Trimethylamine-N-oxide (TMAO) is a common intestinal metabolite. The Choline in the nutrient forms TMA under the action of the gut microbiota, which passes through the liver and eventually forms TMAO. Initial studies of TMAO focused on cardiovascular disease, but as research progressed, TAMO\'s effects were found to be multisystem and closely related to the development of neurological diseases. Intestinal tract is the organ with the largest concentration of bacteria in human body, and the composition and metabolism of gut microbiota affect human health. As a two-way communication axis connecting the central nervous system and the gastrointestinal tract, the brain-gut axis provides the structural basis for TMAO to play its role. This article will review the correlation between TMA/TMAO and neurological diseases in order to find new directions and new targets for the treatment of neurological diseases.

As the global population ages, the prevalence of neurodegenerative diseases is surging. These disorders have a multifaceted pathogenesis, entwined with genetic and environmental factors. Emerging research underscores the profound influence of diet on the development and progression of health conditions. Intermittent fasting (IF), a dietary pattern that is increasingly embraced and recommended, has demonstrated potential in improving neurophysiological functions and mitigating pathological injuries with few adverse effects. Although the precise mechanisms of IF\'s beneficial impact are not yet completely understood, gut microbiota and their metabolites are believed to be pivotal in mediating these effects. This review endeavors to thoroughly examine current studies on the shifts in gut microbiota and metabolite profiles prompted by IF, and their possible consequences for neural health. It also highlights the significance of dietary strategies as a clinical consideration for those with neurological conditions.

Herpes simplex virus type 2 (HSV-2) is a common human pathogen that establishes lifelong latency in neurons of the nervous system. The number of severe central nervous system infections caused by the virus has increased recently. However, the pathogenesis of HSV-2 infection in the nervous system is not fully understood. Here, we demonstrated global proteomic changes in the brain tissue in BALB/c mice vaginally infected with HSV-2. Data are available via ProteomeXchange with identifier PXD034186. A total of 249 differentially expressed proteins were identified in infected brain tissue. The GO and KEGG enrichment analysis of these proteins indicated that they were mainly involved in the regulation of synapse formation and synaptic excitability. In addition, genes affecting autophagy, the development of other neurodegenerative diseases, and signaling pathways relevant to other neurologic diseases were identified. Additional experiments, comparing the brain tissue of asymptomatic and symptomatic mice showed a differential expression of proteins involved in synapse formation and synaptic transmission. Others were involved in autophagy, addiction, and signaling pathways of other neurologic diseases. These results suggest that changes in synaptic structure and function, as well as autophagy, may be related to the development of neurologic abnormalities that follow HSV-2 infection. We also identified a protein GluN2A encoded by Grin2a was continuously expressed at high levels after infection. We propose that GluN2A may be a key molecule in the pathogenesis of HSV-2-induced neurologic diseases.

Background: Undernutrition is the main reason for the use of artificial nutrition in patients with severe neurological diseases. However, the clinical and immunological outcomes of enteral nutrition supplemented with immunomodulatory nutrients in these patients remain unclear. Methods: In this single-center, randomized controlled study, 57 patients with severe neurological diseases were randomly divided into the following two groups according to the type of enteral nutrition they would receive: immune-enhancing (IE) (n = 27) and non-IE (NIE) (n = 30). The IE and NIE groups received enteral nutrition supplemented with immunomodulatory nutrients and standard enteral nutrition, respectively. We compared the nutritional status and the state of cellular immunity between the patients of the two groups. Clinical and immunological variables were evaluated following nutritional treatment. Results: Feeding intolerance was lower in the IE than that in the NIE group (P = 0.04). However, there were no significant differences between the results of the two groups in terms of length of stay in the intensive care unit or hospital, extubation time, or body mass index (P > 0.05). The CD4+ T-lymphocyte count and CD4+/CD8+ ratio in the peripheral blood increased significantly in the IE group. The expression of CD28 activated cell surface markers was higher in the IE than in the NIE group. In addition, increased plasma interferon-γ levels were recorded in the IE group, whereas the levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-8, and IL-10 decreased. Conclusions: Immune-enhanced enteral nutrition could improve the immune status and feeding tolerance in patients with severe neurological diseases. Trial Registration:www.chictr.org.cn/index.aspx, identifier: ChiCTR-IPR-17013909.

Neurodegenerative diseases are heterogeneous in their cause and clinical presentation making clinical assessment and disease monitoring challenging. Because of this, there is an urgent need for objective tools such as fluid biomarkers able to quantitate different aspects of the disease. In the last decade, technological improvements and awareness of the importance of biorepositories led to the discovery of an evolving number of fluid biomarkers covering the main characteristics of neurodegenerative diseases such as neurodegeneration, protein aggregates and inflammation. The ability to quantitate each aspect of the disease at a high definition enables a more precise stratification of the patients at inclusion in clinical trials, hence reducing the noise that may hamper the detection of therapeutical efficacy and allowing for smaller but likewise powered studies, which particularly improves the ability to start clinical trials for rare neurological diseases. Moreover, the use of fluid biomarkers has the potential to support a targeted therapeutical intervention, as it is now emerging for the treatment of amyloid-beta deposition in patients suffering from Alzheimer\'s disease. Here we review the knowledge that evolved from the measurement of fluid biomarker proteins in neurodegenerative conditions.

