肠道菌群与血管性认知损害

血管性认知损害( vascular cognitive impairment,VCI)是由血管危险因素、显性或隐性脑血管病引起的从轻度VCI到血管性痴呆( vascular dementia,VD)的一类综合征.相关数据显示,VD占所有痴呆类型的15％ ～30％,为仅次于阿尔茨海默病的第二大痴呆类型[1] ,严重影响了...     

肠道微生物与阿尔茨海默病发生相关性的研究进展

阿尔茨海默病(AD)以进行性认知功能障碍为特征,是最常见的痴呆类型。近年来,肠道菌群作为寄居在人消化道内的大量微生物,成为研究众多疾病发病机制的热点之一。越来越多的证据表明,肠道微生物通过肠－脑轴与中枢神经系统功能沟通,影响宿主的认知行为,与AD的发生发展密切相关。研究发现,AD动物模型和患者的肠道内微生物群多样性降低。肠道微生物可通过产生肠道代谢产物、神经递质影响宿主大脑神经生化过程,从而增加或降低宿主患AD的风险。部分肠道微生物可驱动外周炎症,进而激活脑内神经胶质和炎症因子,诱发神经毒性反应,最终加速AD的发生发展。该文综述了肠道微生物与AD的相互作用机制,并探讨益生菌对AD防治的潜在价值,以期为AD的预防及治疗提供新思路。 [引用格式:国际神经病学神经外科学杂志, 2021, 48(4): 377-381.]     

肠道微生物群参与动脉粥样硬化相关机制的研究进展

近年来肠道微生物群在健康和疾病中的重要性越来越受到重视。动脉粥样硬化是心脑血管疾病的一种关键致病原因,已有研究发现肠道微生物群与心脑血管疾病的进程有关,肠道微生物群是否可通过促进或改善动脉粥样硬化过程而影响心脑血管疾病值得深入探讨。因此,本文将从感染所致的炎症反应、对改变宿主细胞脂类代谢结构以及微生物代谢过程之间的影响3个方面,综述肠道微生物群对动脉粥样硬化的作用以及其调节动脉粥样硬化的可能机制。     

老年抑郁症与认知损害

本文就老年抑郁症与认知损害的关系,抗抑郁剂治疗对认知功能的影响,认知损害的神经生化机制进行了阐述。 在老年抑郁症的诊断治疗中,认知损害是一个需要考虑的重要问题。这种损害随着年龄增加而成为老年抑郁症的症状之一,也是许多抗抑郁药的副反应之一。尤其老年抑郁症病人更容易发生这样的急性认     

阿尔茨海默病中肠道微生物群与血脑屏障关系研究进展

阿尔茨海默病（Alzheimer disease,AD）是最常见的痴呆类型,给社会带来沉重负担。血脑屏障（bloodbrain barrier,BBB）的改变可能是AD早期事件之一,肠道微生物群及其代谢产物可能通过影响BBB的结构和功能,参与AD的发生和进展。而靶向肠道微生物群和BBB的AD治疗新策略也日益受到重视,地中海饮食、益生菌可改善BBB结构和功能,益生元、粪便移植治疗则尚在动物研究阶段。探讨AD肠道微生物群的变化及其与BBB关系可为探索AD防治新靶点提供依据。     

血管性认知损害

血管性痴呆是发生在中老年人群中最常见的痴呆之一,近年来在深入研究该病防治的基础上,又提出了血管性认知损害（vascular cognitive impairment,VCI）这一新术语。认为深入研究VCI,有助于对血管性因素和血管病引起的认知损害或痴呆的理解以及早期诊断和早期治疗。本文就VCI的有关研究进展做一介绍。     

情感障碍的认知和神经运动功能损害

本文综述了情感障碍患者认知功能损害和神经运动功能损害的研究最新进展,并提出了今后研究方向。     

痴呆、轻度认知损害的电生理研究进展

痴呆(dementia)是各种原因致使脑功能障碍而产生的获得性、持续性智能障碍综合征.随着人口老龄化的加速,痴呆的早期防治已引起了诸多学者的关注,并成为当今研究的热点之一.     

老年人轻度认知功能损害的神经心理测验研究

目的;用神经心理测验研究老年人轻度认知功能损害的特点。方法;为横断面比较研究。研究对象分为两组,即有轻度认知功能损害的老年人（ＭＣＩ组）和认知功能正常的老年人（对照组,ＮＣ组）。以世界卫生组织老年认知功能介成套神经心理测验（ＷＨＯ－ＢＣＡＩ）为主要研究工具。     

酒精性认知损害的研究进展

本文就酒精性认知损害的临床特点、神经病理基础、病因和治疗康复转归等研究近况作一概述。     

Gut microbiota interacts with intrinsic brain activity of patients with amnestic mild cognitive impairment

