Excitotoxicity

Excitotoxicity is a form of cell death caused by an overload of neuronal stimulation, resulting from excessive release of excitatory neurotransmitters such as glutamate and aspartate. These neurotransmitters play an essential role in normal neuronal function, but when these compounds are released in excessive amounts, they cause a continuous influx of calcium ions into the neuron, resulting in nerve cell damage and death. This process is seen in a variety of neurological diseases, including stroke, epilepsy, traumatic brain injury, and amyotrophic lateral sclerosis (ALS). Excitotoxicity is believed to be a major contributing factor to neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease. These diseases are often linked to the progressive depletion of neurons, which is associated with the excitotoxic damage caused by a malfunctioning glutaminergic system. The onset of these conditions can typically be traced to a decrease in glutaminergic neurons, which normally produce the neurotransmitter glutamate. This leads to an enhanced stimulation of NMDA (N-methyl-D-aspartate) receptors, causing a sustained influx of calcium ions that eventually leads to a toxic build-up, leading to excitotoxic cell death. This process is suspected to contribute to the development of these neurological conditions. To reduce the risk of excitotoxicity, the use of drugs that target glutamate receptors has been proposed as a potential therapeutic strategy. By reducing glutamate levels, it is possible to reduce the influx of calcium and consequently reduce nerve cell death. Recent studies on animals have shown promising results in reducing neurological damage associated with excitotoxicity. By understanding the mechanisms of excitotoxicity and developing therapeutic strategies to prevent its damaging effects, it may be possible to reduce the prevalence of neurological conditions such as Alzheimer’s and Parkinson’s disease in the future.