimulated by dopamine. Dopamine agonists are not transformed to dopamine upon administration hence differs from levodopa but resembles dopamine. The drug is used in the initial stages of the illness to relieve symptoms. It mostly employed to people who have recently been identified with Parkinson’s disease and have 60 years or less. This is because the drug has a tendency of holding up the need for levodopa, resulting to postponing of motor fluctuations that might transpire with long-term therapy f levodopa. Additionally, dopamine agonist can be combined with levodopa in the later stages of the illness when levodopa is either unable to control symptoms and dosage increment would result to adverse side effects or severe motor fluctuations because of levodopa. Examples of dopamine include Apomorphine that is an injectible and speedy-active dopamine. It is administered through skin injection due immobility. The usage of Apomorphine is frequently referred to as rescue.

When used singly at initial stages of the disorder, the drug might mitigate symptoms of the disease specifically motor function oriented symptoms including slowness and stiffness. As much as dopamine is not as efficient as levodopa, it supplements it especially when other dopamine agonists or levodopa is inefficient. The combination of dopamine agonist and levodopa decreases the amount of levodopa required to control symptoms hence reducing side effects. The drug enhances motor function throughout the on and off periods. Long-term usage of Levodopa is associated with involuntary movement; hence combining it with dopamine agonists reduces this side effect of levodopa. Another benefit of dopamine agonist is that it extends the effect of levodopa and diminishes motor fluctuations. Amorphine’s rapid activity makes it effective within the first 10 minutes from the period of injection administration (Miller, James-Kracke, Sun, & Sun, 2009).

Similar to other drugs, dopamine agonists have side effects, which include chest pain, discomfort, cold sweats or chills, confusion, hallucinations, dizziness, fainting, twitching, or recurring movement of lips, tongue, arms, face or legs. The above named side effects might require special attention from the doctor. Other popular side effects include skin problems, yawning, blurred vision, runny nose, drowsiness, and sleepiness among others.

 

COMT inhibitors

Cotechol O-methyltransferase inhibitors, abbreviated as COMT, enables huge amounts of levodopa to access the brain, increasing dopamine levels. It aids in provision of much stable and constant supply of levodopa. As a result, it prolongs the benefits of levodopa. This drug is popularly combined with levodopa and is ineffective to symptoms of Parkinson’s disease on its own. However, it is employed to treat individuals having intervals between doses of levodopa, a period called wearing off characterized by ceasing of functioning of levodopa. Other situations where COMT inhibitors are used are in patients that have uncertain “off” periods that do not occur in the time interval of doses of levodopa. The medicine is also advantageous to patients who show response constancy to levodopa, although they want much symptom relief devoid of increasing their dosage of levodopa and those who show an impulsive and uncontainable movement, allowing for the decrement of levodopa dosage that reduces the relentlessness of dyskinesias (Cicchetti, Drouin-Ouelle, & Gross, 2009).

The inhibitor has been observed to be accommodating many patients having Parkinson’s disease. The combination of COMT inhibitor and tolcapone and entacapone has the following abilities: raising of “on” time and lowering of “off” time by 1 to 2 hours per day, decrease motor fluctuations initiated by levodopa’s effect of wearing off, enhance motor performance and capability to accomplish daily activities devoid of quitting any symptom control. Additionally, stalevo, a combination of entacapone, levodopa, and carbidopa is more suitable for some patients since instead of taking two pills, they take only one.

Some severe side effects of entacapone include difficulties in breathing, hives, swelling of face, lips, throat, and tongue. Side effects such as increase or reduction in directed movement, hyperactivity, hallucination and undirected movements of lips, tongues, face, or legs are not severe, but it is important to inform the doctor. Common side effects present to all users of entacapone medicine include nausea or belly pain, diarrhea, dizziness and fatigue. Tolcapone also exhibits certain side effects such as dark urine, itching, light colored stool, progressing nausea, extraordinary drowsiness, tiredness and weakness, and yellow eyes, which are all indications of liver destruction. Other results due to the usage of tolcapone are hallucination, dizziness, headache, infections such as sore throat and sleeping problems.

