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BackgroundReal-time detection of cerebral blood perfusion can prevent adverse reactions, such as cerebral infarction and neuronal apoptosis. Our previous clinical trial have shown that the infusion of therapeutic fluid can significantly change the impedance distribution in the brain. However, whether this alteration implicates the cerebral blood perfusion remains unclear. To explore the feasibility of monitoring cerebral blood perfusion, the present pilot study established a novel cerebral contrast-enhanced electrical impedance tomography (C-EIT) technique.Materials and methodsRabbits were randomly divided into two groups: the internal carotid artery non-occlusion (ICAN) and internal carotid artery occlusion (ICAO) groups. Both of groups were injected with glucose, an electrical impedance-enhanced contrast agent, through the right internal carotid artery under EIT monitoring. The C-EIT reconstruction images of the rabbits brain were analyzed according to the collected raw data. The paired and independent t-tests were used to analyze the remodeled impedance values of the left and right cerebral hemispheres within and between studied groups, respectively. Moreover, pathological examinations of brain were performed immediately after C-EIT monitoring.ResultsAccording to the reconstructed images, the impedance value of the left cerebral hemisphere in the ICAN group did not change significantly, whereas the impedance value of the right cerebral hemisphere gradually increased, reaching a peak at approximately 10 s followed by gradually decreased. In the ICAO group, the impedance values of both cerebral hemispheres increased gradually and then began to decrease after reaching the peak value. According to the paired t-test, there was a significant difference (P < 0.001) in the remodeling impedance values between the left and right hemispheres in the ICAN group, and there was also a significant difference (P < 0.001) in the ICAO group. According to the independent t-test, there was a significant difference (P < 0.001) of the left hemispheres between the ICAN and ICAO groups.ConclusionThe cerebral C-EIT proposed in this pilot study can reflect cerebral blood perfusion. This method has potential in various applications in the brain in the future, including disease progression monitoring, collateral circulation judgment, tumor-specific detection, and brain function research.

Overnutrition-related obesity has become a worldwide epidemic, and its prevalence is expected to steadily rise in the future. It is widely recognized that obesity exerts negative impacts on metabolic disorders such as type 2 diabetes mellitus (T2DM) and cardiovascular diseases. However, relatively fewer reports exist on the impairment of brain structure and function, in the form of memory and executive dysfunction, as well as neurogenerative diseases. Emerging evidence indicates that besides obesity, overnutrition diets independently induce cognitive impairments via multiple mechanisms. In this study, we reviewed the clinical and preclinical literature about the detrimental effects of obesity or high-nutrition diets on cognitive performance and cerebral structure. We mainly focused on the role of brain insulin resistance (IR), microbiota-gut-brain axis, and neuroinflammation. We concluded that before the onset of obesity, short-term exposure to high-nutrition diets already blunted central responses to insulin, altered gut microbiome composition, and activated inflammatory mediators. Overnutrition is linked with the changes in protein expression in brain insulin signaling, leading to pathological features in the brain. Microbiome alteration, bacterial endotoxin release, and gut barrier hyperpermeability also occur to trigger mental and neuronal diseases. In addition, obesity or high-nutrition diets cause chronic and low-grade systematic inflammation, which eventually spreads from the peripheral tissue to the central nervous system (CNS). Altogether, a large number of unknown but potential routes interact and contribute to obesity or diet-induced cognitive impairment. The challenge for future research is to identify effective interventions involving dietary shifts and personalized therapy targeting the underlying mechanisms to prevent and improve cognition deficits.