This review discusses the role of oxidative stress (OS) and inflammation in neurodegenerative diseases (NDDs), with a focus on Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS). OS is defined as an imbalance between oxidants and antioxidants, often due to elevated levels of reactive oxygen species (ROS) or deficient antioxidant defenses. In the brain, high oxygen consumption and the presence of easily oxidizable polyunsaturated fatty acids make it particularly vulnerable to oxidative injury. The review highlights the interconnection between OS and inflammation, where ROS can promote pro-inflammatory gene expression, and inflammation can stimulate ROS production. In AD, OS induced by toxic beta-amyloid (Aβ) peptides leads to lipid, protein, and DNA oxidation, contributing to neuroinflammation and neuronal death. PD is characterized by the loss of dopaminergic neurons, with OS and ROS overproduction playing significant roles in their degeneration. HD is an inherited NDD caused by mutant huntingtin protein, leading to OS and inflammation. ALS affects motor neurons, with OS and inflammation contributing to neuronal damage and cell death. The review also discusses therapeutic approaches targeting OS and inflammation in ALS, including the use of antioxidants, anti-inflammatory compounds, and mitochondrial-targeted antioxidants. While some drugs like Edaravone and Riluzole have shown promise, their efficacy is limited. Clinical trials of compounds like NP001 and Fingolimod have shown some positive results, but more research is needed to fully understand the complex mechanisms of ALS and to develop effective treatments.This review discusses the role of oxidative stress (OS) and inflammation in neurodegenerative diseases (NDDs), with a focus on Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS). OS is defined as an imbalance between oxidants and antioxidants, often due to elevated levels of reactive oxygen species (ROS) or deficient antioxidant defenses. In the brain, high oxygen consumption and the presence of easily oxidizable polyunsaturated fatty acids make it particularly vulnerable to oxidative injury. The review highlights the interconnection between OS and inflammation, where ROS can promote pro-inflammatory gene expression, and inflammation can stimulate ROS production. In AD, OS induced by toxic beta-amyloid (Aβ) peptides leads to lipid, protein, and DNA oxidation, contributing to neuroinflammation and neuronal death. PD is characterized by the loss of dopaminergic neurons, with OS and ROS overproduction playing significant roles in their degeneration. HD is an inherited NDD caused by mutant huntingtin protein, leading to OS and inflammation. ALS affects motor neurons, with OS and inflammation contributing to neuronal damage and cell death. The review also discusses therapeutic approaches targeting OS and inflammation in ALS, including the use of antioxidants, anti-inflammatory compounds, and mitochondrial-targeted antioxidants. While some drugs like Edaravone and Riluzole have shown promise, their efficacy is limited. Clinical trials of compounds like NP001 and Fingolimod have shown some positive results, but more research is needed to fully understand the complex mechanisms of ALS and to develop effective treatments.