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Investigating the role of gut-derived extracellular vesicles in PTSD following TBI

Award Number: R01NS133347
ORGANIZATION: NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 09/05/2024
PERIOD OF PERFORMANCE END DATE: 08/31/2029

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Investigating the role of gut-derived extracellular vesicles in PTSD following TBI - Abstract Veterans and the general public with traumatic brain injury (TBI) have a high risk of developing posttraumatic stress disorder (PTSD) and other psychiatric disorders, such as anxiety and depression. The pathophysiological basis that contributes to comorbid PTSD and other psychiatric disorders following TBI is not yet understood, and there are currently few effective treatments for comorbid TBI/PTSD. Serotonergic dysfunction and neuroinflammation are strongly associated with TBI and psychiatric disorders. Gut microbiota dysfunction induces inflammation and affects tryptophan metabolism, a precursor of serotonin, which is involved in serotonin biosynthesis. Studies conducted on patients with PTSD and other psychiatric disorders, as well as mice exposed to experimental stress, have shown a high correlation between perturbation in gut microbiota and mental disorders. TBI also induces gut microbiota dysbiosis. However, the cause-effect relationship and the underlying mechanisms by which gut microbiota disruption following TBI impacts comorbid PTSD and other psychiatric disorders are still largely unknown. Extracellular vesicles (EVs), small nanovesicles, play a crucial role in cellular communication and carry various molecules. Bacterial EVs in the gut contain bacterial genetic and biomaterials that are associated with virulence and considered causative agents in many diseases, while EVs produced by select probiotics have great therapeutic potential. Our pilot data reveal that administration of TBI-gut-EVs to gnotobiotic mice affects the expression of genes related to host serotonin metabolites and neuroinflammation. In contrast, treatment of TBI animals with EVs derived from select probiotics significantly increases host serotonin levels and alleviates psychiatric-like behavior. Based on our novel findings, we hypothesize that the changes in gut microbiota-derived TBI-gut-EVs are involved in the regulation of serotonergic neurons, neuroinflammation, and PTSD-like behavioral impairments following TBI. The successful completion of this study will not only provide new insight into the pathogenesis of TBI, but also promote the development of novel microbial-based therapy for preventing and/or treating comorbid TBI/PTSD, and potentially other psychiatric disorders.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2025 ( Subtotal = $463,128 )
2025	2025	HENRY FORD HEALTH + MICHIGAN STATE UNIVERSITY HEALTH SCIENCES	426 AUDITORIUM RD	EAST LANSING	MI	48824	INGHAM	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	000	2	8/4/2025	NON-COMPETING CONTINUATION	$463,128
														Subtotal = $463,128

Issue Date FY: 2024 ( Subtotal = $485,152 )
2024	2024	HENRY FORD HEALTH + MICHIGAN STATE UNIVERSITY HEALTH SCIENCES	426 AUDITORIUM RD	EAST LANSING	MI	48824	INGHAM	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	000	1	9/4/2024	NEW	$485,152
														Subtotal = $485,152

Grand Total All Awards = $948,280

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Investigating the role of gut-derived extracellular vesicles in PTSD following TBI

Award Number: R01NS133347

ORGANIZATION: NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 09/05/2024

PERIOD OF PERFORMANCE END DATE: 08/31/2029

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