Parkinson's disease (PD) is a severe brain disease known for their deterioration of nerve cells . The deterioration of the nerve cells results in a decrease in the dopamine level in the patient's brain, causing issues with basic motor functions.(2) Symptoms commonly observed in this disease are tremors, slow body movements, instability in body posture, rigidity, cognitive impairment, disturbance in sleep, and mood. The major contributors to the disease are genetic, environmental factors, and exposure to harmful toxins; however, the exact cause of PD is unknown.(4) Currently, the disease does not have any treatment, only supportive care based on managing the symptoms and enhancing the quality of life of the patient. Current treatment approaches for Parkinson's disease revolve around intricately combining multiple relief efforts such as medication and physical therapy. Medications that target neurochemical imbalances are commonly used.( ) An example of these medications would be Levodopa, a drug that replenishes dopamine levels in the brain, alleviating the motor symptoms caused by PD.(6) Some prescribed medications that are used to complement Levodopa or be used individually are MAO-B inhibitors, COMT inhibitors, and dopamine agonists. Anticholinergic drugs may be utilized to manage tremors. In addition to pharmacotherapy, advanced interventions like deep brain stimulation can be employed to provide relief to a patient.( ) Deep brain stimulation implants electrodes into specific brain regions, in this position it can modulate neural activity and alleviate motor symptoms.( ) Lifestyle modifications have also proved to be effective in aiding symptoms. Regular exercise and physical therapy help maintain mobility. Furthermore, ongoing research aims to find novel therapeutic avenues for PD patients. Gene therapy and targeting drug delivery systems are continuing to be studied to refine treatment strategies and better the quality of life for many Parkinson's patients. The precise function of alpha-synuclein is not fully understood but its aggregation into insoluble fibrils is a recurrence among diseases like Alzheimer's disease and PD studies on the three-dimensional structure of alpha-synuclein have been extensively used. However, the disordered nature of the protein has made this effort quite a task, hindering results in finding a high-resolution structure. Nevertheless, researchers have proposed several models that assisted in gaining insight to the conformational dynamics of this protein. The flexibility of alpha-synuclein is said to be the cause for it is pathogenic properties, as well as its diverse functions.(15) Alphasynuclein is said to form an ensemble of structures with regions capable of forming coils, helices, and beta-sheets. Understanding the precise makeup of the alpha-synuclein and its interactions is crucial for the development of targeted therapies that can combat the neurodegenerative diseases it causes. Alpha-synuclein is a protein present in neurons and is suggested to play a role in their communication. In Parkinson's disease, this protein accumulates in abnormally high concentrations. Then these proteins clump together and form large aggregations called as Lewy Bodies. The detailed mechanism of these Lewy body formation is shown in Figure .