急性一氧化碳中毒后迟发性脑病的预后因素分析

目的探讨影响急性一氧化碳中毒后迟发性脑病（DEACMP）预后的因素。方法回顾性分析2008年7月至2011年3月在川北医学院附属医院神经内科住院的42例DEACMP患者临床资料,根据其恢复情况将患者分为无效组（n=21）和好转组（n：21）,分别比较两组患者年龄、性别、基础疾病、中毒时间、意识丧失时间、假愈期、入院时日常生活活动量表（ADL）评分、并发症、是否在急性期接受高压氧（HBO）治疗、头颅CT是否异常、头颅MRI是否异常以及是否使用神经节苷脂（GM1）、依达拉奉、多奈哌齐治疗等可能影响DEACMP预后的因素。结果年龄、假愈期、人院时ADL评分以及并发症与DEACMP患者预后相关（P〈0．05）,其中年龄和最低ADL评分更具意义（P〈0．01）,而其余因素对DEACMP患者预后无明显影响（P〉0．05）。结论年龄较大、假愈期较短、入院时ADL评分较低以及出现并发症均提示DEACMP患者预后不良,应高度警惕。     

急性一氧化碳中毒后迟发性脑病的危险因素及脑电图变化

目的 探讨急性一氧化碳(CO)中毒后迟发性脑病(DEACMP)的危险因素及脑电图变化.方法 对83例抢救成功的急性CO中毒昏迷患者按是否发生迟发性脑病分为DEACMP组(32例)和非DEACMP组(51例),比较两组年龄、性别、既往心脑血管病史评分、中毒后昏迷时间及随访期间6次EEG评分,分析DEACMP发生的危险因素.结果 与非DEACMP组比较,DEACMP组年龄、既往心脑血管病史评分、昏迷时间和6次EEG评分的差异均有统计学意义(P＜0.05～0.01).相关分析显示DEACMP发生与年龄、既往心脑血管病史评分、CO中度后昏迷时间呈正相关(r=0.311、0.435、0.631,均P＜0.01).多元逐步回归分析显示既往心脑血管病史评分、中毒后昏迷时间进入方程.DEACMP组EEG具有随假愈期好转后又恶化再缓慢改善的特点,与临床过程平行.结论 CO中毒后昏迷时间长和既往心脑血管病史为DEACMP重要危险因素;DEACMP患者EEG变化与临床过程平行.     

急性一氧化碳中毒后迟发性脑病患者血清皮质醇、促肾上腺皮质激素水平及其临床意义

目的 探讨急性一氧化碳中毒后迟发性脑病(DEACMP)患者血清皮质醇(COR)、促肾上腺皮质激素(ACTH)水平的变化及其临床意义.方法 采用酶联免疫吸附法动态检测33例DEACMP患者血清COR、ACTH的水平,并与32例急性一氧化碳(CO)中毒后未发生DEACMP患者和32例正常对照者进行比较;采用日常生活能力量表(ADL)、常识-记忆-注意测验(IMCT)、长谷川痴呆量表(HDS)动态检查DEACMP患者的病情变化.结果 DEACMP组急性期血清COR水平明显高于急性CO中毒组和正常对照组(均P＜0.05);ACTH水平明显高于急性CO中毒组(P＜0.05),与正常对照组比较无显著差异(P＞0.05).DEACMP组恢复期血清COR、ACTH水平较急性期均有不同程度的降低,但只有COR水平有显著差异(P＜0.05).DEACMP组急性期ADL、HDS、IMCT评分与恢复期比较均有显著差异(均P＜0.01).DEACMP组急性期、恢复期血清COR水平变化与HDS和ADL评分变化之间呈显著正相关(P＜0.05).结论 DEACMP患者血清COR、ACTH水平动态变化与病情变化基本一致,动态检测血清COR、ACTH水平变化可作为DEACMP病情变化和治疗效果的生物学指标之一.     

急性一氧化碳中毒后迟发性脑病预后的早期预测因素

目的探讨急性一氧化碳中毒后迟发性脑病(Delayed Encephalopathy after Acute Carbon Monoxide Poisoning DEACMP)患者一般情况、早期症状与疾病最终预后相关的因素,并筛选出预测性指标以指导早期的干预和治疗.方法收集1998年6月～2004年6月湘雅医院收治的123例DEACMP患者并随防6月,随防结束时进行ADL评分,按ADL得分情况将DEACMP患者划分为预后好和预后差2组,应用Logistic模型分析疾病最终预后的相关因素和预测因素.结果123例患者中32例预后好;非脑力劳动者且昏迷时间较短的患者预后好;最终预后好的可能性是脑力劳动者的3.33倍,昏迷时间短于72 h者是长于72者的20.17倍.结论患者是否为非脑力劳动者及急性一氧化碳中毒期昏迷时间的长短能在一定程度上预测DEACMP患者的预后.     

