Neuroprotection最新文献

Background: Some research suggests that vitamin E may help prevent intraventricular hemorrhage (IVH) in preterm neonates. However, consolidated evidence regarding its effects on brain vascular health in this population is lacking. This study systematically reviews primary research on this topic. This study examines the effectiveness of vitamin E supplementation in preventing IVH in preterm neonates than a placebo, thus addressing gaps in the literature.

Methods: The Cochrane, Dimensions, Embase, and PubMed databases were searched for relevant studies based on specific inclusion criteria. Subsequently, the relevant data were extracted, and statistical analysis was conducted using R studio (version 4.3.1) by applying appropriate models to account for heterogeneity and generate a combined estimate. The results were interpreted considering potential biases and limitations.

Results: Five studies involving 554 patients were included. Among them, 274 (49.45%) received vitamin E. The results (relative ratio 0.57; 95% confidence interval 0.35-0.92; p = 0.02; I ² = 56%) demonstrated a reduction in the incidence of IVH in patients who received administration of vitamin E (n = 274) compared with those who received a placebo (n = 280).

Conclusion: These findings highlight the potential therapeutic benefits of vitamin E supplementation in preterm neonates, which show a significant reduction in IVH incidence than placebo. Further research and clinical trials are required to fully explore its protective effects in this population.

Neuroinflammation, a key defense mechanism of the nervous system, is associated with changes in inflammatory markers and stimulation of neuroimmune cells such as microglia and astrocytes. Growing evidence indicates that the gut microbiota and its metabolites directly or indirectly regulate host health. According to recent studies, bacterial dysbiosis in the gut is closely linked to several central nervous system disorders that cause neuroinflammation, including multiple sclerosis, Alzheimer's disease, Parkinson's disease, sepsis-associated encephalopathy, and ischemic stroke. Recent findings indicate a bidirectional communication network between the gut microbiota and central nervous system that influences neuroinflammation and cognitive function. Dysregulation of this system can affect the generation of cytotoxic metabolites, promote neuroinflammation, and impair cognition. This review explores the lesser-studied microbiota-derived metabolites involved in neuroinflammation-bile acids, trimethylamine-N-oxide, and indole derivatives-as targets for creating new treatment tools for neuroinflammatory illnesses, as well as possible biomarkers for early diagnosis and prognosis.

Stroke is the leading cause of acquired disability. The development of acute ischemic stroke treatments, such as mechanical thrombectomy and tissue plasminogen activator, has resulted in more patients surviving the initial insult. However, long-term complications, such as post-stroke cognitive impairment (PSCI) and dementia (PSD), are at an all-time high. Notably, 80% of stroke survivors suffer from cognitive impairment, and a history of stroke doubles a patient's lifetime risk of developing dementia. A combination of greater life expectancy, an increase in the number of strokes in young individuals, and improved survival have inherently increased the number of years patients are living post-stroke, highlighting the critical need to understand the long-term effects of stroke, including how pathological changes in the brain might give rise to functional and behavioral changes in stroke survivors. Even with this increased risk of PSCI and PSD in stroke survivors, understanding of how the stroke itself develops into these conditions remains incomplete. Recently, secondary neurodegeneration (SND) following stroke has been linked with PSCI and PSD. SND is the degeneration of brain regions outside the original stroke site. Degeneration in these sites is thought to arise due to functional diaschisis with the infarct core; however, observation of SND pathology in multiple regions without direct connectivity to the stroke infarct suggests that the degeneration in these regions is likely more complex. Moreover, pathological hallmarks of dementia, such as a deposition of neurodegenerative proteins and iron, cell death, inflammation and blood-brain barrier alterations, have all been found in regions such as the thalamus, hippocampus, basal ganglia, amygdala and prefrontal cortex following stroke. Hence, in this review, we present the current understanding of PSCI and PSD in the context of SND and outline how remote anatomical and molecular changes may drive the development of these conditions.

Background: Despite the World Health Organization's prioritization of familial hypercholesterolemia (FH), its global diagnostic rate remains critically low, leading to inadequate treatment and control, thereby increasing the risk of atherosclerotic cardiovascular disease. This study aimed to investigate the comorbidity burden of FH in China and analyze the differences between familial and general hypercholesterolemia (HC) populations.

Methods: Using a national medical insurance database from 2013 to 2017 including 13,976 patients with FH and 13,976 matched control patients with HC, we utilized case-control methods to compare the composition ratio, comorbidity rates, medical expenses, and healthcare burden of patients with FH to those of control patients.

Results: The FH population had a higher comorbidity rate of more than one cardiometabolic disease (83.7% [11,697/13,976]) compared to the HC group (70.3% [9279/13,976]; χ² = 250.45, p < 0.0001). The rates of coronary heart disease, hypertension, stroke, and diabetes were higher in patients with FH (39.2% [5475/13,976], 71.0% [9925/13,976], 14.2% [1982/13,976], and 31.2% [4363/13,976], respectively) compared to those in the HC group (30.4% [4255/13,976], 61.4% [8587/13,976], 11.5% [1601/13,976], and 28.1% [3923/13,976], respectively; all p < 0.0001). In the 40-49 age group, patients with FH had a significantly higher average number of comorbidities compared to control patients with HC (1.2 vs. 0.9; t  = 15.67, p < 0.0001). Notably, the comorbidity count in patients with FH aged 40-49 years even exceeded that in patients with HC aged 50-59 years. Furthermore, the annual per capita medical cost for patients with FH was significantly higher at 5045.5 Chinese yuan (CNY) compared to 4184.7 CNY for patients with HC (t = 12.54, p < 0.0001).

