1. Introduction
Brain inflammation may contribute to a wide variety of neurodegenerative pathologies. Major regulators of brain inflammation that may exert a direct effect on neurons are reactive oxygen species (ROSs). ROSs are emerging as important players in the etiology of neurodegenerative disorders [1]. Due to the reduced capacity of neuronal regeneration and high metabolic rate, the brain is believed to be profoundly liable to the damaging effects of ROS and the dopaminergic neurons in the substantia nigra of Parkinson' disease (PD) patients are undoubtedly susceptible. Different data sets suggest that oxidative stress is at the center of various neurodegenerative diseases. Postmortem brain tissues from patients with neurodegenerative diseases including Alzheimer's disease (AD), PD, Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS) clearly show increased levels of ROS in affected brain regions [2–4]. Though one cannot assume that only ROSs are the major cause of these disease states, it is necessary to question what is responsible for this increased ROS generation.
ROSs are a wide range of small signaling molecules which are highly reactive unpaired valence electrons. ROSs include superoxide (O2 −), hydrogen peroxide (H2O2), hydroxyl radical (OH•), and peroxynitrite (ONOO−) [5]. Although ROSs have some biological advantages, excessive generation may lead to threatened homeostasis of the biological system [6–9]. ROSs are constantly generated through a variety of pathways, including both enzyme-catalyzed reactions and nonenzyme reactions [10]. Whenever the balance between ROS generation and the natural antioxidant defense system is lost, a series of events may occur deregulating cellular functions which may lead to various pathological conditions for almost all vital organs [11]. ROS can react with vital cell components and alter intrinsic membrane properties like fluidity, ion transport, loss of enzyme activity, protein cross-linking, inhibition of protein synthesis, and DNA damage ultimately resulting in cell death [12]. 
A more direct effect on neurons is the ROS produced by the activation of the several inflammatory enzymes such as nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, the expression of the inducible nitric oxide synthase (iNOS), myeloperoxidase, lipoxygenase, and cyclooxygenase (COX). These enzymes contribute to the pathogenesis of various neurodegenerative diseases including PD. Earlier studies postulated that NADPH oxidase and iNOS are not expressed in normal CNS conditions, but in PD patients and in 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) intoxicated mice. Both are clearly expressed and activated in glial cells in the ventral midbrain. These two major inflammatory enzymes that produce ROS may have a pathogenic role in PD, because when they are lacking in mutant mice, they show less loss of dopaminergic neurons [13–15].
In this paper, we discuss recent inhibitors of ROS-generating inflammatory oxidative enzymes, in particular the NADPH oxidase and iNOS as a therapeutic strategy for the treatment of PD. We also summarize claims by recent patents for several agents as potential NADPH oxidase and iNOS inhibitors.