Neuroprotection suggests to the relative storage of neuronal structure and/or function. In the case of an ongoing insult (a neurodegenerative insult) the relative preservation of neuronal integrity implies a decreasing 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, spinal cord injury, stroke, traumatic brain 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. In spite of contrasts in indications or wounds related with CNS clutters, numerous of the instruments behind neurodegeneration are the same.Common instruments incorporate expanded levels in oxidative stretch, mitochondrial brokenness, excitotoxicity, provocative changes, press amassing, and protein aggregation. Of these instruments, neuroprotective medications regularly target oxidative stretch and excitotoxicity—both of which are profoundly related with CNS disarranges. Not as it were can oxidative stretch and excitotoxicity trigger neuron cell passing but when combined they have synergistic impacts that cause indeed more debasement than on their own. In this way restricting excitotoxicity and oxidative push may be a exceptionally vital perspective of neuroprotection. Common neuroprotective medications are glutamate opponents and cancer prevention agents, which point to constrain excitotoxicity and oxidative.

  • Epileptic seizure
  • Partial and generalized seizure
  • Progressive myoclonic epilepsies
  • Cerebral trauma and tumour
  • Cerebrovascular and autoimmune diseases
  • Disorders of chromosome function
  • Differential diagnosis

Related Conference of Neuroprotection

Neuroprotection Conference Speakers