AimsTo explore the potential relationships among gut microbiota (GM), local brain spontaneous activity, and neuropsychological characteristics in amnestic mild cognitive impairment (aMCI) patients.MethodsTwenty aMCI and 22 healthy control (HC) subjects were recruited. The GM composition was determined by 16S ribosomal RNA gene sequencing. Resting‐state functional magnetic resonance imaging scans were performed, and fractional amplitude of low‐frequency fluctuations (fALFF) was calculated across different frequencies. The Spearman or Pearson correlation analysis was used to analyze the relationship between spontaneous brain activity and cognitive function, and GM composition.ResultsaMCI patients had altered GM state and local spontaneous brain activity as compared with HC subjects. Correlation analysis showed that aMCI and HC groups had different “GM‐intrinsic brain activity interaction” patterns. In aMCI group, at the typical band (0.01‐0.08 Hz), the relative abundance (RA) of Bacteroides from phylum to genus level was negatively correlated with fALFF value of cerebellar vermis IV‐V, and the Ruminococcaceae RA was negatively correlated with fALFF values of left lenticular nucleus and pallidum. The Clostridiaceae RA and Blautia RA were positively correlated with the left cerebellum lobules IV‐V at the slow‐4 band (0.027‐0.073 Hz). The Veillonellaceae RA was positively correlated with fALFF values of left precentral gyrus at the slow‐5 band (0.073‐0.08 Hz). Correlation analysis showed that Clostridium members (Lachnospiraceae and Blautia) were positively, while Veillonellaceae was negatively, correlated with cognition test. Bacteroides was positively correlated with attention and computation, and negatively correlated with the three‐stage command score.ConclusionsaMCI patients have a specific GM‐intrinsic brain activity‐cognitive function interaction pattern.     

肠道菌群及其代谢产物与卒中后认知功能障碍相关性的研究进展

卒中后认知功能障碍（PSCI）在脑卒中患者中较为常见,影响了卒中患者的生活质量及预后,其危险因素的研究也越来越受到人们的重视。肠道菌群及其代谢产物作为近年来的研究热点之一,已被证实与中枢神经系统疾病的发生发展密切相关,尤其是脑卒中患者。有文章表明,肠道菌群及其代谢产物与早期认知功能下降及PSCI均密切相关。本文将综述肠道菌群及其代谢产物和脑卒中的相互作用机制,卒中后肠道菌群的变化,以及改变的肠道菌群和代谢产物对脑卒中及PSCI的影响,并探讨胆碱、益生菌、抗生素等在PSCI防治方面的潜在价值,为PSCI的防治提供新思路。     

Microbial lipopolysaccharide-induced inflammation contributes to cognitive impairment and white matter lesion progression in diet-induced obese mice with chronic cerebral hypoperfusion

Aims

White matter lesions (WMLs) are involved in the pathological processes leading to cognitive decline and dementia. We examined the mechanisms underlying the exacerbation of ischemia-induced cognitive impairment and WMLs by diet-induced obesity, including lipopolysaccharide (LPS)-triggered neuroinflammation via toll-like receptor (TLR) 4.

Methods

Wild-type (WT) and TLR4-knockout (KO) C57BL/6 mice were fed a high-fat diet (HFD) or low-fat diet (LFD), and subjected to bilateral carotid artery stenosis (BCAS). Diet groups were compared for changes in gut microbiota, intestinal permeability, systemic inflammation, neuroinflammation, WML severity, and cognitive dysfunction.

Results

In WT mice, HFD induced obesity and increased cognitive impairment and WML severity compared with LFD-fed mice following BCAS. HFD caused gut dysbiosis and increased intestinal permeability, and plasma LPS and pro-inflammatory cytokine concentrations. Furthermore, HFD-fed mice had higher LPS levels and higher neuroinflammatory status, including increased TLR4 expression, in WMLs. In TLR4-KO mice, HFD also caused obesity and gut dysbiosis but did not increase cognitive impairment or WML severity after BCAS. No difference was found between HFD- and LFD-fed KO mice for LPS levels or inflammatory status in either plasma or WMLs.

Conclusion

Inflammation triggered by LPS–TLR4 signaling may mediate obesity-associated exacerbation of cognitive impairment and WMLs from brain ischemia.     

Gut microbiota and gastrointestinal health: current concepts and future directions

Background  The microbial community of the human gut – the enteric microbiota – plays a critical role in functions that sustain health and is a positive asset in host defenses. In recent years, our understanding of this so‐called human ‘super organism’ has advanced, following characterization of fecal metagenomes which identified three core bacterial enterotypes, and based on basic and clinical research into the impact and consequences of microbiota biodiversity and change on gastrointestinal disorders and diseases. Purpose  This article considers current knowledge and future perspectives on the make‐up and function of human gut microbiota, with a particular focus on altered microbiota and gastrointestinal disorders, nutritional influences on the gut microbiota, and the consequences for gastrointestinal health, as well as improved understanding of gut‐microbiota–brain communication.     

Acanthopanax senticosus extract alleviates radiation-induced learning and memory impairment based on neurotransmitter-gut microbiota communication

Background

Acanthopanax senticosus (AS) is a medicinal and food plant with many physiological functions, especially nerve protection. Its extract has many functional components, including polysaccharides, flavonoids, saponins, and amino acids. Our previous study indicated that AS extract protected against nerve damage caused by radiation. However, little is known about the gut-brain axis mechanism of AS and its impact on radiation-induced learning and memory impairment.

