Owing to the high consumption of oxygen and enrichment in PUFA, the brain is the most vulnerable part of the body.ROS cause a damaging eect on neurons and accumulate in the brain, resulting in neurodegenerative diseases.Though metals are crucial for the enzyme mediated reactions in cellular metabolism and cell signaling, mutation in mitochondrial DNA and metal overload in the aged brain subsequently lead to oxidative stress.A cascade of events takes place that ultimately impair neuronal proteins, leading to neuroinammation and neurological disorders manifested in loss of cognitive function. Mitochondrial dysfunction also plays a substantial role in the imbalance in ROS and the antioxidant system in the cellular environment.In the present scenario, research is believed to focus on the development of antioxidants that can eciently scavenge free radicals and combat oxidative stress.The foremost impediment in ways of delivery of antioxidantdrugs is the bloodbrain barrier, posing selective permeability to a specic set of substances only.Several antioxidant therapeutic targets are developed that are capable of neuroprotection prior to OS, preventing free radical production as well as modulating normal metal homeostasis.Additionally, antioxidants are formulated to cure neuronal inammation as well as free radical scavenging. Interestingly, saron has been found to act as an antioxidant, playing a key role in the protection of CNS diseases.Low cytotoxicity, commercially availability, and ability to cross the bloodbrain barrier make it a suitable candidate to combat various diseases. To stop the degeneration of neurons in the brain, stemcell oriented therapy is the sole hope for regional reconstruction.Thus, severe nerve damage should be controlled via balancing the ROS generation and its scavenging by antioxidants.Although preclinical studies have shown promising results, the benet of antioxidant therapy for neurodegenerative diseases is still controversial in humans. Following the notion prevention is better than cure should help in delaying the neurodegeneration.Ageing and lifestyle are other major factors that play a key role in the onset of neurodegenerative diseases.However, changing ones lifestyle, developing ecient antioxidants, and early diagnosis may also assist in the treatment of neurodegenerative disorders.Ongoing research worldwide is opening new avenues and hope for future therapeutic targets to control these neurodegenerative diseases.This Fluocinolone acetonide article is an open access article distributed under the terms and conditions of the Creative Commons Attribution. These proteins lack any Dextrorphan tartrate signicant primary sequence homology, yet their aggregates possess very similar features, speci cally, high sheet content, brillar morphology, relative insolubility, and protease resistance.Besides structure, the aggregates may possess similar pathways of assembly.Two alternative assembly pathways have been proposed: the nucleationelongation and the templateassisted mode.These two modes may be complementary, not mutually exclusive.Strategies for interfering with aggregation, which may provide novel therapeutic approaches, are under development.The structural similarities between protein aggregates of dissimilar origin suggest that therapeutic strategies successful against one disease may have broad utility in others.Deposits of aggregated prion protein, some of which have the structural features of amyloid, are observed in brain tissues from humans and animals with these related diseases.Huntingtons disease is causally linked to an expanded polyglutamine repeat domain. No proteolysis or covalent modication appears to be required to initiate aggregation.