Investigation of the Enhancement of Neuroprotective Efficacy of Water Soluble Ashwagandha Extract Alone and in Combination with Ubisol- Q10 for Parkinson’s Disease

Parkinson’s disease (PD) is the second most common chronic and progressive neurodegenerative disease and the most common movement disorder. PD is characterized by the progressive loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc), leading to symptoms such as tremors, bradykinesia, postural instability, and rigidity. Biochemical pathologies of PD include oxidative stress, autophagy and mitochondrial dysfunction, and neuroinflammation. Current treatments for PD provide only symptomatic relief and fail to halt progression of neurodegeneration. Prolonged treatment can result in adverse motor/behavioural side effects. Previous studies have shown that supplementary antioxidants such as coenzyme Q10 have neuroprotective abilities and can target mechanisms of oxidative stress and mitochondrial and autophagic dysfunction, however, it has limited bioavailability since it is lipophilic.A water-soluble formulation of CoQ10 (Ubisol-Q10) was created to increase bioavailability. Ubisol-Q10 was shown to protect cultured neurons from paraquat (PQ) (an environmental toxin known to cause PD) toxicity and DA neurons in PQ induced rodent models of PD. Ethanolic ashwagandha has also been shown to provide neuroprotective, anti-inflammatory, and even neuro-regenerative properties in PQ induced rodent models of PD. Similar to CoQ10, ashwagandha extract phytochemicals are lipophilic, resulting in poor bioavailability. The same technology used in Ubisol-Q10 was used to enhance solubility of ashwagandha extract. Previously, we investigated the efficacy of combined Ubisol-Q10 and ethanolic ashwagandha treatments and we have begun to test the enhanced efficacy of the combination of both water-soluble formulations. Both physiological and behavioral components of PD progression in response to treatment in rats will be studied in this project. We anticipate that this combinatorial treatment will halt the progression by reducing oxidative stress, stabilizing mitochondrial function and activating autophagy mechanisms