Investigation of Phytochemical and Antidepressants Activity of Cinnamon Powder Extract

Abstract

Neurodegenerative disease is the most common type of mobility issue, but unfortunately, there is now no medication that can alter the course of the disease. We don't know what causes this ailment. In mouse models of Parkinson's disease induced with 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine, the oral administration of cinnamon powder and sodium benzoate may prevent the death of dopaminergic cells, dysregulation of striatal neurotransmitters, and motor impairments. The mechanisms driving its function include controlling autophagy, antioxidant effects, Parkin, DJ-1, and glial cell line-derived neurotrophic factor activation, TLR/NF-κB pathway modulation, and excessive proinflammatory response prevention. Moreover, research carried out in both laboratory and living organism settings has shown that cinnamon extracts may impact the oligomerisation and aggregation of α-synuclein. This article's goal is to discuss recent findings about this phytochemical's potential as a novel treatment for Parkinson's disease (PD). We highlight additional areas of mechanism that require investigation and possible constraints that must be overcome before this phytochemical may be used in PD trials. Neurodegenerative disease is the most common type of mobility impairment, and unfortunately, there is now no medication that can alter this disease. We don't know what causes this ailment. There has been a recent uptick in interest in medicinal plant use because of the novelty, safety, and relative affordability of this field. The characteristic flavour and aroma of cinnamon, a spice that is often used, may have neuroprotective effects on people with Parkinson's disease (PD) and other neurodegenerative diseases. The essential oils of Cinnamomum species, such as cinnamaldehyde and sodium benzoate, have shown in vitro that they can protect cells from oxidative stress, ROS generation, and autophagy dysregulation. Consequently, these oils may exert a neuroprotective effect. The in vivo evidence suggests that cinnamon powder and sodium benzoate, when administered orally to Parkinson's disease models in mice, may prevent the death of dopaminergic cells, dysregulation of striatal neurotransmitters, and motor deficits. In this essay, we will go over the latest research on this phytochemical and its potential as a novel treatment for Parkinson's disease (PD). Incorporating this phytochemical into experimental PD treatments requires further investigation into additional molecular aspects and the potential overcoming of constraints and obstacles.