Free «Parkinson's Disease» Essay

Parkinson's Disease

Parkinson’s disease (PD) is a disorder which affects the central nervous system. Hesitation, trembling, bradykinesia, rigidity of the muscles are some of the most conspicuous signs of the illness. This pathology is caused by the dying or impairing of nerve cells in the substantia nigra (SN). The latter is a region of the basal ganglia which is responsible for producing the brain’s dopamine (DA). This chemical is a monoamine neurotransmitter that regulates brain processes directed to control the emotional response and movement of the body. One of dopamine’s functions is to send information to the areas in the brain responsible for the activation or inhibition of the movement process. In other words, dopamine acts as a greasing substance in the chemical chains and, thereby, helps stimulate an excitatory loop and suppress the inhibitory one (Smith 2012). Dopamine’s level decreases after the death of dopaminergic cells and, as follows, this process impedes the passing of the messages to their destination. Hence, the symptoms of Parkinson’s disease appear in the patient’s body.

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Based on the foregoing, it becomes evident that dopamine substitution or regulation is necessary for maintaining the mental and physical health of susceptible patients. Levodopa (L-DOPA), a compound that can be converted into dopamine in the brain, is still the best standard therapy for Parkinson’s disease. The conversion occurs under the action of dopa decarboxylase. Its inhibitors, such as benserazide and carbidopa, can delay L-DOPA’s metabolism before the chemical reaches the dopaminergic neurons. As a result, the side effects of the drug can be reduced, but L-DOPA still causes fluctuations and dyskesias in the patient’s motor system. That is the reason why scientists use alternatives in PD therapy, focusing on dopamine regulating elements. There are several factors that influence the regulation of dopamine. One of the contributing entities is the dopamine transporter (DAT), which regulates the consumption of dopamine neurons. DAT activity controls the level of dopamine receptor stimulation. The drugs that are purposed to fulfil this action are called dopamine agonists.

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A dopamine agonist contains a molecule that binds to and activates dopamine receptors similarly to dopamine itself (Life Extension 2014). In contrast to L-DOPA, metabolites of receptor agonists provide a longer term of stimulation and act without producing free radicals, which are toxic to DA neurons. Dopamine agonists comprise such chemicals as pergolide, pramipexole, ropinirole, bromocriptine, piribedil, apomorphine, cabergoline, and lisuride (Goldenberg 2008). Another component which is considered to affect dopamine levels is monoamine oxidise (MAO) enzyme B. MAO-B inhibitors act as compounds which diminish the breakdown of free dopamine and thereby raise the amount of dopamine available to neurons (Sommer & Stacy 2014). Selegiline, for example, blocks the breakdown of DA and leads to the mend of patient’s early Parkinson’s disease. Rasagiline, medication based on selegiline, slows down the PD progression. MAO-B inhibitors demonstrate efficacy while working alone or in combination with L-DOPA. Catechol-O-methyltransferase (COMT) inhibitor is another drug responsible for catabolism of levodopa and dopamine. It works only in combination with levodopa. This chemical allows a greater amount of the specified element to achieve the brain and, thus, to increase the degree of dopamine there. Tolcapone and entacapone are COMT agents which are presently marketed in the USA. Before levodopa application, antagonists of muscarinic acetylcholine receptors were widely used to treat PD (Goldenberg 2008). These anticholinergic agents are destined to restore the balance between dopamine and acetylcholine by lowering the level of the latter. The medications of this subgroup allow people with PD to experience reduction in tremor and muscle stiffness. Comparatively, amantadine, an antiviral agent known for its suppressing activity to side effects of L-DOPA, has the same effect. Recent investigations discovered amantadine as a N-Methyl-D-aspartate receptor antagonist (Sommer & Stacy 2014).

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The drugs which turn down dopamine activity through blocking but not stimulating dopamine receptors are identified as dopamine antagonists. This method can help treat conditions caused by drug abuse. Under the action of these medications, the dopamine receptors will be blocked and the reuptake of dopamine will be inhibited. Medical practitioners prescribe them in the form of atypical antipsychotics, antiemetics, and antidepressants. Current researches explore the roles of alpha2-adrenergic receptor antagonists in confronting dyskinesia caused by L-DOPA. In addition, candidates of adenosine A2 receptor antagonists are presently under investigation as well. It is believed that adenosine has a significant influence on the basal ganglia’s activity which, in its turn, is responsible for generating the symptoms of PD. Besides the explorations in dopamine antagonist perspectives, future therapies will focus on gene therapy, transplantation of dopaminergic embryonic tissue, and neuroprotective treatments.

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