Background: Aging is the primary risk factor for the onset of Alzheimer's disease (AD). Inflammaaging is a major feature in the process of aging, and the chronic neuroinflammation caused by inflamma-aging is closely related to AD. As the main participant of neuroinflammation, the polarization of microglia (MG) could influence the development of neuroinflammation. Objective: This study aims to observe the impact of YHD on microglia (MG) polarization and neuroinflammation to delay the onset and progression of AD. Methods: In vivo experiment, four-month senescence accelerated mouse prone 8 (SAMP8) were used as the model group, the SAMR1 mice of the same age were used as the control group. In YHD group, 6.24 g/kg YHD was intragastrically administrated continuously for 12 weeks, and Ibuprofen 0.026 g/kg in positive control group. Morris Water Maze test was used to evaluate the learning and memory ability, Nissl's staining and immunofluorescence double staining for neuron damage and MG M1/M2 polarization, Enzyme-Linked Immunosorbent Assay (ELISA) for neuroinflammation biomarkers in hippocampus, Western blot for key protein expression of TREM2/NF kappa B signaling pathway. In vitro experiments, 10 mu M/l A(31-42 induced BV-2 cell model was used to re-verify the effect of YHD regulating MG polarization to reduce neuroinflammation. Also, TREM2 small interfering RNA (siRNA) was used to clarify the key target of YHD. Results: YHD could improve the learning and memory ability of SAMP8 mice evaluated by the Morris Water Maze test. Like Ibuprofen, YHD could regulate the M1/M2 polarization of MG and the levels of neuroinflammatory markers TNF-alpha and IL-10 in hippocampus, and relieve neuroinflammation and neuron loss. In addition, YHD could also regulate the expression of PU.1, TREM2, p-NF-kappa B P65 in the TREM2/NF-kappa B signaling pathway. Further in vitro experiments, we found that YHD had a significant regulatory effect on A(31-42-induced BV-2 cell polarization, and it could significantly increase PU.1, TREM2, decrease p-NF-kappa B P65, p-IKK(3, TNF-alpha, IL-6, IL-1(3. At the same time, using siRNA to inhibit TREM2, it proved that TREM2 was a key target for YHD to promote A(31-42-induced BV-2 cell M2 polarization to reduce neuroinflammation. Conclusions: YHD could regulate the TREM2/NF-kappa B signaling pathway through TREM2, thereby to adjust MG polarization and reduce AD-related neuroinflammation.

目的 研究轻度老年性痴呆患者日常生活能力与中医证候相关性.方法 应用统计软件进行多重线性回归,以ADL量表及分项为因变量,中医常见症状为自变量,选择逐步回归法,探索影响日常生活能力的主要中医常见症状.结果 研究发现ADL量表评分与善误、腰膝酸软、行动迟缓最为相关.ADL使用工具能力与善误、行动迟缓最为相关.ADL生活自理能力与善误、行动迟缓、腰膝酸软最为相关.ADL室内活动能力与行动迟缓最为相关.ADL日常生活能力与善误、腰膝酸软、行动迟缓最为相关.ADL饮食能力与反应迟钝、少言寡语最为相关.结论 轻度老年性痴呆患者日常生活能力与中医症状密切相关,从肾论治老年性痴呆结合中医康复提高患者日常生活能力具有很好的临床价值.

目的:观察益肾化浊方对快速老化小鼠亚系 8(SAMP8)小鼠谷氨酸受体2(GluR2)内化作用的影响,探讨其改善阿尔茨海默病学习记忆能力的作用机制.方法:采用激光共聚焦、蛋白质印迹法(Western Blotting)和免疫共沉淀检测小鼠海马神经元突触后膜GluR2 相对表达量,相关蛋白的表达以及各蛋白间相互结合情况.结果:经益肾化浊方干预后,SAMP8 小鼠突触后膜GluR2 含量较前增多,降低了谷氨酸受体2L-丝氨酸(GluR2 Ser880)蛋白水平,提高了AMPA受体结合蛋白(ABP)、谷氨酸受体结合蛋白(GRIP)水平,同时促进了GluR2-N-乙基马来酰亚胺敏感因子(NSF)结合,抑制了GluR2-转接蛋白复合物(AP2)结合.结论:益肾化浊方可抑制SAMP8 小鼠AMPA受体GluR2 内化作用,该作用与减轻GluR2 磷酸化和上调内化抑制蛋白GRIP、ABP的表达,促进GluR2-NSF的结合,减少GluR2-AP2 的结合有关.

