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Definition: How does neuroprotective therapy target glutamate excitotoxicity?

Glutamate is the most abundant excitatory neurotransmitter in the central nervous system and plays a crucial role in normal brain function. However, excessive release of glutamate or impaired clearance can lead to an excessive activation of glutamate receptors, resulting in a cascade of harmful events known as excitotoxicity.

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Excitotoxicity is characterized by an influx of calcium ions into neurons, leading to mitochondrial dysfunction, oxidative stress, and ultimately cell death. This process is implicated in various neurodegenerative disorders, including Alzheimer’s disease, Parkinson’s disease, and stroke.

Neuroprotective therapy aims to counteract glutamate excitotoxicity through several mechanisms. One approach is to reduce the release of glutamate or enhance its clearance from the synaptic cleft. This can be achieved by targeting specific transporters responsible for glutamate reuptake or by modulating the activity of enzymes involved in glutamate synthesis.

Another strategy is to block or modulate glutamate receptors to prevent excessive activation. This can be done by using receptor antagonists or by targeting downstream signaling pathways that mediate excitotoxicity.

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Furthermore, neuroprotective therapy may involve the administration of antioxidants to counteract the oxidative stress induced by excitotoxicity. Antioxidants can scavenge free radicals and reduce the damage caused by reactive oxygen species.

In summary, neuroprotective therapy targets glutamate excitotoxicity by reducing glutamate release, enhancing its clearance, blocking or modulating glutamate receptors, and providing antioxidant support. These interventions aim to protect neurons from the harmful effects of excessive glutamate activation and promote their survival and function.

Keywords: glutamate, excitotoxicity, neuroprotective, excessive, function, neurons, release, clearance, activation