急性一氧化碳中毒后迟发性脑病患者血清内皮素-1、TNF-α的表达水平及其临床意义

目的 探讨血清内皮素-1(ET-1)、TNF-α的水平及其动态变化与急性一氧化碳(CO)中毒后迟发性脑病(DEACMP)患者病情变化的关系.方法 应用酶联免疫吸附法(ELISA)动态测定31例DEACMP患者血清ET-1、TNF-α水平,用日常生活能力量表(ADL)、常识-记忆-注意测验(IMCT)、长谷川痴呆量表(HDS)动态检查DEACMP患者病情变化,并与30例急性CO中毒后未发生迟发性脑病患者(急性CO中毒组)和30例同期健康体检者(正常对照组)进行比较.结果 急性CO中毒组、DEACMP组患者急性期血清ET-1、TNF-α水平明显高于正常对照组,差异均有统计学意义(P＜0.05);DEACMP组患者急性期TNF-α水平明显低于急性CO中毒组,差异有统计学意义(P＜0.05),ET-1水平与急性CO中毒组比较差异无统计学意义(P＞0.05).DEACMP患者恢复期血清ET-1水平明显低于急性期,差异有统计学意义(P＜0.05).DEACMP患者急性期ADL得分均高于常模(正常值≤20分),IMCT和HDS得分均低于常模(正常值分别为≥19分和＞16分).DEACMP患者恢复期ADL得分明显低于急性期,IMCT和HDS得分明显高于急性期,差异均有统计学意义(P＜0.05).DEACMP患者急性期和恢复期ADL、IMCT和HDS得分两两之间均有明显相关性(P＜0.05).结论 动态检测血清ET-1、TNF-α水平可以作为判定DEACMP患者病情程度的指标.     

急性脑卒中患者营养不良、卒中后并发症及不良预后的危险因素分析

目的 探讨影响急性脑卒中患者营养不良、卒中后并发症及不良预后的危险因素.方法 收集122例急性脑卒中患者的一般资料,进行营养状况和神经功能缺损程度评估.3个月后采用改良Rankin量表(mRS)评估预后.分析各因素与急性脑卒中患者营养不良、卒中后并发症及不良预后的关系.结果 随访结束时,共91例患者纳入本次研究.年龄及NIHSS评分为入院时营养不良的危险因素(P＜ 0.05～0.001);年龄、高胆固醇血症、入院营养不良、鼻饲为7d时营养不良的危险因素(P＜0.05 ～0.001).多因素Logistic回归分析显示,入院营养不良为7d发生营养不良的独立预测因素(OR=14.15,95％CI:3.32～61.76,P＜0.001).年龄、入院NIHSS评分、入院营养不良、鼻饲、7d时NIHSS评分、7d时营养不良及营养状况恶化为发生并发症的危险因素(均P＜0.01).多因素Logistic回归分析显示,入院NIHSS评分及入院营养不良为并发症的独立预测因素(OR=1.11,95％CI:1.04 ～ 1.48,P＜0.05;OR=6.56,95％CI:1.18 ～42.72,P＜0.05).年龄、入院NIHSS评分、7d时NIHSS评分、7d时营养不良及营养状况恶化为预后不良的危险因素(P ＜0.05 ～0.01).多因素Logistic回归分析显示,7d时营养不良及7d时NIHSS评分为预后不良的独立预测因素(OR =-4.32,95％CI:1.15 ～ 18.89,P＜0.05;OR=1.81,95％CI:1.21 ～2.43,P＜0.01).结论 入院营养不良为7d发生营养不良的独立危险因素,入院NIHSS评分及营养不良为并发症的独立危险因素,7d时营养不良及NIHSS评分为预后不良的独立危险因素.     