中医脑络与大脑微循环在分布、走行、吻合等特点上有相似之处,功能上脑络可以运载营卫气血,营养脑髓,为脑的活动提供物质基础,这与现代医学中大脑微循环调节脑部血流量、维持脑组织功能的作用相对应.病理上,脑梗死在中医学中“脑络瘀阻”的病理改变与现代医学所指因大脑微循环障碍导致的缺血缺氧状态具有一定的相似性.在脑梗死的治疗中,采用益气活血通络法、活血化瘀通络法、开窍醒神通络法皆可有效促进脑梗死患者脑血流恢复,改善脑梗死后大脑微循环障碍.因此,中医学中“通络”可部分解释为改善大脑微循环障碍.

目的:观察益肾化浊方对快速老化模型小鼠(SAMP8小鼠)学习记忆能力、神经元突触效能和突触AMPA受体亚基GluR1含量的影响,探讨益肾化浊方治疗阿尔茨海默病的作用机制.方法:将40只7月龄SAMP8小鼠随机分为模型组和益肾化浊方组,每组各20只,同时选取同月龄抵抗快速老化小鼠(SAMR1小鼠)20只作为对照组.益肾化浊方组小鼠每日按6.24 g/kg的剂量予益肾化浊方水煎液灌胃1次,对照组和模型组小鼠每日给予等量蒸馏水灌胃1次.各组小鼠连续灌胃4周后,通过Morris水迷宫实验检测学习记忆能力,利用透射电子显微镜观察小鼠海马CA1区神经元和突触超微结构变化,并用激光共聚焦显微镜观察小鼠海马突触后膜上GluR1的含量.结果:Morris水迷宫实验显示,与对照组比较,模型组小鼠逃避潜伏期明显延长、穿越平台次数明显减少,差异有统计学意义(P＜0.05);与模型组比较,益肾化浊方组小鼠逃避潜伏期明显缩短、穿越平台次数明显增加,差异有统计学意义(P＜0.05).透射电子显微镜观察发现,与模型组比较,益肾化浊方组小鼠神经元细胞核呈椭圆形,核膜尚清晰完整,染色质细腻,核仁明显,细胞器病变改善;突触前膜、后膜结构尚清晰可见,突触间隙明显.激光共聚焦显微镜观察发现,对照组小鼠海马神经元突触后膜的GluR1含量丰富,模型组含量极少,益肾化浊方组含量较模型组增加.结论:益肾化浊方可通过促进AMPA受体亚基GluR1的表达,调控神经元细胞“胞吐-内化”过程,有效保护神经元和突触超微结构的完整性,改善SAMP8小鼠突触传递效能,进而改善其学习记忆能力.

Background: Studies have found that autophagy could promote the clearance of Aβ. To promote and maintain the occurrence of autophagy in Alzheimer's disease (AD) might be a potential way to reduce neuronal loss and improve the learning and memory of AD. Objective: To investigate the possible mechanisms of Yishen Huazhuo Decoction (YHD) against AD model. Methods: Forty 7-month-old male SAMP8 mice were randomly divided into model (P8) group and YHD group, 20 in each group, with 20 SAMR1 mice as control (R1) group. All mice were intragastrically administered for 4 weeks, YHD at the dosage of 6.24g/kg for YHD group, and distilled water for P8 group and R1 group. Morris water maze (MWM) test, Nissl’s staining, TEM, TUNEL staining, immunofluorescence double staining, and western blot analysis were applied to learning and memory, structure and ultrastructure of neurons, autophagosome, apoptosis index, Aβ, LAMP1, and autophagy related proteins. Results: The escape latency time of YHD group was significantly shorter on the 4th and 5th day during MWM test than those in P8 group (P=0.011, 0.008<0.05), and the number of crossing platform in YHD group increased significantly (P=0.02<0.05). Nissl’s staining showed that the number of neurons in YHD group increased significantly (P<0.0001). TEM showed in YHD group, the nucleus of neurons was slightly irregular, with slightly reduced organelles, partially fused and blurred cristae and membrane of mitochondria. The apoptosis index of YHD group showed a decreasing trend, without statistically significant difference (P=0.093>0.05), while Caspase3 expression in YHD group was significantly lower (P=0.044<0.05). YHD could promote the clearance of Aβ1-42 protein, improve the expression of Beclin-1 and p-Bcl2 proteins, reduce mTOR and p62 proteins. Conclusions: YHD could induce autophagy initiation, increase the formation of autophagosomes and autolysosome, promote the degradation of autophagy substrates, thereby to regulate autophagy, thereby to promote the clearance of Aβ1-42 to improve memory impairment in SAMP8 mice.

