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Parasitic diseases continue to afflict millions of people globally. However, traditional vaccine development strategies are often difficult to apply to parasites, leaving an immense unmet need for new effective vaccines for the prevention and control of parasitic infections. As parasites commonly use extracellular vesicles (EVs) to interact with, interfere with, or modulate the host immune response from a distance, parasite-derived EVs may provide promising vaccine agents that induce immunity against parasitic infections. We here present achievements to date and the challenges and limitations associated with using parasitic EVs in a clinical context. Despite the many difficulties that need to be overcome, we believe this direction could offer a new and reliable source of therapeutics for various neglected parasitic diseases., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Neurogenesis, the formation of new neurons in the adult brain, is important for memory formation and extinction. One of the most studied external interventions that affect the rate of adult neurogenesis is physical exercise. Physical exercise promotes adult neurogenesis via several factors including brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF). Here, we identified L-lactate, a physical exercise-induced metabolite, as a factor that promotes adult hippocampal neurogenesis. While prolonged exposure to L-lactate promoted neurogenesis, no beneficial effect was exerted on cognitive learning and memory. Systemic pharmacological blocking of monocarboxylate transporter 2 (MCT2), which transports L-lactate to the brain, prevented lactate-induced neurogenesis, while 3,5-dihydroxybenzoic acid (3,5-DHBA), an agonist for the lactate-receptor hydroxycarboxylic acid receptor 1 (HCAR1), did not affect adult neurogenesis. These data suggest that L-lactate partially mediates the effect of physical exercise on adult neurogenesis, but not cognition, in a MCT2-dependent manner.