Longterm followup studies from near onset will be needed to establish this relationship.In the meantime, denitive clinical trials should continue to measure an appropriate disability endpoint.The peripheral benzodiazepine binding site in the brain in multiple sclerosis.Brain and reasch YK11 spinal cord abnormalities in multiple sclerosis.Primary progressive multiple sclerosis: a year clinical and MR study.Effect of natalizumab on conversion of gadolinium enhancing lesions to T hypointense lesions in relapsing multiple sclerosis.Signal intensity on MRI of basal ganglia in multiple sclerosis.NeuroRx, Vol, No, The excess of oxidants causes a reduction of antioxidants, which in turn produce an oxidationreduction imbalance in organisms.Paucity of the antioxidant system generates oxidativestress, characterized by elevated levels of reactive species. Mitochondria play a key role in ATP supply to cells via oxidative phosphorylation, as well as synthesis of essential biological molecules.Various redox reactions catalyzed by enzymes take place in the oxidative phosphorylation process.An inecient oxidative phosphorylation may generate reactive oxygen species, leading to mitochondrial dysfunction.Mitochondrial redox metabolism, phospholipid metabolism, and proteolytic pathways are found to be the major and potential source of free radicals.A lower concentration of ROS is essential for normal cellular signaling, whereas the higher concentration and longtime exposure of ROS cause damage to cellular macromolecules such as DNA, lipids and proteins, ultimately resulting in necrosis and apoptotic cell death.Normal and proper functioning of the central nervous system is entirely dependent on the chemical integrity of brain.It is well established that the brain consumes a large amount of oxygen and is highly rich in lipid content, becoming prone to oxidative stress.A high consumption of oxygen leads to excessive production of ROS.Apart from this, the neuronal membranes are found to be rich in polyunsaturated fatty acids, which are highly susceptible to ROS.There is a need to understand the processes and role of oxidative stress in neurodegenerative diseases.This review is an eort towards improving our understanding of the pivotal role played by OS in neurodegenerative disorders.Although oxygen is crucial for life and is involved in signal transduction, gene transcription, and other cellular activities, coincidently, it also has a deleterious eect on biomolecules in the form of free radical and reactive oxygen species. The adverse eect of oxygen is the result of its univalent metabolic reduction status, which is responsible for the generation of ROS.The other most important species is nitric oxide, which carries out the regulatory function of relaxation and proliferation of vascular smooth muscle cells, leukocytes adhesion, angiogenesis, platelets aggregation, thrombosis, vascular tone, and haemodynamics, among others. Nitric monoxide in its free form is harmful for biomolecules.There are various chemical species comprising of free radicals, containing oxygen such as the hydroxyl radical. In the present scenario, ROS stands for both oxygen radicals as well as nonradicals that are conveniently converted into radicals. Halliwell had established that a free radical is a species having one or more unpaired electrons and existing independently on its own. Free radicals are supposed to play a substantial role in various biochemical reactions, as well as in biological evolution.Oxygen is the most important and vital entity for all living organisms including neuronal cells involved in tissue formation, whereas when present in excess, it has deleterious eects.