Neuroprotection

Common mechanisms of neuronal injury include decreased delivery of oxygen and glucose to the brain, energy failure, increased levels in oxidative stress, mitochondrial dysfunction, excitotoxicity, inflammatory changes, iron accumulation, and protein aggregation.

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.

A number of glutamate antagonists have been explored as options in CNS disorders, but many are found to lack efficacy or have intolerable side effects.

[6][7] The increased levels of oxidative stress are widely targeted in neuroprotective treatments because of their role in causing neuron apoptosis.

Listed below are common antioxidants shown to be effective in reducing oxidative stress in at least one neurodegenerative disease: NMDA receptor stimulants can lead to glutamate and calcium excitotoxicity and neuroinflammation.

Nerinetide, a 20 amino acid linear peptide that prevents PSD-95 interaction with NMDA receptors,[40] shows benefit in patients with ischaemic stroke who go on to receive thrombolysis.

Continued research is being done in an effort to find any method effective in preventing the onset or progression of neurodegenerative diseases or secondary injuries.