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Modulation and mechanism for the neuroprotective effects of 17-beta-estradiol: Relevance to depressive symptoms in Parkinson’s disease

P. Kumar, N. Baquer (New Delhi, India)

Meeting: 2016 International Congress

Abstract Number: 378

Keywords: Aging, Estrogen, Oxidative stress, Parkinsonism

Session Information

Date: Monday, June 20, 2016

Session Title: Parkinson's disease: Non-motor symptoms

Session Time: 12:30pm-2:00pm

Location: Exhibit Hall located in Hall B, Level 2

Objective: The objective of this study was to investigate neuroprotective potential of 17β estradiol (E2) treatment on the activities of acetylcholinesterase and monoamine oxidase, membrane fluidity, neurolipofuscin, glucose transporter-3 (GLUT3) expression and testing learning memory, occurring in brains of female rats of 3 months (young), 12 months (adult) and 24 months (old) age groups, and to see whether these changes are restored to normal levels after exogenous administration of 17β estradiol (E2).

Background: Parkinson’s disease (PD) is a neurodegenerative disease and a movement disorder characterized by loss of dopaminergic neurons in the substantia nigra causing dopamine depletion in the striatum. Recently, there has been a growing interest in the action and functions of the ovarian steroid hormone estradiol, particularly on whether they are neuroprotective for such age related disease and neurodegenerative conditions like stroke, PD and Alzheimer’s disease.

Methods: The aged rats (12 and 24 months old) (n= 8 for each group) were given subcutaneous injection of 17b-estradiol (0.1 µg/g body weight) daily for one month. After 30 days of hormone treatment, experimental animals of all the groups were sacrificed and brains were isolated for further study.Learning was tested in a Morris water maze with expression of synaptic molecules synaptophysin and synapsin I and ultrastructural studies of brain region by magnetic resonance imaging.

Results: The results obtained in the present work revealed that normal aging was associated with significant increases in the activity of monoamine oxidase and neurolipofuscin accumulation in aging rats, and a decrease in acetylcholinesterase activity, membrane polarization and GLUT3 expression. E2 treatments improved attention and memory functions of the aging rats with enhanced the levels of synaptic molecules synaptophysin and synapsin I. Ultrastructural studies revealed that the changes were more pronounced in the aged treated rats in terms of presence of lipofuscin and lysosomal degradation. Our data showed that exogenous administration of E2 brought these changes to near normalcy in aging female rats.

Conclusions: Based on our studies and others, we conclude that E2 have therapeutic potential for adjunctive therapy along with dopamine replacement in PD.

To cite this abstract in AMA style:

P. Kumar, N. Baquer. Modulation and mechanism for the neuroprotective effects of 17-beta-estradiol: Relevance to depressive symptoms in Parkinson’s disease [abstract]. Mov Disord. 2016; 31 (suppl 2). https://www.mdsabstracts.org/abstract/modulation-and-mechanism-for-the-neuroprotective-effects-of-17-beta-estradiol-relevance-to-depressive-symptoms-in-parkinsons-disease/. Accessed June 14, 2025.
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