急性CO中毒迟发脑病的影响因素及MRI特点分析

目的探讨急性CO中毒迟发脑病的影响因素及MRI特点。方法回顾性分析45例急性CO中毒后昏迷病人的病例资料,按是否发生迟发脑病分为迟发脑病组(22例)和对照组(23例),比较2组临床相关资料的差异。结果迟发脑病组在年龄、昏迷时间、中毒程度、并发症、高压氧治疗时间与对照组相比差异有统计学意义(P<0.05),迟发脑病组MRI改变分为弥漫性白质病变、皮质改变及基底节神经核团改变三种,多合并存在。结论年龄、昏迷时间、中毒程度、并发症是急性CO中毒后发生DEACMP的重要影响因素,高压氧治疗对DEACMP的预防及改善预后均有一定帮助。对急性CO中毒患者,应根据每个人病情特点,结合头颅MR检查结果进行个体化评估,对一些有潜在DEACMP发病可能的病例,应积极进行规律长疗程的高压氧治疗以尽可能改善预后。     

急性一氧化碳中毒后迟发性脑病患者血清促肾上腺皮质激素释放激素水平及其临床意义

目的探讨急性一氧化碳中毒后迟发性脑病(DEACMP)患者血清促肾上腺皮质激素释放激素(CRH)水平的变化及其临床意义。方法应用酶联免疫吸附法动态测定33例DEACMP患者血清CRH水平,并与32例急性一氧化碳中毒(ACMP)后未发生DEACMP患者和32例正常对照者进行比较;采用日常生活能力量表(ADL)、常识-记忆-注意测验(IMCT)、长谷川痴呆量表(HDS)动态检查DEACMP患者的病情变化。结果 DEAC-MP组急性期血清CRH水平明显高于正常对照组(P<0.05),与ACMP组急性期比较无显著差异(P>0.05);AC-MP组急性期明显高于正常对照组(P<0.05)。DEACMP组恢复期血清CRH水平明显低于急性期(P<0.05),但仍明显高于ACMP组随访期和正常对照组(均P<0.05);ACMP组随访期血清CRH水平明显低于急性期(P<0.05),与正常对照组比较无显著差异(P>0.05)。DEACMP组急性期ADL、HDS、IMCT评分与恢复期比较均有显著差异(均P<0.05)。DEACMP组急性期、恢复期患者血清CRH水平变化与HDS评分变化之间呈显著正相关性(P<0.05)。结论下丘脑-垂体-肾上腺皮质轴参与了DEACMP的发病机制,CRH的水平变化与病情变化基本一致。     

高血压脑出血手术治疗近期预后的影响因素

目的探讨高血压脑出血手术治疗近期预后的影响因素.方法回顾经手术治疗的80例高血压脑出血的临床资料,分析性别、年龄、术前GCS评分、术前有无瞳孔异常、出血部位、出血是否破入脑室、脑实质内血肿量、手术时机、术后有无再出血9个因素对预后的影响.日常生活能力(ADL)1～3级为预后良,ADL 4～6级为预后差.结果预后良组与预后差组的术前GCS评分、术前有无瞳孔异常、出血部位、脑实质内血肿量、手术时机及术后有无再出血之间有显著性差异(P＜0.05),两组的性别、年龄及出血是否破入脑室之间无显著性差异(P＞0.05).仅术前GCS评分和术后有无再出血两个因素被引入Logistic回归方程作为影响预后的有意义因素(x2=54.820,P＜0.001).术前GCS评分与ADL分级存在负相关(rs=-0.765,P＜0.001).结论术前GCS评分和术后有无再出血是判断高血压脑出血手术治疗近期预后最具参考性的指标,系统了解影响预后的因素有助于规划治疗和估计预后.     

高血压性脑干出血的临床特点和预后分析

目的探讨高血压性脑干出血的临床特点和预后。方法对103例高血压性脑干出血患者的临床资料进行回顾性分析,以治疗或随访3个月后的日常生活活动能力(ADL)分级作为预后评价指标。采用卡方检验对可能影响患者预后的因素(包括性别、年龄、出血量、出血部位、出血破入脑室、GCS评分、瞳孔变化、并发症及收缩压和舒张压)进行单因素分析,对其中差异有统计学意义(P0.05)者采用有序多分类Logistic回归方法进行多因素分析,寻找影响患者预后的主要因素;并对出血量因素进行受试者工作特征曲线(ROC)分析。结果 103例患者预后为ADLⅠ级14例、ADLⅡ级10例、ADLⅢ级11例、ADLⅣ级15例、ADL V级7例、ADLⅥ级46例。单因素分析结果显示出血量、出血部位、出血破入脑室、GCS评分、瞳孔变化、并发症及入院时收缩压等因素差异有统计学意义(P0.05),进一步多因素分析显示出血量、出血部位和并发症是影响患者预后的重要因素(均P0.05)。ROC曲线分析显示死亡风险的出血量阈值为≤6 mL。结论高血压性脑干出血的预后较差,其预后主要取决于出血量、出血部位和并发症。     

