Parkinson Disease Case Study

Parkinson Disease (PD) is neurodegenerative disorder caused by the degeneration of the dopminergic neurons in the midbrain. The degeneration of the dopaminergic neurons results in the development of symptoms such as rigidity, tremor, bradykinesia, etc. The exact cause of degeneration of the dopaminergic neurons is not yet known. A large number of the drugs are used in treatment of PD, but all the drugs produce only symptomatic relief. No drug is currently available which can completely cure PD. Also out of the known therapeutic options for treatment of PD, there is no drug which can completely stop the process of the degeneration of dopaminergic neurons in midbrain. Thus there is need of potential drugs that may inhibit the process of degeneration

MAPK, PKC and PI3K pathways are basically involved in the growth and the differentiation of neuronal cells. As flavonoids and polyphenols are known for modulation of these pathways, so it can be emphasized that flavonoids/polyphenols may exert the beneficial effect in the treatment of PD. The aim of present review is to demonstrate the role of the flavonoids and polyphenols in the treatment of the PD and the mechanism by which they exert beneficial effect.

Key Words: Flavonoids; Parkinson’s disease, Basal ganglia; Dopamine; Substantia nigra

Introduction

Parkinson’s disease (PD) is a neurodegenerative disorder characterized by the progressive loss of the dopaminergic neurons in the substantia nigra pars compacta (SNc) region of the midbrain (Dauer and Przedborski, 2003) (Fig.1). The salient pathologic feature of idiopathic PD is relatively selective degeneration of dopaminergic neurons in

Projection neurons of the striatum are referred to as the medium spiny neurons (MSNs) that use gamma aminobutyric acid (GABA). There are two main types of MSNs in the striatum, one that co-contain substance P and GABA and projects primarily to GPi and SNr co-contain mRNA for the dopamine D1 receptors; and other that contains enkephalin and GABA and projects primarily to the GPe contains high mRNA expression levels for the D2 receptor subtype (Gerfen et al., 1990a; Gerfen et al., 1990b; Aubert et al., 2000). Striatal neurons discharge in response to firing of corticostriatal glutamatergic neurons, which leads to inhibition of BG output neurons and disinhibition (direct) or inhibition (indirect) of neurons in the targets of the BG. The output of the BG is thus a complex spatiotemporal pattern of increased and decreased firing, which leads to an inhibitory output signal under resting conditions that is reduced during BG associated behavior (Chevalier and Deniau,