IV immunoglobulin (Ig) therapy has been widely used for the treatment of neurologic disorders, autoimmune diseases, immunodeficiency-related diseases, blood system diseases, and cancers. In this review, we summarize the efficacy and tolerability of IVIg and SCIg therapy in neurologic diseases.
We summarized and analyzed the efficacy and tolerability of IVIg and SCIg in neurologic diseases, by analyzing the literature pertaining to the use of IVIg and SCIg to treat nervous system diseases.
In clinical neurology practice, IVIg has been shown to be useful for the treatment of new-onset or recurrent immune diseases and for long-term maintenance treatment of chronic diseases. Moreover, IVIg may have applications in the management of intractable autoimmune epilepsy, paraneoplastic syndrome, autoimmune encephalitis, and neuromyelitis optica. SCIg is emerging as an alternative to IVIg treatment. Although SCIg has a composition similar to that of IVIg, the applications of this therapy are different. Notably, the bioavailability of SCIg is lower than that of IVIg, but the homeostasis level is more stable. Current studies have shown that these 2 therapies have pharmacodynamic equivalence.
In this review, we explored the efficacy of IVIg in the treatment of various neurologic disorders. IVIg administration still faces many challenges. Thus, it will be necessary to standardize the use of IVIg in the clinical setting. SCIg administration is a novel and feasible treatment option for neurologic and immune-related diseases, such as chronic inflammatory demyelinating polyradiculoneuropathy and idiopathic inflammatory myopathies. As our understanding of the mechanisms of action of IVIg improve, potential next-generation biologics can being developed.

Many neurologic diseases are related to autoimmune dysfunction and a variety of molecules or reaction pathways are involved in the regulation of immune function of the nervous system. Soluble CD83 (sCD83) is the soluble form of CD83, a specific marker of mature dendritic cell, which has recently been shown to have an immunomodulatory effect. Indoleamine 2,3-dioxygenase (IDO; corresponding enzyme intrahepatic, tryptophan 2,3-dioxygenase, TDO), a rate-limiting enzyme of extrahepatic tryptophan kynurenine pathway (KP) participates in the immunoregulation through a variety of mechanisms solely or with the synergy of sCD83, and the imbalances of metabolites of KP were associated with immune dysfunction. With the complement of sCD83 to IDO-KP, a previously known immunomodulatory axis, this review focused on an expanded neuroimmunomodulation axis: sCD83-IDO-KP and its involvement in nervous system diseases.

In neurologically critically ill patients with mechanical ventilation (MV), the development of acute respiratory distress syndrome (ARDS) is a major contributor to morbidity and mortality, but the role of ventilatory management has been scarcely evaluated. We evaluate the association of tidal volume, level of PEEP and driving pressure with the development of ARDS in a population of patients with brain injury.
We performed a secondary analysis of a prospective, observational study on mechanical ventilation.
We included 986 patients mechanically ventilated due to an acute brain injury (hemorrhagic stroke, ischemic stroke or brain trauma). Incidence of ARDS in this cohort was 3%. Multivariate analysis suggested that driving pressure could be associated with the development of ARDS (odds ratio for unit increment of driving pressure 1.12; confidence interval for 95%: 1.01 to 1.23) whereas we did not observe association for tidal volume (in ml per kg of predicted body weight) or level of PEEP. ARDS was associated with an increase in mortality, longer duration of mechanical ventilation, and longer ICU length of stay.
In a cohort of brain-injured patients the development of ARDS was not common. Driving pressure was associated with the development of this disease.

OBJECTIVE: To examine the characteristics and the prognostic influence of pulmonary infections in neurologic disease patients with mild-to-severe hypoproteinemia.
METHODS: We used a retrospective survey method to analyze the characteristics and prognoses of 220 patients with hypoproteinemia complicated with pulmonary infection in the Internal Medicine-Neurology Intensive Care Unit at the First Affiliated Hospital of Chongqing Medical University from January 2010 to December 2013. The patients were divided into mild, moderate and severe hypoproteinemia groups according to their serum albumin levels. The analysis included patient age, sex, acute physiology and chronic health evaluation (APACHE II score), and characteristics of the pulmonary infection, nutritional support and prognosis, among others.
RESULTS: Differences in the general information of the 220 cases of hypoalbuminemia patients complicated with varying degrees of pulmonary infection (APACHE II score, age, disease distribution) were statistically significant. The pulmonary infection onset time and pathogen susceptibility in the patients with mild-to-severe hypoalbuminemia were not significantly different. Pulmonary infection onset was more frequently observed within the first 3-11 days following admission in all groups. The nutritional support method did not significantly influence serum albumin protein levels. However, the neurological intensive care unit stay length, total hospitalization cost and disease distribution were significantly different among the patient groups.
CONCLUSIONS: Patients with cerebrovascular disease, intracranial infections and epilepsy complicated with pulmonary infection represent the high-risk groups for hypoalbuminemia. The Acinetobacter baumannii complex represents the main group of pathogenic bacteria causing lung infections, and the high-risk period for lung infections is 3-11 days after the occurrence of hypoalbuminemia. Patients with severe hypoalbuminemia complicated with pulmonary infection have the worst prognoses.

Multimodality imaging of positron emission tomography/computed tomography (PET/CT) provides both metabolic information and the anatomic structure, which is significantly superior to either PET or CT alone and has greatly improved its clinical applications. Because of the higher soft-tissue contrast of magnetic resonance imaging (MRI) and no extra ionizing radiation, PET/MRI imaging is the hottest topic currently. PET/MRI is swiftly making its way into clinical practice. However, it has many technical difficulties to overcome, such as photomultiplier tubes, which cannot work properly in a magnetic field, and the inability to provide density information on the object for attenuation correction. This paper introduces the technique process of PET/MRI and summarizes its clinical applications, including imaging in oncology, neurology, and cardiology.