Environmental factors in the development and progression of late-onset Alzheimer＇s disease

Late-onset Alzheimer＇s disease （LOAD） is an age-related neurodegenerative disorder characterized by gradual loss of synapses and neurons, but its pathogenesis remains to be clarified. Neurons live in an environment constituted by neurons themselves and glial cells. In this review, we propose that the neuronal degeneration in the AD brain is partially caused by diverse environmental factors. We first discuss various environmental stresses and the corresponding responses at different levels. Then we propose some mechanisms underlying the specific pathological changes, in particular, hypothalamic-pituitary adrenal axis dysfunction at the systemic level; cerebrovascular dysfunction, metal toxicity, glial activation, and Aβ toxicity at the intercellular level; and kinase-phosphatase imbalance and epigenetic modification at the intracellular level. Finally, we discuss the possibility of developing new strategies for the prevention and treatment of LOAD from the perspective of environmental stress. We conclude that environmental factors play a significant role in the development of LOAD through multiple pathological mechanisms.     

Edema and neuronal apoptosis in the hippocampus and cortex of elderly rats following transient cerebral ischemia/reperfusion injury

BACKGROUND： Previous studies of cerebral ischemia have used young animals, with an ischemic time greater than 5 minutes （safe time limit）. Despite an increased understanding of neuronal apoptosis, it remains uncertain whether brief cerebral ischemic events of 5 minutes or less damage brain tissue in elderly rodents. OBJECTIVE： To investigate the effects of transient cerebral ischemia （5 minutes）/reperfusion injury on brain cortical and hippocampal edema, aquaporin-4 （AQP-4） expression, and neuronal apoptosis in aged rats, and to compare ischemic sensitivity between cortex and hippocampus. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Institute of Cerebrovascular Disease, Qingdao University Medical School from April 2008 to March 2009. MATERIALS： Rabbit anti-AQP-4 polyclonal antibody, TUNEL kit, and SABC immunohistochemistry kit were purchased from Wuhan Boster Bioengineering, China. METHODS： A total of 160 healthy, male, aged 19-21 months, Wistar rats were randomly assigned to 4 groups： sham-surgery, and ischemia 1-, 3-, and 5-minute groups, with 40 rats in each group. The global cerebral ischemia model was established using the Pusinelli four-vessel occlusion, and the three cerebral ischemia groups were subdivided into reperfusion 12-hour, 1-, 2-, 3-, and 7-day subgroups, with 8 rats in each subgroup. The sham-surgery group was subjected to exposure of the first cervical bilateral alar foramina and bilateral common carotid arteries. MAIN OUTCOME MEASURES： The dry-wet weight assay was used to measure brain water content and histopathology of the cortex and hippocampus was observed following hematoxylin-eosin staining. In addition, cortical and hippocampal AQP-4 expression was detected by streptavidin-biotin complex immunohistochemistry, and neuronal apoptosis was detected by the TUNEL method. RESULTS： There was no significant difference in brain water content or AQP-4 expression in the cortex and hippocampus between ischemia 1- and 3-minute groups and the sham-surgery group or brain water content or AQP-4 expression in the cortex between ischemia 5-minute group and sham-surgery group （P 〉 0.05）. However, brain water content and AQP-4 expression in the hippocampus after 5 minutes of cerebral ischemia were significantly increased compared with the sham-surgery group （P 〈 0.05 or P 〈 0.01）. Several TUNEL-positive cells were observed in the cortex and hippocampus of the sham-surgery group and ischemia 1-minute group, as well as in the cortex of the ischemia 3-minute group. In addition, the number of apoptotic neurons in the hippocampus of ischemia 3-minute group and in the cortex and hippocampus of ischemia 5-minute group was significantly increased （P 〈 0.05 or P 〈 0.01 ）. Neuronal apoptosis was increased after 12 hours of ischemia/reperfusion, and it reached a peak by 2 days （P 〈 0.01）. CONCLUSION： Transient cerebral ischemia （5 minutes） resulted in increased hippocampal edema, AQP-4 expression, and neuronal apoptosis. Moreover, cerebral ischemia had a greater effect on neuronal apoptosis than brain edema or AQP-4 expression, and the hippocampus was more sensitive than the cortex.     

