Recent investigations suggest that gut microbiota affects the brain activity through the microbiota-gut-brain axis under both physiological and pathological disease conditions like Parkinson’s disease. Further dopamine synthesis in the brain is induced by dopamine producing enzymes that are controlled by gut microbiota via the microbiota-gut-brain axis. Also alpha synuclein deposition and the associated neurodegeneration in the enteric nervous system that increase intestinal permeability, oxidative stress, and local inflammation, accounts for constipation in Parkinson’s disease patients. The trigger that causes blood brain barrier leakage, immune cell activation and inflammation, and ultimately neuroinflammation in the central nervous system is believed to be due to the chronic low-grade inflammation in the gut. The non-motor symptoms that appear years before motor symptoms could be reliable early biomarkers, if they could be correlated with the established and reliable neuroimaging techniques or behavioral indices. The future directions should therefore, focus on the exploration of newer investigational techniques to identify these reliable early biomarkers and define the specific gut microbes that contribute to the development of Parkinson’s disease. This ultimately should pave the way to safer and novel therapeutic approaches that avoid the complications of the drugs delivered today to the brain of Parkinson’s disease patients.
Parkinson's Disease (PD) is a neurodegenerative disorder in the nigrostriatal pathway of animals and humans and is responsible for most of the movement disorders, including rigidity. The present study aimed to determine the effect of chronic cigarette smoke, alcohol intake, and frequent sexual mating on 1-Methyl-4-phenyl-1,2,3,6-tertahydro pyridine (MPTP)-induced rat model of PD. After treatment, the effect of these factors was determined by biochemical and molecular evaluation. Dopamine (DA) concentration, antioxidant enzymes, and mitochondrial activity decreased after treatment with cigarette smoke, alcohol, and frequent sexual mating when compared to the values in the control group. Excessive exposure of these factors may lead to neurodegeneration, dopaminergic toxicities, and, ultimately, clinical parkinsonism. Earlier literature from different publisher suggested that nicotine and cigarette smoke can protect the dopaminergic neurons in the substantia nigra against MPTP toxicity. In this study, we assessed the effect of the above three factors on an MPTP-treated rat model and concluded that they have a neurodegenerative effect and were found to be toxic to dopaminergic neurons in the substantia nigra. Further investigation is required to understand the exact etiology of clinical parkinsonism.
Abstract::
Sirtuins are NAD+ dependent enzymes that have a predominant role in neurodegenerative disorders and also regulate the inflammatory process, protein aggregation, etc. The relation between Sirtuins with that of the nervous system and neurodegeneration are widely studied consequently. Sirtuins have a strong role in metabolic syndrome in mitochondria also. The activities of Sirtuins can be altered by using small molecules that would be developed into drugs and it is proven that manipulation of SIRT1 activity influences neurodegenerative disease models. They are especially thrilling since using small molecules, which would be developed into a drug, it is feasible to alter the activities of sirtuins. Different functions of Sirtuins are depended upon their subcellular localization. In this review paper, we are discussing different Sirtuins, differential expression of sirtuins, and expression of sirtuin in the brain and briefly about sirtuin3 (SIRT3).
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