Apart from the brain, A accumulation is also observed in subcellular areas such as golgi apparatus and endoplasmic reticulum. It is well studied that deposition of betaamyloid plaque causes major damage, also to mitochondria.Thus, the connection among mitochondrial dysfunction, tau phosphorylation, and betaamyloid draws considerable attention towards innovative therapeutic interventions.Apart from ROS elevation in AD patients, an increase in RNS is also observed.It is depicted that RNS elevation with modications is found both in astrocytes as well as in neurons in an AD brain.Gradual modication in astrocyte is identied with an increase in the expression of neuronal isozymes.The direct association of iNOS and eNOS with A aggregates indicating towards beta amyloid assisted in the induction of nitric oxide synthases. NO is found to be involved in the promotion of vascular smooth muscle relaxation and thus leads to the proper regulation of blood ow.Elevation in NO is demonstrated as the main cause of generation of ONOO, which in turn damages the biomolecules. It is well documented that oxidative stress and ROSRNS play a considerable role in the manifestation of AD; however, use of antioxidants to control and prevent AD is still unsettled.The main reason behind this is that most of the antioxidants have permeability limitations, owing to which antioxidants are unable to cross the bloodbrain barrier.With the advent of nanotechnology, nanoparticles might prove an ecient vehicle for drug delivery into the CNS. Using multiple antioxidants, their correct dosage, netuned equilibrium in all antioxidants used along with measurements of biomarkers in Imiquimod patients can lead to positive results.As neurons regulate and control the voluntary movements of the body, their deterioration leads to impaired motor function, bradykinesia, postural instability, rigidity, and tremor at rest.Various exogenous sources such as overuse of herbicides, pesticides, exposure to organic chemicals, carbon monoxide, carbon disulphide, plant derived toxins, and bacterial as well as viral infections are supposed to play a substantial role in the manifestation of PD.The familial forms of PD exhibited various mutations in a number of genes.In order to understand the pathophysiology of PD, it is essential to unveil the mechanism by which mutation led to degeneration of nigralneuron. Several reports indicate that the involvement of ROS and oxidative stress might be one of the major factors causing PD. The exact pathway and mechanism of PD is still incredulous, but it is believed and demonstrated in many reports that in particular, the substantia nigra of PD patients are found to have elevated levels of oxidized lipids, proteins, and DNA, along with reduced levels of glutathione. It is also observed that inammatory markers such as tumor necrosis factor in microglia were suppressed and nonfunctional in PD patients. The presence of high levels of trace element aggravates cell damage occurring in substantia nigra owing to lipid peroxidation.Along with ferrous ion, other trace elements are also found to be involved in neurodegeneration. Apart from ROS, it is Pyridoxine evidenced that RNS also plays major role in nitrosative stress.NO obstructs various enzymes in addition to complex I and IV of the mitochondrial electron transport chain, resulting in elevated levels of ROS.