Method

In ⁶⁰Co-γ ray-irradiated mice, we investigated the changes in behavior, neurotransmitters and gut microbiota after different days of administration of AS extract as a dietary supplement.

Results

The AS extract improved learning and memory ability in mice, and the neurotransmitter levels in the hippocampus and colon started to change from the 7th day, which accompanied changes of the gut microbiota, a decreased abundance of Helicobacter on the 7th day and an increased abundance of Lactobacillus on the 28th day. Among the marker bacteria, Ruminococcus and Clostridiales were associated with 5-HT synthesis, and Streptococcus were associated with 5-HT and ACH synthesis. In addition, the AS extract increased the tight junction protein, inhibited inflammation levels in colon, and even increased the relative protein expression of BDNF and NF-κB and decreased the relative protein expression of IκBα in the hippocampus of irradiated mice.

Conclusion

These results will lay the foundation for further study on the mechanism of the gut-brain axis of AS in preventing radiation-induced learning and memory impairment.     

Gut microbiota in brain tumors: An emerging crucial player

In recent decades, various roles of the gut microbiota in physiological and pathological conditions have been uncovered. Among the many interacting pathways between the host and gut flora, the gut–brain axis has drawn increasing attention and is generally considered a promising way to understand and treat brain tumors, one of the most lethal neoplasms. In this narrative review, we aimed to unveil and dissect the sophisticated mechanisms by which the gut-brain axis exerts its influence on brain tumors. Furthermore, we summarized the latest research regarding the gastrointestinal microbial landscape and the effect of gut–brain axis malfunction on different brain tumors. Finally, we outlined the ongoing developing approaches of microbial manipulation and their corresponding research related to neuro-malignancies. Collectively, we recapitulated the advances in gut microbial alterations along with their potential interactive mechanisms in brain tumors and encouraged increased efforts in this area.     

Conceptualization of mild cognitive impairment: a review

BACKGROUND: Several factors have prompted renewed interest in the concept of declines in cognitive function that occur in association with aging, in particular the area between normal cognition and dementia. We review the changing conceptualization of what has come to be known as mild cognitive impairment (MCI) in an effort to identify recent developments and highlight areas of controversy. METHODS: Standard MEDLINE search for relevant English-language publications on mild cognitive impairment and its associated terms, supplemented by hand searches of pertinent reference lists. RESULTS: Many conditions cause cognitive impairment which does not meet current criteria for dementia. Within this heterogenous group, termed 'Cognitive Impairment, No Dementia' (CIND), there are disorders associated with an increased risk of progression to dementia. Still, the conceptualization of these latter disorders remains in flux, with variability around assumptions about aging, the relationship between impairment and disease, and how concomitant functional impairment is classified. Amongst patients with MCI, especially its amnestic form, many will progress to Alzheimer's disease (AD). In contrast with clinic-based studies, where progression is more uniform, population-based studies suggest that the MCI classification is unstable in that context. In addition to Amnestic Mild Cognitive Impairment (AMCI), other syndromes exist and can progress to dementia. For example, an identifiable group with vascular cognitive impairment without dementia shows a higher risk of progression to vascular dementia, Alzheimer's disease and mixed dementia. CONCLUSIONS: Recent attempts to profile patients at an increased risk of dementia suggest that this can be done in skilled hands, especially in people whose symptoms prompt them to seek medical attention. Whether these people actually have early AD remains to be determined. The more narrowly defined MCI profiles need to be understood in a population context of CIND.     

晚发型抑郁障碍与轻度认知功能损害患者的认知功能差异研究

目的 探讨晚发型抑郁障碍患者与轻度认知功能损害患者的认知功能损害的差异.方法 研究对象为2012年7月～2013年8月上海市精神卫生中心老年科住院与门诊就诊符合DSM—Ⅳ诊断标准且起病年龄≥60岁的抑郁障碍患者,共26例为晚发型抑郁障碍组（LOD组）,另选择26例轻度认知功能损害的患者（MCI组）与26例正常老年人（NC组）.认知功能评估采用简明精神状态量表（MMSE）、蒙特利尔量表（MoCA）.结果 MMSE总分、MMSE分测验中计算力与注意力及MoCA总分、MoCA分测验中连线、注意、持续注意、计算、复述、延迟回忆在LOD组与MCI组差比较异无统计学意义（P＞0.05）,两组与NC组比较差异有统计学意义（P＜0.05）.三组在MMSE分测验的时间定向、延迟回忆、三步指令、书写书面指令及MoCA分测验的复制图、画钟、命名比较,MCI组均值最低,与NC组比较差异有统计学意义（P＜0.05）,与LOD组比较差异无统计学意义（P＞0.05）.结论 LOD组认知功能在注意力、延迟回忆、连线测验方面与MCI组损害程度相当.MCI组认知功能受损范围较LOD组广泛.