Transplantation of microbiota from drug-free patients with schizophrenia causes schizophrenia-like abnormal behaviors and dysregulated kynurenine metabolism in miceOriginal paper
Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease, four years before the first published case study.
Read MoreWhat was studied?
Researchers tested whether fecal microbiota from drug-free schizophrenia patients could transfer disease-like traits to animals. They transplanted patient and healthy-control feces into antibiotic-treated, specific pathogen-free mice.
How was it studied?
After colonization, mice were assessed for behavior (locomotor activity, learning, memory) and for tryptophan-kynurenine pathway metabolites in blood and brain. Colonic filtrates from transplanted mice were also applied to cultured hepatocytes and forebrain cortical slices to test effects on kynurenic acid synthesis.
What did they find?
Mice given patient microbiota showed psychomotor hyperactivity and impaired learning and memory versus mice given control microbiota. They also had elevated kynurenine-kynurenic acid pathway activity, higher prefrontal dopamine, and higher hippocampal serotonin. Sixty donor-derived bacterial species and 78 functional modules, including tryptophan biosynthesis, differed between groups.
Why it matters
The findings suggest gut microbiota composition can causally contribute to schizophrenia-like behavior, partly by dysregulating tryptophan-kynurenine metabolism. This supports the microbiota-gut-brain axis as a mechanistic pathway in schizophrenia, per PubMed (DOI: https://doi.org/10.1038/s41380-019-0475-4).