[目的]初步了解临床中成人不寐患者的一般情况、睡眠情况及中医证候特征与规律.[方法]利用研制的成人不寐中医证候临床流行病学调查问卷和匹兹堡睡眠质量指数(PSQI)对2017年8月—2018年2月以不寐为主诉的成人患者进行预调查,用Excel建立数据库,并运用SPSS及Modeler进行统计分析.[结果]共回收有效问卷75份,其中被调查者66.67％为女性,平均(56.20±14.19)岁,以60～79岁年龄的人数最多,61.33％的患者是高中及以上学历,44％的患者是脑力劳动为主者;76％的患者有既往病史,涉及43个疾病.90.67％的患者为慢性不寐,81.33％为入睡困难,92％为混合型不寐,PSQI(15.12±3.22)分.73.33％患者的病因病机是情志失调,37个常见中医症状,30.67％属心脾两虚证.[结论]本次预调查的成人不寐患者以女性、老年人、脑力劳动者为主,文化程度较高,常伴有多种内科疾病;以慢性病程为主,以入睡困难者最多,多为混合型不寐;最主要的病因病机是情志失调,常见中医症状除睡眠相关主症外,常伴随精神情绪及日间功能下降症状,证候类型以心脾两虚最多.

Background and purpose Tianzhi granule (TZ) is usually used for patients with vascular dementia (VaD) in China. The aim was to assess the effect of TZ by a randomized clinical trial (RCT). Methods A 24-week RCT was conducted in 16 centres. Participants were grouped into TZ, donepezil or placebo. The co-primary outcomes were the Vascular Dementia Assessment Scale-cognitive subscale (VADAS-cog) and Clinician's Interview-based Impression of Change-plus caregiver information (CIBIC-plus). Results A total of 543 patients with mild to moderate VaD were enrolled, of whom 242 took TZ granules, 241 took donepezil, and 60 took placebo. The least-squares mean changes from baseline and 95% CI were 6.20 (5.31, 7.09) (TZ group), 6.53 (5.63, 7.42) (donepezil group) and 3.47 (1.76, 5.19) (placebo group), both TZ and donepezil showed small but significantly improvement compared with placebo group. The percent of improvement on the global impression which was measured by CIBIC-plus was 73.71% in TZ and 58.18% in placebo, there was significant different between TZ and placebo group (P = 0.004). No significant differences were observed between TZ and donepezil. No significant differences of adverse events were found. Conclusions TZ and donepezil could bring symptomatic benefit for mild to moderate VaD. Trial registration The protocol had retrospectively registered at clinical trial.gov, Unique identifier: NCT02453932, date of registration: May 27, 2015; https://www.clinicaltrials.gov/ct2/show/NCT02453932?term=NCT02453932&rank=1

目的 通过收集整理文献,采用关联规则对针刺治疗血管性痴呆的配伍规律进行研究.方法 在数据库中检索针刺治疗血管性痴呆的中英文临床研究文献,经筛选后对使用穴位进行提取,采用SPSS Statistics17.0和SPSS Model-er14.10对数据进行关联规则分析.结果 文献中共使用穴位90个,其中使用频次在10次以上的穴位共23个.关联规则结果显示,置信度在90％以上的配伍组合有20组,以上下配穴和局部配穴为主.结论 基于关联规则的针刺治疗血管性痴呆的配伍规律研究是可行的,研究结果可作为依据服务于临床.

目的 观察益肾化浊方对快速老化小鼠SAMP8海马β淀粉样蛋白( Aβ)和磷酸化tau( p-tau)蛋白表达及肝肾功能的影响.方法 将7月龄SAMP8随机分成SAMP8组、益肾化浊方(YSHZ)组,选择抗快速老化小鼠SAMR1作为对照;益肾化浊方按照6. 24 g/kg灌胃干预,SAMR1组和SAMP8组给予等体积的蒸馏水,每日灌胃1次,持续4 w;治疗后采用免疫组化法检测海马CA1区Aβ和p-tau蛋白表达,酶联免疫吸附试验(ELISA)检测血清天门冬氨酸氨基转移酶( AST)、谷丙转氨酶(ALT)水平、肌氨酸氧化酶法检测血清肌酐(Cr)水平、二乙酰-肟法检测血清尿素氮(BUN)水平.结果 与SAMR1组比较, SAMP8、YSHZ组Aβ、p-tau表达量、ALT水平显著升高(P<0. 05),AST水平显著降低( P<0. 05),Cr、BUN水平无显著变化( P>0. 05);与SAMP8组比较,YSHZ组Aβ、p-tau表达量显著降低(P<0. 05),ALT、AST、Cr、BUN水平无显著变化( P>0. 05).结论 YSHZ可降低7月龄SAMP8海马CA1区Aβ和p-tau的表达,从而减轻两者的神经毒性作用,对肝肾功能未出现明显的损伤作用.