Monoamine oxidase inhibitors (MAOIs)

This medication treats Parkinson’s disease symptom by inhibiting the breakdown of dopamine and extending its effects. Additionally, MAOIs averts the elimination of dopamine between nerve endings and improve its discharge from the nerve cells. Examples of MAOIs include, rasagiline and selegiline, both are selective forms of monoamine oxidase inhibitors. This drug is administered in the initial stages of the disorder to treat placid symptoms such as resting tremor. Some researches propose that rasagiline and selegiline are able to decrease the progression of the disorder, but the issue is arguable by some medical experts. Rasagiline and selegiline might be supplemented to levodopa management especially in advanced cases of Parkinson’s disease to decrease motor fluctuations, rise the levodopa’s time of effect, and reduce the levels of levodopa required to manage symptoms (Jackson-Lewis & Smeyne, 2005). Early stages of Parkinson’s disease require MAO-B to improve symptoms. Combination of rasagiline or selegiline with levodopa is able to decrease motor fluctuations and raise the length of “on” periods when administered to people in the sophisticated stage of the disease.

Some severe side effects of MAOIs include difficulty in breathing, hives, swelling of lips, tongue, face or throat and indications of high blood pressure such as acute chest pains, broadened eye pupils, acute headache, inflexible or sore neck,and fast or slow heart beat. Common side effects present when MAOIs are used include belly pain or heartburn, dizziness, muscle pains, nausea and vomiting, and sleeping problems.

Amantadine

This is a remedy applied to manage and inhibit influenza viruses’ infection. However, it is essential in treating other signs of illnesses. Yokoyama, Kuroiwa, Yano, & Araki (2008) point out that, the drug induces the discharge of dopamine in the brain and blocks receptors for acetylcholine, a brain chemical that provokes movement. Acetylcholine and dopamine amounts need to be balanced for a normal control of muscle and motor. Amantadine is applied to people in their initial stages of the disorder and has gentle to modest symptoms. Moreover, it can be combined with levodopa to decrease dyskinesias during the later stages of Parkinson’s disease. Common side effects of Amantadine include agitation, anxiety, dizziness, loss of appetite, sleeping problems and blotchy marks on the skin.

Anticholinergic agents

            This drug obstructs cholinergic nerve impulses, which aid in directing muscles of arms, legs, and body and prevent the activities of acetylcholine. Acetylcholine is a primary chemical messenger like dopamine, assists in controlling muscle mobility, sweat gland function and intestinal function (Cicchetti, Drouin-Ouelle, & Gross, 2009).

Brain Surgery

            Failure of drugs to relieve symptoms of Parkinson’s disease leads to consideration of brain surgery as a form of treatment, though it is not a cure. Administration of drugs continues even after surgery, but it can decrease the amount and number of drugs required in the symptom’s management. There are three surgery options namely, deep brain simulation, pallidotomy, and thalamotomy. Deep brain simulation employs electrical impulses to kindle the target portion of the brain. This treatment method can be combined with other drugs in case the symptoms surpass the drugs. Deep brain simulation is commonly used to treat advanced stages of the disorder because it does not damage brain tissues and is linked to fewer risks. Pallidotomy entails the specific destruction of a brain component, globus pallidus that generates symptoms whereas thalamotomy entails the destruction of a particular brain constituent, thalamus, which causes symptoms (Zhou, Huang, & Przedborski, 2008).

Future treatment of Parkinson’s disease

Various researches are concerned with attempts to substitute dopamine with drugs that imitate its role and actions or preventing the breakdown of uninfected nerve cells is being conducted. Some anticipated future treatments include gene therapy, cytoplasmic hybrid cells, and stem cells.

Gene therapy

Gene therapy method of treatment involves the usage of genes as drugs. It functions by providing normal genes to people affected by Parkinson’s disease to overcome the symptoms or cure (Lindvall & Kokaia, 2010). This method is most probably employable to people in early stages of the disease that have active nerve cells and available medications have no control over symptoms. Parkinson’s disease is rarely inherited and to affirm this certain researches have shown that there are few genetic mutations of genes in some affected families. This provides some relaxed association to Parkinson’s disease. This genetic vulnerability and other causalities increase the chances of the condition. Notably, gene therapy is not restricted to providing potential treatment to diseases caused by genetic factors.

