Anti-Parkinsonian effects of Bacopa monnieri: insights from transgenic and pharmacological Caenorhabditis elegans models of Parkinson’s disease

Abstract

Neurodegenerative Parkinson’s Disease (PD) is associated with aggregation of protein alpha synuclein and selective death of dopaminergic neurons, thereby leading to cognitive and motor impairment in patients. The disease has no complete cure yet; the current therapeutic strategies involve prescription of dopamine agonist drugs which turn ineffective after prolonged use. The present study utilized the powerful genetics of model system Caenorhabditis elegans towards exploring the anti-parkinsonian effects of a neuro-protective botanical Bacopa monnieri. Two different strains of C. elegans; a transgenic model expressing “human” alpha synuclein [NL5901 (Punc-54::alphasynuclein::YFP+unc-119)], and a pharmacological model expressing green fluorescent protein (GFP) specifically in the dopaminergic neurons [BZ555 (Pdat-1::GFP)] treated with selective catecholaminergic neurotoxin 6-hydroxy dopamine (6-OHDA), were employed for the study. Bacopa monnieri was chosen for its known neuroprotective and cognition enhancing effects. The study examined the effect of the botanical, on aggregation of alpha synuclein, degeneration of dopaminergic neurons, content of lipids and longevity of the nematodes. Our studies show that Bacopa monnieri reduces alpha synuclein aggregation, prevents dopaminergic neurodegeneration and restores the lipid content in nematodes, thereby proving its potential as a possible anti-Parkinsonian agent. These findings encourage further investigations on the botanical, and its active constituent compounds, as possible therapeutic intervention against Parkinson’s disease.