**Abstract**

Neurons are basic structural and functional units of the nervous system with major function being that of integration and interpretation of neuronal input or information. The lifespan of a nerve cell generally last throughout the individual lifetime. However, some physiologic or pathologic processes may affect the neuron causing premature death of this cell or tissue. This premature neurological death caused by pathologic circumstances is what we call neurotoxicity. The biochemical mechanisms put forward to explain neurotoxicity are not fully known. Nonetheless, whatever the mechanism involved, the outcome usually results in apoptosis, pyropoptosis, or necrosis. Examples of these mechanisms include excitotoxicity, oxidative stress, glial cell destruction, vascular interruptions, and inflammation. The idea about possibly protecting neurons against insults using pharmacologic means leads to the birth of the neuroprotection concept. This new concept has emerged based on ongoing research, suggesting it is possible through physical and pharmacological means to prevent or avoid neurotoxicity by the abovementioned mechanisms but with the exception of vascular interruption mechanisms. We will present in this chapter a synoptic view of the inflammatory mechanisms implicated in neurotoxicity and bring out the possible implications in neuroprotection.

**Keywords:** neuroprotection, neurotoxicity, inflammation, inflammasome, NLRP3, metabolic syndrome
