Session Information
Date: Monday, October 8, 2018
Session Title: Parkinson's Disease: Non-Motor Symptoms
Session Time: 1:15pm-2:45pm
Location: Hall 3FG
Objective: To investigate melatonin therapeutic potential effects in Parkinson’s disease.
Background: Sleep disorders constitute major nonmotor features of Parkinson’s disease (PD) that have a substantial effect on patients’ quality of life and can be related to the progression of the neurodegenerative disease[1]. the etiology of sleep disorders in PD remains undefined, so, the assessment of the components of the circadian system, including melatonin, could give therapeutically valuable insight[2]. Our work focus on melatonin as a regulator of the sleep/wake cycle and also as an effective antioxidant and mitochondrial function protector. We investigate melatonin therapeutic potential effects in PD. The answer to this question impact deeply on sleep disorders treatment and also neuroprotection in PD.
Methods: In this study, we administered melatonin as an antioxidant factor and neuroprotective agent to prevent neural death. A Parkinson’s disease model was induced in rats by subcutaneous injection of rotenone at the back of their necks. Melatonin was administered for 7 days, the count and the volume of the LC neurons examined due to stereology methods. The enzymatic test for GSH measurement of Caspase-3, C-Fos was done to assess the antioxidant property and apoptosis process and neural activity respectively. Immunohistochemistry of Anti-TH factors was done to assess the noradrenergic neurons and the Iba-1 test was also done to show the microglial migration.
Results: Melatonin leads to a reduction in the level of apoptotic factor Caspase-3 expression followed by PD. According to stereology analysis, the count of adrenergic neurons and the volume of the nucleus reduces in the administered-melatonin group. The apoptotic protein Caspase-3 reduces to prevent neural death. Microglial migration to the LC occurs after neural death and the melatonin increases GSH levels in this group.
Conclusions: Melatonin with neuroprotective property can be used to treatment of adrenergic-depended sleep disorders and prevention of neural apoptosis.
References: 1.Videnovic A, Noble C, Reid KJ, Peng J, Turek FW, Marconi A, Rademaker AW, Simuni T, Zadikoff C, Zee PC. Circadian melatonin rhythm and excessive daytime sleepiness in Parkinson disease. JAMA neurology. 2014 Apr 1;71(4):463-9. 2.Fertl E, Auff E, Doppelbauer A, Waldhauser F. Circadian secretion pattern of melatonin in Parkinson’s disease. Journal of Neural Transmission-Parkinson’s Disease and Dementia Section. 1991 Mar 1;3(1):41-7.
To cite this abstract in AMA style:
F. Yadolahi, M. Mehrpour. Neuroprotective effect of exogenous melatonin on apoptosis of neuroadernergic neurons in a rat model of Parkinson’s disease [abstract]. Mov Disord. 2018; 33 (suppl 2). https://www.mdsabstracts.org/abstract/neuroprotective-effect-of-exogenous-melatonin-on-apoptosis-of-neuroadernergic-neurons-in-a-rat-model-of-parkinsons-disease/. Accessed September 7, 2024.« Back to 2018 International Congress
MDS Abstracts - https://www.mdsabstracts.org/abstract/neuroprotective-effect-of-exogenous-melatonin-on-apoptosis-of-neuroadernergic-neurons-in-a-rat-model-of-parkinsons-disease/