目的:观察针灸治疗带状疱疹后遗神经痛的临床疗效.方法:将64例带状疱疹后遗神经痛患者随机分为治疗组和对照组,每组各32例,治疗组采用针灸治疗,对照组单用针刺治疗.结果:总有效率治疗组为93.75％,对照组为87.50％,组间比较,差异有统计学意义(P＜0.05);2组NRS评分治疗前后组内比较及治疗后组间比较,差异均有统计学意义(P＜0.05).结论:针灸治疗带状疱疹后遗神经痛疗效优于单纯针刺治疗.

目的 观察益肾化浊方对SAMP8小鼠学习记忆能力和海马CA1区神经元、肿瘤坏死因子-α(TNF-α)、核因子-κB(NF-κB)表达的影响,探讨其可能的作用机制.方法 将7月龄SAMP8小鼠随机分为SAMP8组和益肾化浊方低、中、高剂量组,选择SAMR1小鼠作为对照;益肾化浊方低、中、高剂量组分别给予3.12、6.24、12.48 g/kg益肾化浊方药液灌胃,SAMR1组和SAMP8组给予等体积蒸馏水灌胃,每日1次,连续4周;采用Morris水迷宫实验评价小鼠学习记忆能力,尼氏染色观察小鼠海马CA1区神经元变化,免疫组化检测小鼠海马CA1区TNF-α和NF-κB的表达.结果 水迷宫实验结果显示,各组小鼠平均游泳速度差异无统计学意义(P>0.05);与SAMR1组比较,SAMP8组小鼠逃避潜伏时间显著增加、穿越平台次数显著减少(P<0.05);与SAMP8组比较,益肾化浊方中剂量组小鼠逃避潜伏时间显著减少、穿越平台次数显著增加(P<0.05).尼氏染色结果显示,与SAMR1组比较,SAMP8组小鼠海马CA1区神经元数量显著减少(P<0.05);与SAMP8组比较,益肾化浊方中剂量组小鼠海马CA1区神经元数量显著增加(P<0.05).免疫组化染色结果显示,与SAMR1组比较,SAMP8组小鼠海马CA1区TNF-α和NF-κB表达显著增加(P<0.05);与SAMP8组比较,益肾化浊方中剂量组小鼠海马CA1区TNF-α和NF-κB表达显著减少(P<0.05).结论 中剂量益肾化浊方可有效改善7月龄SAMP8小鼠学习记忆能力,该作用机制可能与其减少海马CA1区神经元丢失、抑制炎症因子TNF-α、NF-κB的表达有关.

快速老化小鼠是一种在生命早期即出现身体各部位功能衰老现象的鼠系,且不同亚系的病理特征各异.不同亚系小鼠的病理表现多与人类衰老的病理学特征相似,因此常用于老年病相关实验的动物模型,如骨质疏松症、阿尔茨海默病、神经退行性病变等.中医药具有多途径、多靶点的作用优势,在老年性疾病的治疗中发挥着重要作用.近年来,越来越多的中医药防治老年性疾病的基础研究选择SAM系小鼠作为研究模型,有助于揭示中药的作用机制.现将不同亚系的SAM小鼠特征及其在中医药治疗老年病作用机制研究中的应用现状进行简要概述.

