Itt írjon a(z) ParkinsonTreatment-ról/ről

Treatment of Parkinson’s disease

What is Parkinson’s disease?

Parkinson’s disease is a condition that affects dopaminergic neurotransmission. Dopamine is essential for controlling movement, cognition, and emotion in the Central Nervous System. Parkinson’s Disease damages dopamine neurotransmission, leading to impaired movement in the form of rest tremor, rigidity, and slowness of movement (bradykinesia) (W.M.M. Schuepbach et al, 2013). The condition can also cause non-motor symptoms, including cognitive impairment, dementia, psychosis, apathy, tiredness, sleep disorders, and disturbances of mood (Goldman, J., Holden, S., 2014)

What causes it?

Parkinson’s disease is caused by the progressive loss of dopaminergic neurons or the disturbance of dopamine signalling (Lu et al, 2017).

Treatment

Unfortunately there is currently no real cure for Parkinson’s disease. Current treatment for Parkinson’s disease involves managing the symptoms of the condition as it progresses (J Clin Invest. 2013). The main goal is to give patients the highest quality of life possible by slowing down the advance of disease and treating and minimising the symptoms.

Pharmaceutical treatments

Levodopa (also known as L-DOPA) is an amino acid that is the precursor of many important neurotransmitters, such as dopamine, epinephrine, and norepinephrine (together they are known as catecholamines). It also mediates the release of neurotrophic factors from the Central Nervous System. Levodopa can be synthetically produced as a purified psychoactive drug, and has been used for many years in treating Parkinson’s disease. By taking Levodopa medication, the patient can make up for the lost dopaminergic neurons, thus allowing for more normal dopamine signalling (Brichta et al; 2013).

A study carried out between 2000 and 2009 showed that levodopa provides small but continuing benefits, as compared to levodopa-sparing therapy (the latter is a treatment in which the use of levodopa is avoided or limited for as long as is practically possible). It is thought that levodopa provides better short-term control of the motor symptoms in patients with newly diagnosed Parkinson’s disease. It also seems to cause fewer side-effects than dopamine agonists or MonoAmine Oxidase Type B Inhibitors (MAOBI) (UK PD MED Collaborative Group, 2014)

Unfortunately, according to Lu et al (2017), chronic use of Levodopa leads to L-DOPA-Induced Dyskinesia (LID) (involuntary muscle movements such as twitching or tics); however, if one stops taking Levodopa, dyskinesia may also evolve (Mizuno et al, 2016). Lu et al (2017) mention that the negative effects of Levodopa can be reduced if the drug is used in combination with Dopa agonists or if dopa agonists are used in monotherapy.

MonoAmine Oxidase Type B Inhibitors (MAOBI) have been used in levodopa sparing therapy. They were found to be a treat that is at least as effective as dopa agonists (UK PD MED Collaborative Group, 2014) There has also been research in using Exanatide, often given to patients with Type 2 Diabetes, to treat Parkinson’s disease. Exenatide has been shown to have some neuroprotective and neurorestorative properties, and it might be a more cost effective treatment. In a recent study, patients with moderate Parkinson’s disease were given subcutaneous injections of Exenatide for about 12 months. The results of the study showed that the drug was well-tolerated by these patients, although weight loss was common. The results seem promising, but further research is needed (Aviles-Olmos, I. et al; 2017).

Mitochondria-targeted Antioxidants

It has been suggested that mitochondrial dysfunction and oxidative stress have an important role in the dopaminergic neurodegeneration of Parkinson's disease. Thus, therapies that target and improve their function mitochondria could help to prevent or treat Parkinson’s disease. A class of compounds called Mitochondria-targeted antioxidifants has been developed. They are created by conjugating lipophilic triphenylphosphonium cation to an antioxidant moiety. Studies seem promising, but further research is needed, as the pharmacological effects on these drugs are not entirely known (Huajun et al, 2013).