Neuroprotection refers to the relative preservation of
neuronal structure and/or function. In the case of an ongoing insult (a
neurodegenerative insult) the relative preservation of neuronal integrity implies a reduction in the rate of neuronal loss over time, which can be expressed as a differential equation. It is a widely explored treatment option for many central nervous system (CNS) disorders including
neurodegenerative diseases, stroke, traumatic
brain injury,
spinal cord injury, and acute
management of neurotoxin consumption (i.e. methamphetamine overdoses).
Neuroprotection aims to prevent or slow disease progression and secondary injuries by halting or at least slowing the loss of neurons. Despite differences in symptoms or injuries associated with CNS disorders, many of the mechanisms behind
neurodegeneration are the same. Common mechanisms include increased levels in oxidative stress, mitochondrial dysfunction, excitotoxicity, inflammatory changes, iron accumulation, and protein aggregation. Of these mechanisms, neuroprotective treatments often target
oxidative stress and excitotoxicity—both of which are highly associated with CNS disorders. Not only can
oxidative stress and excitotoxicity trigger
neuron cell death but when combined they have synergistic effects that cause even more degradation than on their own. Thus limiting excitotoxicity and
oxidative stress is a very important aspect of neuroprotection. Common neuroprotective treatments are glutamate antagonists and antioxidants, which aim to limit excitotoxicity and
oxidative stress respectively.
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