Abstract

Parkinson disease (PD) is the second most common age-related neurodegenerative disease after Alzheimer disease, characterized by loss of dopaminergic neurons in substantia nigra pars compacta, accompanied by motor and non-motor symptoms. Idiopathic PD is the most common cause of Parkinsonism (primary Parkinsonism) while, certain medication and different groups of neurological disorder may be causes of secondary Parkinsonism. The presence of intraneuronal proteinaceous cytoplasmic inclusions “Lewy Bodies” and the loss of the nigrostriatal dopaminergic neurons are the main neuropathological hallmarks of PD. However, the etiology of the disease is still undefined; several studies assume that oxidative stress, mitochondrial defects, neuroinflammation, apoptosis and excitotoxicity play vital roles in the pathogenesis and progress of the disease. Experimental models of PD can be induced by several neurotoxins such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, 6-hydroxydopamine, rotenone and paraquat which produce neuropathological and neurochemical changes that are identical to those seen in PD. The primary drug for PD treatment is L-dopa; however, drug-induced dyskinesia and motor complications restricted its use as long term treatment. Dopamine agonists are alternative options for initial treatment of PD and have been reported to retard the onset of motor complications. Combination of L-dopa with other medications, such ascatechol-O-methyltransferase inhibitors and monoamine oxidase B inhibitors has the ability to alleviate L-dopa-induced motor complications. Anticholinergic drugs can be used to control the symptoms of PD but their cognitive and autonomic side effects make them unsuitable for the elderly.

Highlights

  • Parkinson's disease (PD) is considered as a multisystem neurodegenerative disease in which there is a gradual loss of dopaminergic neurons in the substantia nigra pars compacta (SNc), which is one of the basal ganglia nuclei, with resulting striatal dopamine (DA) deafferentation, leads to distinctive motor dysfunctions including, bradykinesia, resting tremor and muscular rigidity.[3,4]

  • In the absence of the Dopa decarboxylase inhibitors (DDC-I), L-dopa is extensively decarboxylated in the intestine and other peripheral sites and this decreases the concentration of the drug reaches the brain

  • This study proposed that neuroprotective mechanisms of bee venom are explained mainly by decreasing neuroinflammation and suppressing the proinflammatory cytokines, such as TNF-α, IL-1 and inducible nitric oxide synthase (iNOS) expression.[180]

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Summary

INTRODUCTION

Parkinson's disease (PD) is considered as a chronically progressive age-related neurodegenerative disease which affects 1% of the worldwide population over the age of 60 wherein, the percentage increases to 5 % in individuals after the age of 85 years.[1,2] PD is considered as a multisystem neurodegenerative disease in which there is a gradual loss of dopaminergic neurons in the substantia nigra pars compacta (SNc), which is one of the basal ganglia nuclei, with resulting striatal dopamine (DA) deafferentation, leads to distinctive motor dysfunctions including, bradykinesia, resting tremor and muscular rigidity.[3,4] These symptoms of motor disturbances are usually considered as clinical diagnostic criteria for PD.[5,6]. Other drugs such as dopamine depleting drugs (reserpine), anti-emetic (metoclopramide), calcium channel blockers (flunarizine, cinnarizine, diltiazem and verapamil), amiodarone, lithium and alpha-methyldopa are considered as DIP.[16,20]

Vascular Parkinsonism
Degeneration of nigrostriatal dopaminergic neurons
Intraneuronal proteinaceous cytoplasmic inclusions “LBs”
MAO-B Inhibitors
Findings
CONCLUSION
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