Traumatic brain injury (TBI) heavily impacts the body: it damages the brain tissue and the peripheral nervous system and shifts homeostasis in many types of tissue. An acute brain injury compromises the “brain–gut-microbiome axis”, a well-balanced network formed by the brain, gastrointestinal tract, and gut microbiome, which has a complex effect: damage to the brain alters the composition of the microbiome; the altered microbiome affects TBI severity, neuroplasticity, and metabolic pathways through various bacterial metabolites. We modeled TBI in rats. Using a bioinformatics approach, we sought to identify correlations between the gut microbiome composition, TBI severity, the rate of neurological function recovery, and blood metabolome. We found that the TBI caused changes in the abundance of 26 bacterial genera. The most dramatic change was observed in the abundance of Agathobacter species. The TBI also altered concentrations of several metabolites, specifically citrulline and tryptophan. We found no significant correlations between TBI severity and the pre-existing gut microbiota composition or blood metabolites. However, we discovered some differences between the two groups of subjects that showed high and low rates of neurological function recovery, respectively. The present study highlights the role of the brain–gut-microbiome axis in TBI.

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Brain-derived neurotrophic factor (BDNF) is principally involved in the phenomena of neuroplasticity of the brain and long-term synaptic potency (LTP) in the hippocampus. This article covers the role played by BDNF as a diagnostic marker of vascular cognitive disorders. The relationship between etiology and the degree of cognitive impairment with the level of BDNF is ambiguous. Especially if we take into account the fact that vascular pathology can be a trigger for molecular mechanisms of neurodegeneration. The lowest BDNF level can be found among patients with dementia in Alzheimer’s disease, and there is evidence that patients with neurodegenerative disease without cognitive impairment have a decreased BDNF level. Patients with vascular cognitive impairment have a less expressed decrease of BDNF level, although it can depend on severity of stroke. In case of vascular cognitive impairment, it is possible to improve cognitive state thanks to increased BDNF level in hippocampus after physical activity. That opens new opportunities in rehabilitation. Genetic polymorphism of BDNF leads to the problems with cognitive rehabilitation and increases the risk of post-stroke dementia and dementia in Alzheimer’s disease. Supposedly, changes in the structure of BDNF-propeptide, which is involved in the processes of long-term synaptic depression (LTD) of the hippocampus, are the main cause in this case.

The purpose of this study is assessing informative capability of the most frequently used scales and neuropsychological tests evaluating cognitive function for mild cognitive impairment (MCI) and vascular dementia (VD). A total of 104 patients with cerebrovascular disorder including 39 male and 65 female were divided into two subgroups depending on severity of the cognitive impairment. The first group consisted of 51 patients with MCI and the second one consisted of 53 patients with VD confirmed by MMSE and MoCA-test. The obtained correlation analysis data testifies to difficulties in the interpretation of these routinely used scales not only because of the differences between investigated parameters of the patients with MCI and VD, but also because of the main goal of their creation. Most of the scales were created for patients with dementia and now their sensitivity for MCI is doubtful. The MoCA test, Clock Drawing Test (CDT) and ADAS-cog subscale are more sensitive and has greatest informative capability for patients with MCI and dementia, while MMSE is more informative mostly for patients with dementia. Neuropsychological tests DAD and NPI remain informative in varying degrees of cognitive impairment. In the diagnosis and differential diagnosis of the degree of cognitive impairment of vascular genesis, one should use not only a complex of scales and neuropsychological tests, but also methods that comprehensively reflect the vascular genesis of the process of formation of cognitive impairment.