The pathogenesis of ALS is complex and involves a combination of genetic, environmental, and cellular factors. While the exact cause of ALS remains incompletely understood, several key mechanisms have been implicated in the degeneration of motor neurons characteristic of the disease. ALS primarily affects motor neurons, which are the nerve cells responsible for transmitting signals from the brain and spinal cord to the muscles, controlling voluntary muscle movement. The progressive degeneration and death of motor neurons lead to muscle weakness, atrophy, and eventual paralysis. Glutamate is the primary excitatory neurotransmitter in the CNS, including the motor neurons. In ALS, dysregulation of glutamate signaling occurs, leading to excessive levels of glutamate in the synaptic cleft. This excitotoxicity can damage motor neurons, contributing to their degeneration and death. Motor neurons are particularly vulnerable to oxidative stress, which occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the body's ability to neutralize them with antioxidants. Oxidative stress can damage cellular structures, including proteins, lipids, and DNA, leading to motor neuron dysfunction and death. Abnormal protein aggregation is a hallmark feature of ALS pathology.