OBJECTIVETo explore the acupoint selection rules of acupuncture for Alzheimer's disease (AD) in modern clinical practice by complex network technology.METHODSThe relevant articles of clinical trials were retrieved from CNKI published before December 2017. Using Microsoft Excel 2010, the database was established. Using Gephi 0.8.2 software, the complex network mode was built and its topological structure was analyzed.RESULTSFinally, 81 articles were eligible and 114 acupoint prescriptions were extracted. The constructed complex network of acupoint prescriptions for AD was characteristics as small world effect and scale-free property, the crucial acupoints included Baihui (GV 20), Sishencong (EX-HN 1), Fengchi (GB 20), Yintang (GV 29), Shenmen (HT 7), Shenting (GV 24), Zusanli (ST 36), Fenglong (ST 40) and Taichong (LR 3). In acupoint combination, Baihui (GV 20), Neiguan (PC 6), Shenmen (HT 7) and Sanyinjiao (SP 6) were the most common, and the combination of the distal and nearby points was predominant. Using k-core for acupoint optimization, 29 core acupoints were screened and they were mostly located on the governor vessel and the head and neck, with the highest use frequency. 82.76% of acupoints were specific acupoints and the influential points were dominant. Using community structure partition, these acupoints were classified into two groups, i.e. deficiency syndrome and excess syndrome.CONCLUSIONThe selection of local acupoints is the first choice in acupuncture treatment for AD. The combination of distal and nearby points is the most common and the special points are the core. In clinical practice, the great consideration is provided on mind regulation, integration of disease and symptoms, the mutual treatment of the primary and the secondary as well as the deficiency and the excess.

目的 制订成人不寐中医证候临床流行病学调查问卷.方法 回顾中国知网(CNKI)相关文献,归纳整理不寐中医病因病机、四诊信息、中医证候及证候要素;将所得信息条目池制订专家咨询表进行2轮专家咨询,并结合专家意见形成成人不寐中医证候调查问卷;通过临床预调查及信度与效度的初步检验形成正式调查表.结果 成人不寐中医证候流行病学调查问卷包括病因病机7条、中医四诊信息236项、中医证型17个、证候要素12条,临床预调查显示具有较好的可操作性,信度分析克朗巴赫α系数为0.933,建构效度分析KMO检验为0.614,Bartlett球形检验P ＜0.01,结果显示具有较高的可靠性和一定的有效性,由此最终建立流行病学调查表.结论 该调查问卷具有一定的临床应用价值,为今后深入开展成人不寐中医证候流行病学调查奠定基础.

OBJECTIVE:To observe the effect of electroacupuncture (EA) on neurological behavior and activity of Toll-like receptor 2 / nuclear factor kappa B (TLR2/NF-κB) signaling of the ischemic cerebral area in cerebral ischemia-reperfusion injury (CIRI) rats, so as to explore its mechanisms underlying improvement of CIRI. METHODS:A total of 120 male SD rats were randomly divided into blank control, sham operation, model, EA and EA＋NF-κB inhibitor (Pyrrolidine Dithiocarbamate Hydrochloride, PDTC, EA＋PDTC) groups which were further divided into 3, 7, 14 and 28 d subgroups (n＝6 in each subgroup). The CIRI model was established by occlusion of the middle cerebral artery for 90 min, followed by reperfusion. EA (1－20 Hz, 6 V) was applied to "Shuigou" (GV26), "Neiguan" (PC6), "Sanyinjiao" (SP6) and "Weizhong" (BL40) for 30 min, once a day for 28 days. For rats of the EA＋PDTC group, PDTC solution (120 mg/kg) was intraperitoneally injected on the 3rd day after successful modeling and before EA intervention. The neurological deficit severity (Zea Longa score) was assessed 3, 7, 14 and 28 days after modeling. The expression levels of TLR2, Interleukin-1 receptor-associated kinase (IRAK) and NF-κB mRNAs in the ischemic penumbra region of brain tissue were detected by real-time fluorescence quantitative PCR. RESULTS:Following modeling, the neurological deficit scores were significantly increased from the 3rd day on after CIRI (P<0.05), the expression levels of TLR2 mRNA on day 3, 7, 14 and 28, and IRAK mRNA on day 3 and 7, as well as NF-κB mRNA on day 3, 7 and 14 were significantly up-regulated in the model group relevant to the blank control group (P<0.05). After EA intervention, the neurological deficit scores were significantly decreased in the EA group on day 3, 7 and 28 and in the EA＋PDTC group on day 3, 7, 14 and 28 in comparison with those of the model group (P<0.05). In addition, the expression levels of TLR2 mRNA and NF-κB mRNA on day 3, 7 and 14 in the EA group, and on day 3, 7, 14 and 28 in the EA＋PDTC group, IRAK mRNA on day 3 in the EA and EA＋PDTC group were significantly down-regulated (P<0.05), but those of IRAK mRNA on day 14 and 28 in the EA group were significantly up-regulated in comparison with those of the model group (P<0.05). The effect of the EA＋PDTC was obviously superior to that of simple EA in down-regulating the expression of TLR2 (on day 28), and IRAK (on day 3, 14, 28), and NF-κB (on day 3, 7 and 14) (all P<0.05). CONCLUSION:EA stimulation can improve the symptoms of neurological deficits in CIRI rats, which may be related to its effect in suppressing the expression of TLR2, NF-κB and IRAK mRNAs of the ischemic cerebral tissue, i．e., down-regulating the activity of TLR2/NF-κB signaling.

