Interestingly, various proteins are also found to play a crucial role in familial forms of PD.PTEN induced putative kinase I, and synuclein are the proteins that Sertraline hydrochloride displayed their link with PD. DJ is found to play as a marker and sensor for oxidative stress, as well as a redoxchaperone protein. It is also evidenced that neurons with mutations in protein LRRK are more vulnerable to mitochondrial toxins. There are various factors involved in the progression of neurodegeneration leading to PD; however, the exact mechanism is still illusive.Although PD involves a cascade of events thatultimately play a substantial role in the aggravation of the disease, it is important to decipher the exact pathway via which this disease progression can be stopped.Various genetic as well as environmental factors are involved in PD, for example, mutation in various proteins is shown to be involved in mitochondrial perturbation as well as to enhance oxidative stress.Metal mediated toxicity also plays a crucial role in the elevation of ROS, enhancing oxidative stress in cellular environment and causing damage to neurons.The main challenge in PD pathology is the varied complexity of an individual case; therefore, a substantial case study will be required for better understanding of PD.Appropriate antioxidants should be identied as therapeutic candidates for the treatment.Like the AD, the main hurdle to be resolved in treatment of PD is the ineective drug delivery, restricted because of the bloodbrain barrier.Mitochondrial DNA deletions are identied in pigmented neurons present in substantia nigra of aged and PD brains.Additionally, the morphology and mitochondrial function concomitantly deteriorate with advancing age, leading to the accumulation of defective mitochondria.Recent advances in in vitro studies have opened new avenues to understand PD pathology and have illuminated novel insights to develop therapeutic candidates to target the Riboflavin reasons for PD.ALS is a fatal neurodegenerative disorder characterized by the progressive degeneration of upper and lower motor neurons in the spinal cord, cortex, and brainstem. It was found that approximately of familial ALS cases are the result of mutation in the gene responsible for encoding the superoxide dismutase, whereas of ALS cases are sporadic. Various reports indicated the involvement of several factors in ALS, such as excitotoxicity, mitochondrial dysfunctiondysregulation, endoplasmic reticulum stress, neuroinammation, and oxidative stress. However, the interlinking of these events in this complex disease is still a puzzle.OS mediated protein injury, lipid peroxidation, and DNA and RNA oxidation has been observed in ALS patients.Even OS biomarkers are profoundly found in SALS patients urine, cerebro spinal uid; blood; and individual tissues or in combination with one or more biomolecules such as elevation in malodialdehyde, and lipid peroxidation product. Various antioxidants were used to scavenge free radicals, research has shown that vitamin E in combination with PUFA reduced the risk of ALS development.Edavarone is also investigated as a free radical scavenger and it was demonstrated that it eciently removes lipid peroxide and hydroxyl radicals via transferring electron to the radical, leading to a protective eect on neurons.Edavarone is also shown to eliminate nitrosative stress in the CSF of ALS patients.