高血压脑出血的显微外科治疗进展

高血压脑出血（Hypertensive intrac-rebral hemorrhage,HICH）是具有高发病率、高病死率、高致残率的急性脑血管疾病,占所有脑卒中患者的10%-20%,早期病死率可高达49.4%。随着人口老龄化,其发病率逐年提高;而外科手术的干预,使其病死率有所下降,但致残率居高不下。如何提高手术疗效和患者生存质量,一直是神经外科医师努力的方向。微侵袭血肿清除术因其手术创伤小,恢复快,是目前国内治疗高血压脑出血的重要手段。     

神经内镜联合亚低温治疗高血压基底节区脑出血

目的 探讨神经内镜联合亚低温在治疗高血压基底节区脑出血中的临床应用价值.方法 回顾性分析我院神经内镜治疗高血压基底节区脑出血患者40例的临床资料,并对治疗结果进行分析.结果 神经内镜治疗组22例(甲组),神经内镜联合亚低温治疗组18例(乙组),术后3个月根据GCS评分,甲组恢复良好1例,中残4例,重残6例,植物生存6例,死亡5例;乙组恢复良好4例,中残8例,重残3例,植物生存1例,死亡2例,两组比较差异有统计学意义(P＜0.05).两组颅内压比较第1天两者差异不明显,但第2、3天亚低温组颅内压明显降低.结论 神经内镜是治疗高血压基底节区脑出血较为有效的手术方式,联合亚低温治疗能有效降低颅内压,改善术后神经功能恢复,具有较好的临床应用价值.     

Total saponins of Panax ginseng effects on proliferation and differentiation of human embryonic neural stem cells and in a Parkinson’s disease mouse model

BACKGROUND： Total saponins of Panax ginseng （TSPG） exhibits neuroprotection against Parkinson＇s disease in the substantia nigra. OBJECTIVE： To investigate the effects of TSPG on human embryonic neural stem cells （NSCs） proliferation and differentiation into dopaminergic neurons using in vitro studies, and to observe NSC differentiation in a mouse model of Parkinson＇s disease, as well as behavioral changes before and after transplantation. DESIGN, TIME AND SETTING： In vitro neural cell biology trial and in vivo randomized, controlled animal trial were performed at the Institute of Basic Medical Sciences, Chongqing Medical University between September 2004 and December 2007. MATERIALS： TSPG （purity 〉 95%） was isolated, extracted, and identified by Chongqing Academy of Chinese Materia Medica. Recombinant human basic fibroblast growth factor （bFGF） and recombinant human epidermal growth factor （EGF） were purchased from PeproTech, USA. A total of 25 C57/BL6J mice, aged 18-20 weeks were included. Twenty were used to establish a Parkinson＇s disease model with i.p. injection of MPTP （1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine） and TSPG alone or combined with interleukin-1 （IL-1）-treated NSCs prior to transplantation into the corpus striatum. The remaining five mice were pretreated for 3 days with TSPG prior to MPTP injection, serving as the TSPG prevention group. METHODS： Primary NSCs were isolated, cultured and purified from embryonic cerebral cortex. Immunocytochemistry was employed to detect specific antigen expression in the NSCs. In vitro experiment： （1） to induce proliferation, NSCs were treated with TSPG, EGF＋bFGF, or TSPG＋EGF＋bFGF, respectively; （2） to induce dopaminergic neuronal differentiation, NSCs were treated with TSPG, IL-1, or TSPG＋IL-1, respectively. MAIN OUTCOME MEASURES： In vitro experiment： the effects of TSPG on NSCs proliferation were evaluated with flow cytometry and MTT assay. Tyrosine hydroxylase expression was determined by immunocytochemistry assay to observe effects of TSPG on dopaminergic neuronal differentiation. In vivo experiment： differentiation of grafted NSCs in the mouse brain was determined by immunohistochemical staining. Behavioral changes were evaluated by spontaneous activity frequency, memory function, and score of paralysis agitans. RESULTS： （1） NSCs were cultured and passaged for more than three passages. Immunocytochemistry revealed positive nestin staining, as well as neurofilament protein and glial fibrillary acidic protein. （2） TSPG significantly increased NSC proliferation, in particular when combined with EGF and bFGF, which was twice as effective as FGF or bFGF alone. TSPG also induced dopaminergic differentiation in NSCs, in particular when TSPG was added together with IL-1, resulting in an effect five times greater than that of IL-1 alone. （3） At day 30 following transplantation, most NSCs in the TSPG prevention group differentiated into dopaminergic neurons, and the scores of paralysis agitans, spontaneous activity, and memory function were significantly increased compared with TSPG alone or TSPG＋IL-1 groups （P 〈 0.05）. CONCLUSION： TSPG stimulated NSC proliferation, in particular when combined with FGF and bFGF. TSPG significantly induced dopaminergic neuronal differentiation of NSCs, and the effect was greater when combined with IL-1. In addition, TSPG greatly improved behavior in the Parkinson＇s disease mouse model following NSC transplantation. Following NSC transplantation, TSPG pretreatment exhibited superior efficacy over either TSPG alone or TSPG in combination with IL-1, in terms of behavioral improvements in the Parkinson＇s disease mouse model.     

