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Gut Microbiome May Provide Novel Therapies for Neurological Disorders


Researchers at the Baylor College of Medicine report that they have found that microbes in the gut may contribute to certain symptoms associated with complex neurological disorders. Their study “Dissecting the contribution of host genetics and the microbiome in complex behaviors,” published in Cell, also suggests that microbe-inspired therapies may one day help to treat them.


Mauro Costa-Mattioli, PhD, professor and Cullen Foundation Endowed Chair in neuroscience and director of the Memory and Brain Research Center at Baylor, discovered with his team that different abnormal behaviors are interdependently regulated by the host’s genes and microbiome. Specifically, the team found that in mouse models for neurodevelopmental disorders, hyperactivity is controlled by the host’s genetics, whereas social behavior deficits are mediated by the gut microbiome.

From a therapeutic perspective, they found that treatment with a specific microbe that promotes the production of compounds in the biopterin family in the gut or treatment with a metabolically active biopterin molecule improved the social behavior but not motor activity.


“The core symptoms of many neurological disorders have traditionally been thought to be caused by genetic variants affecting brain development and function. However, the gut microbiome, another important source of variation, can also influence specific behaviors. Thus, it is critical to unravel the contributions of host genetic variation, the microbiome, and their interactions to complex behaviors,” write the investigators.


“Unexpectedly, we discovered that different maladaptive behaviors are interdependently regulated by the microbiome and host genes in the Cntnap2 −/− model for neurodevelopmental disorders. The hyperactivity phenotype of Cntnap2 −/− mice is caused by host genetics, whereas the social-behavior phenotype is mediated by the gut microbiome. Interestingly, specific microbial intervention selectively rescued the social deficits in Cntnap2 −/− mice through upregulation of metabolites in the tetrahydrobiopterin synthesis pathway. “


Our findings that behavioral abnormalities could have distinct origins (host genetic versus microbial) may change the way we think about neurological disorders and how to treat them.”

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