The long-term usage if levodopa and dopamine agonists enable exposure of the drugs’ side effects and this explains why extensive research on gene therapy is being conducted. Gene therapy offers two essential products in the treatment of Parkinson’s namely neurotrophic factors and proteins that raise dopamine levels. Neurotrophic factors comprise of GDNF, glial cell derived neurotrophic factor. GDNF is a potent upholder of growth and survival these cells. Straight administration of molecules has been tried with victims of the disorder. These trials revealed that it is relatively hard to hold up high amounts of the factors in there targeted area. Protein factor is an option for levodopa or dopamine agonist administration since it raises the ability of nerve cells to generate their own dopamine. Various viruses such as adenovirus have been employed to deliver the therapeutic genetic substances to the targeted brain area of the affected people (Yokoyama, Kuroiwa, Yano, & Araki, 2008). The method is still under research.

Stem cell research

Another research focused on the treatment of Parkinson’s disease is the stem cell research. This research aims at critical analysis of how organisms develop from a particular cell and how healthy cells can substitute destroyed cells. Stem cell researchers are investigating how the destroyed dopamine-generating cells can be replaced with other uninfected dopamine-generating cells drawn from stem cells (Lindvall & Kokaia, 2010). The research is moving forward at a steady pace and its applicability is assumed to start after approximately 5 to 10 years.

Stem cells have the capability to divide and generate more duplicate of themselves and develop into wide range of cells such as skin, blood, brain and bone cells through differentiation. The capabilities of the cells to restore itself and its adaptability have provided a potential avenue that can be employed to revamp brain cells. They are obtained from aborted fetuses, blood cells from umbilical cords, bone marrow, and adult brain. Embryonic Stem (ES) cells are derived from embryos and have a supplementary ability to transform to all human body cell without choosing. Stem cell mode of treatment was developed due to noteworthy side effects of drugs and surgery could not offer any cure (Lindvall & Kokaia, 2010).  However, the major drawback that is being encountered in the stem cell research is the difficulty to find out how stem cells remain in the state of being unspecialized.

Cytoplasmic hybrid

Cytoplasmic hybrid cells provide a new-fangled avenue for scientists to acquire stem cells for a potential research that may set in motion new forms of treating Parkinson’s disease. Hybrid cells comprise of two elements of varied species. Cytoplasmic cells are generated when DNA material of a cell are introduced to another cell of a different species. DNA is injected into the cell cytoplasm. Experiments that involve the transfer of human genetic material into the cells of other species are underway. As a result, hybrid cells might be regarded to be significantly human in nature. Cytoplasmic hybrid cells explain the functioning of stem cells, but cannot be applied as Parkinson’s disease treatment (Miller, James-Kracke, Sun, & Sun, 2009).

In conclusion, Parkinson’s disease is caused when dopamine-producing cells are destroyed due to toxicity and other factors. The disorder causes immobility due to stiffness and tremor. Parkinson’s treatment aims at alleviating the symptoms since there is no permanent cure for the disorder. The available methods of treatment aim at stimulating the dopamine-generating system to produce dopamine or offer dopamine substitution. Current treatment methods available include the medication, surgery and home treatments. Future treatment prospects include the application of stem cells, cytoplasmic hybrid cells, and genetic therapy.

 

References

Archibald, N., & Burn, D. (2008). Parkinson’s disease. Medicine , 630.

Cicchetti, F., Drouin-Ouelle, J., & Gross, R. (2009). Environmenmental toxins and parkinson’s      disorder:what we have learnt from pesticide-induced animal models. Trends in           pharmarcological sciences , 14-15.

Jackson-Lewis, V., & Smeyne, R. (2005). MPTP model of Parkinson’s Disease. Memphis: John    Wiley & Sons.

Lindvall, O., & Kokaia, Z. (2010). Stem cells in human neurodegenerative disorders — time for   clinical translation? Journal of clinical investigation , 120.

Miller, R., James-Kracke, M., Sun, G., & Sun, A. (2009). Oxidative and inflammatory pathways  in Parkinson’s disease. Mendeley , 55-65.

Yokoyama, H., Kuroiwa, H., Yano, R., & Araki, T. (2008). Targeting reactive oxygen species,      reactive nitrogen species and inflammation in MPTP neurotoxicity and Parkinson’s    disease. Mendeley , 293-301.

Zhou, C., Huang, Y., & Przedborski, S. (2008). Mitochondria and Oxidative Stress in       Neurodegenerative Disorders . Annals of the New York Academy of Sciences , 93-104.

 

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