阿尔茨海默病治疗的研究进展

阿尔茨海默病（AD）是一种隐匿性起病,进行性恶化的神经退行性疾病,临床最初表现为认知功能障碍,并有可能在5～10年内完全衰退。患者往往伴随严重的记忆力丧失、精神行为异常、人格改变、言语功能障碍,无法独立生活,最终近乎于植物状态。Ferri等采用DISMOD软件在全球60岁以上人群中估计,全球的痴呆患者人数到2040年将达到8llO万左右。     

墨蝶呤还原酶基因与精神分裂症相关性的研究进展

墨蝶呤还原酶（SPR）催化四氢生物蝶呤（BH4）从头合成途径的最后一步反应。SPR基因遗传缺陷或突变可导致BH。的合成紊乱,影响单胺类神经递质（如多巴胺、5-羟色胺及谷氨酸等）的合成或释放,进而参与包括精神分裂症在内的多种神经精神系统疾病的发生发展过程。此外,SPR基因敲除小鼠表现出持续增强的自主活动等类精神分裂症症状,说明该基因在精神分裂症的发病中扮演重要的角色。进一步研究SPR基因及其单核苷酸多态性的功能,可为阐明精神分裂症的发病机制提供重要的线索,也为新一代抗精神病药物的研制及开发开拓新的视野。现对SPR基因与精神分裂症的相关研究做一综述。     

Targeting 13-secretase with RNAi in neural stem cells for Alzheimer＇s disease therapy

There are several major pathological changes in Alzheimer＇s disease, including apoptosis of cho- linergic neurons, overactivity or overexpression of 13-site amyloid precursor protein cleaving enzyme 1 （BACE1） and inflammation. In this study, we synthesized a 19-nt oligonucleotide targeting BACE1, the key enzyme in amyloid beta protein （AI3） production, and introduced it into the pSilenCircle vector to construct a short hairpin （shRNA） expression plasmid against the BACE1 gene. We transfected this vector into C17.2 neural stem cells and primary neural stem cells, resulting in downregulation of the BACE1 gene, which in turn induced a considerable reduction in reducing AI3 protein production. We anticipate that this technique combining cell transplantation and gene ther- apy will open up novel therapeutic avenues for Alzheimer＇s disease, particularly because it can be used to simultaneously target several pathogenetic changes in the disease.     

Disrupted structural and functional brain connectomes in mild cognitive impairment and Alzheimer＇s disease

Alzheimer＇s disease （AD） is the most common type of dementia, comprising an estimated 60-80% of all dementia cases. It is clinically characterized by impairments of memory and other cognitive functions. Previous studies have demonstrated that these impairments are associated with abnormal structural and functional connections among brain regions, leading to a disconnection concept of AD. With the advent of a combination of non-invasive neuroimaging （structural magnetic resonance imaging （MRI）, diffusion MRI, and functional MRI） and neurophysiological techniques （electroencephalography and magnetoencephaJography） with graph theoretical analysis, recent studies have shown that patients with AD and mild cognitive impairment （MCI）, the prodromal stage of AD, exhibit disrupted topological organization in large-scale brain networks （i.e., connectomics） and that this disruption is significantly correlated with the decline of cognitive functions. In this review, we summarize the recent progress of brain connectomics in AD and MCI, focusing on the changes in the topological organization of large-scale structural and functional brain networks using graph theoretical approaches. Based on the two different perspectives of information segregation and integration, the literature reviewed here suggests that AD and MCI are associated with disrupted segregation and integration in brain networks. Thus, these connectomics studies open up a new window for understanding the pathophysiological mechanisms of AD and demonstrate the potential to uncover imaging biomarkers for clinical diagnosis and treatment evaluation for this disease.