Abstract: Neurodegenerative diseases are often studied in isolation due to the vast differences in their underlying causes, the diversity in neuron types affected, and the variations in their clinical symptoms. However, there are common elements among these diseases, namely neuroinflammation, mitochondrial pathology, and an association with the gut–brain–immune axis that together suggest that these diseases are more similar to each other than they first seem (Zhang et al., 2023). Despite this, efforts have generally focused on developing therapies aimed at the source of the diseases while less focus has been on developing therapies that might impact a mutual downstream pathway. Reasons for this may include (1) the bias that each disease is unique and must be approached by targeting the initiating cause(s), (2) our lack of understanding of how all the common elements fit together among these diseases, and (3) the uncertainty that a shared element might be a successful target. Indeed, if it is challenging to target even one individual cause of one neurodegenerative disease, how could we expect to target a member of a downstream pathway for an effective treatment of multiple diseases? The discovery of an orally delivered bacteria that is broadly efficacious in neurodegenerative disease models through the production of an agonist of the lysophosphatidic acid receptor 3 (LPAR3), a G-protein coupled receptor involved in mitochondrial health, has presented a door to new possibilities (Acton et al., 2024).