NLRP3 and Alzheimer disease: Exosomes, particularly from N2a cells, neurons, and microglia, are a primary way p‐Tau is secreted, emphasizing their role in AD pathology.[211, 212] Still, a study showed that even when exosomal secretion was inhibited, and secreted p‐Tau reduced, there was little effect in blocking NLRP3 in microglia, pointing to non‐exosomal p‐Tau (soluble p‐Tau) as a potential trigger.[209] Exosomes can also instigate neuroinflammation, heightening AD risk and neuron death.