In recent years, we have seen a silent epidemic of autoimmune disorders, including neuroautoimmunities; harmful bacteria and the toxins they release are the prime suspects in the pathogenesis of these conditions. Pathogenic bacterial invasions can occur through oral and nasal pathways, or through breakdowns in the endothelial gut and blood–brain barriers. These breakdowns in the gut can result in periodontitis, inflammatory bowel disease, irritable bowel syndrome, autoimmune disorders, and even neuroimmune disorders like Alzheimer’s disease. Oral pathogens, especially enterobacters, release lipopolysaccharides, and bacterial cytolethal distending toxins (BCdTs) that can disrupt tight junction proteins and damage the enteric neurons via molecular mimicry and other mechanisms. The breakdown of the endothelial barriers and tight junctions results in the release of self-proteins and the production of antibodies against them. This breakdown allows macromolecules, bacterial components, or even the entire bacteria to enter the brain, allowing for the pathogenesis of neuroautoimmunity and neurodegenerative disorders. Once in the brain, these invasive molecules can provoke an immune reaction that results in the generation of antibodies, including blood–brain barrier (BBB)- and brain-reactive autoantibodies. The measurement of these antibodies against bacterial toxins, tight junction proteins, BBB proteins, and brain-specific antigens may provide early signals to practitioners, and pave the way for the development of novel therapeutic strategies focused on removing triggers, manipulating the gut microbiota, reducing LPS and BCdTs, and repairing the integrity of gut barrier function. These interventions and others like them may ultimately play a role in the prevention and treatment of future autoimmune and neurodegenerative disorders. All of this underscores the importance of the gut–brain–immune connection in understanding and dealing with the explosion of autoimmune disorders.