Develop the following points into a single cohesive narrative summary of the articles I’ve read that focus on post-tbi gut microbiome processes, neuropsychiatric disorders, ongoing chronic symptoms, and and, in a separate paragraph, state where that leaves us and future directions:

-one study found that dysbiosis matters most in the acute phase of moderate to severe injury post-tbi when discussing increased risk tasking and impulsive behaviors, in an animal model.

-one author focused on growth hormone deficiency impacting 20% of people post TBI, which contributes to ongoing cognitive impairment, and creates a brain injury associated fatigue, and notes that TBI patients have different ways of processing nutrients, which influence the microbiome. This lead them to the next study

-They found that there were long-term gut microbiome changes in clinical populations that required long-term care and presented with complex comorbidities, years after their TBI had occurred.

-in response, another author conducted a study in a similar population (but different part of the country) and found that the gut microbiome returns to stasis shortly after the acute (7-day window) phase of injury.

-in a preclinical animal model study that referenced the two previous authors, the researchers found no significant correlations between TBI severity and pre-exsiting gut microbiota composition, but they did find a decrease in a bacteria that is historically suggestive of increased pain signaling.

-one animal model study found decreases in two anti-inflammatory bacteria post-concussion. Previously a decrease in one of these has been associated with peripheral inflammation in patients suffering from cognitive impairment and brain amyloidosis.

-another article explains that TBI has been considered a chronic condition, and argues that this neurodegenerative component is mediated via: gut dysbiosis, gut microbiota influence on inflammation via the production of pro-inflammatory cytokines, autonomic dysregulation, and gut-microbiota influenced production (or inhibition of production) of metabolites that may have typically been neuroprotective.

-Another review argues that TBI yields gut dysregulation and creates the opportunity for secondary insult, which over time, can develop into chronic neurodegenerative diseases, like Parkinsons and Alzheimer’s (proteinopathies). They propose DHA/probiotic supplementation as a potential treatment avenue.

-One animal model study found that while the initial immune response from TBI can help to repair damage by clearing away damaged tissue and debris (via microglial activation), but when it persists too long it can lead to chronic diseases. So they use a fecal microbiome transplant (FMT). They found that this improved cognitive function and reduced neuroinflammation in mice with TBI. It also lead to changes in gut microbiome composition and increased anti-inflammatory cytokines in the brain. They found dysbiosis was more severe 28 days after TBI than after 7 days, suggesting it was progressive. They also found evidence that persistent microglial activation after TBI is dependent on the progressive dysobiosis of gut microbiota. They also saw that the enzyme Lyz2 was responsible for chronic microglia activation.

-Other studies have suggested that high fat diet and obesity contributes to the production of Lyz2 in fat tissue.

-In another review, it was noted that early life stress/abuse/trauma could make it more likely to develop neuropsychiatric disorders later in life. 

-The final review suggested that neuropsychiatric illness tends to occur when there are alterations in gut-microbiome composition throughout life.