Conclusion: With a large number of patients with dyslipidemia, the type and number of comorbidities significantly impact the healthcare burden. FH presents with earlier onset, more comorbidities, and heavier cardiovascular-related medical burdens than HC. Early identification, intervention, and comprehensive management of comorbidities in the FH population are crucial for neuroprotection and prevention of atherosclerotic cardiovascular disease.

The human brain functions as a highly integrated system. Interconnected cellular and molecular networks within this system process sensory information, cognitive functions, and motor responses. The brain also exhibits a remarkable potential for plasticity-driven adaptive learning and memory. Importantly, neuroplasticity serves as a key mechanism of neuroprotection while also enabling the brain to compensate for injury through adaptive structural remodeling. Understanding the brain as a dynamic system requires examining how its components interact to produce adaptive physiological responses and complex behaviors, such as social interactions. Key molecules, such as brain-derived neurotrophic factor (BDNF) and oxytocin (OT), play pivotal roles in maintaining the brain's dynamic complexity and integrative functioning. In this review, we introduce the concept of "neurosocial plasticity", which refers to the brain's ability to adapt both neural circuitry and social behavior through the dynamic interaction between BDNF and OT. This concept highlights how BDNF-OT interactions may support both neural plasticity and the capacity for adaptive social functioning. We then explore how their co-localization, co-expression, and co-regulation may regulate neural and social plasticity, ultimately shaping the brain's adaptability and the development of social behaviors across various contexts.

Oral microbiota is the second largest microbial colony in the body and forms a complex ecological community that influences oral and brain health. Impaired homeostasis of the oral microbiota can lead to pathological changes, resulting in central nervous system (CNS) diseases. However, the mechanisms and clinical value of how the oral microbiome influences the brain remain unclear. This review summarizes recent clinical findings on the role of the oral microbiota in CNS diseases and proposes potential approaches to understand the way the oral microbiota and brain communicate. We propose three underlying patterns involving neuroinflammation, neuroendocrine regulation, and CNS signaling between oral microbiota and CNS diseases. We also summarize the clinical characteristics and potential utilization of the oral microbiota in ischemic stroke, Alzheimer's and Parkinson's disease, intracranial aneurysms, and mental disorders. Although the current findings are preliminary and clinical evidence is incomplete, oral microbiota is a potential biomarker for the clinical diagnosis and treatment of CNS diseases.

Stroke, a leading cause of mortality and morbidity worldwide, is a complex cerebrovascular disease. Stroke risk factors are diverse, encompassing age, sex, and ethnicity. Comorbid conditions, including hypertension, hyperglycemia, hyperlipidemia, and atrial fibrillation, exacerbate stroke outcomes, contributing to the overall stroke burden within populations. In addition to these factors, lifestyle-related diseases can impact individuals across all age groups, and often include as comorbidities linked to stroke. Socioeconomic conditions, healthcare access, and the quality of clinical data significantly influence the prevalence of comorbidities. Asia, the largest continent and home to 60% of the world's population, includes many developing nations undergoing diverse economic transitions. In Southeast Asian countries, stroke prevalence is high, imposing a substantial burden on healthcare systems and economies. Research disparities in stroke are often attributed to insufficient demographic data on comorbidities. Hence, the review discusses all previously published results of hospital-based studies and data from national registries. It has been noticed that due to insufficient documentation on stroke-related comorbidities in various developing countries of Southeast Asia, stroke management becomes difficult. Therefore, this review aims to discuss the association between various comorbidities and stroke, with special emphasis on the incidence and prevalence of stroke burden in Southeast Asian countries.

Chronic neuroinflammation and protein aggregation are the fundamental events mainly responsible for the progression of neurodegenerative diseases (NDs). Potential neurotoxic changes in the intra- and extracellular environment are typical hallmarks of many NDs. Treatment of ND is challenging, as the symptoms in these patients arises when a significant numbers of neurons have already been destroyed. Heat shock proteins (HSPs) can bind to recipient cells that are susceptible to stress, such as neurons, in the extracellular environment, therefore enhancing stress resistance. Among all, HSP60, HSP70, and HSP90 are highly conserved molecular chaperones involved in protein folding and assembly, maintaining cellular homeostasis in the central nervous system. Notably, α-synuclein accumulation is a major pathophysiology in Parkinson's disease, where HSP90 modulates the assembly of α-synuclein in vesicles to prevent its accumulation. Moreover, HSP90 regulates the activity of the glycogen synthase kinase-3β protein, which is crucial in diabetes mellitus-associated neurocognitive disorder. Therefore, understanding the molecular mechanism by which HSPs facilitate protein aggregation and respond to inflammatory stimuli, including metabolic disease such as diabetes, is essential for understanding the significance of HSPs in NDs. This review emphasizes the role of various HSPs in the progression of NDs such as Alzheimer's, Parkinson's, multiple sclerosis, and Huntington's disease, including diabetes, which is one of the major risk factors for neurodegeneration.