目的 观察益肾化浊方对AD模型大鼠海马区Ca2浓度及钙相关记忆蛋白表达的影响,初步探讨益肾化浊方治疗AD的部分作用机制.方法 将30只雄性SD大鼠随机分为假手术组,模型组和益肾化浊方组.采用右侧侧脑室注射Aβ25-35建立AD模型,造模成功后益肾化浊方组大鼠按照4.32g·kg-1·d-1剂量给予药液灌胃,假手术组和模型组给予等体积蒸馏水灌胃,持续4周.采用Rhod 2-AM荧光探针法和Western blot检测各组大鼠海马区突触Ca2+浓度及CaMKⅡ、NR2B、CREB、BDNF和TrkB蛋白的表达.结果 (1)Rhod 2-AM荧光探针法检测结果显示:与假手术组比较,模型组大鼠钙离子浓度显著升高(P＜0.01);与模型组相比,益肾化浊方组钙离子浓度显著减低(P＜0.01),差异具有统计学意义.(2)Western blot检测结果显示:与假手术组比较,模型组大鼠海马区NR2B、CaMKⅡ、CREB、BDNF和TrkB蛋白的表达显著降低(P＜0.01);与模型组比较,益肾化浊方组NR2B、CaMKⅡ、CREB、BDNF和TrkB蛋白显著升高(P＜0.01),差异具有统计学意义.结论 益肾化浊方治疗AD的作用机制可能与调节海马突触体内Ca2+浓度,减轻Aβ诱发的神经毒性;同时增加钙相关记忆蛋白的表达有关.

BACKGROUND:Abnormal amyloid β (Aβ) accumulation and deposition in the hippocampus is an essential process in Alzheimer's disease (AD).OBJECTIVE:To investigate whether Oleanolic acid (OA) could improve memory deficit in AD model and its possible mechanism.METHODS:Forty-five SD rats were randomly divided into sham operation group, model group, and OA group. AD models by injection of Aβ25-35 were built. Morris water maze (MWM) was applied to investigate learning and memory, transmission electron microscope (TEM) to observe the ultrastructure of synapse, western blot to the proteins, electrophysiology for long-term potentiation (LTP), and Ca2+ concentration in synapse was also measured.RESULTS:The latency time in model group was significantly longer than that in sham operation group (P=0.0001); while it was significantly shorter in the OA group than that in model group (P=0.0001); compared with model group, the times of cross-platform in OA group significantly increased (P=0.0001). TEM results showed OA could alleviate neuron damage and synapses changes induced by Aβ25-35. The expressions of CaMKII, PKC, NMDAR2B, BDNF, TrkB, and CREB protein were significantly improved by OA (P=0.0001, 0.036, 0.041, 0.0001, 0.0001, 0.026, respectively) compared with that in model group; the concentration of Ca2+ was significantly lower in OA group (1.11±0.42) than that in model group (1.68±0.18); and the slope rate (P=0.0001) and amplitude (P=0.0001) of f- EPSP significantly increased in OA group.CONCLUSION:The present results support that OA could ameliorate Aβ-induced memory loss of AD rats by maintaining synaptic plasticity of the hippocampus.

肾是人体最为重要的脏腑之一,肾之所以重要与肾所化生和闭藏之物——“肾精”有密切关系,肾中精气作为构成人体最基本的物质基础,其盛衰直接影响人体生命的全过程.从某种程度上来说,肾精与干细胞在来源、分布、功能上具有相近之处,肾精的物质基础主要或部分体现为干细胞及其功能,肾精亏虚导致的老年性痴呆(AD),势必影响到神经干细胞及其功能.文章以“肾-痴呆-千细胞”为主线,逐层揭示三者之间的关系,探寻中医基础理论与现代医学科学融合与渗透的契合点,以期为AD的防治提供新的理论依据.

目的 探讨轻度阿尔茨海默病(AD)患者认知功能与日常生活能力(ADL)的临床特点及相关性.方法 采用描述性分析方法对144例轻度AD患者的认知评定量表(ADAS-cog)与ADL量表进行分析,并以ADL作为因变量,ADAS-cog分项为自变量进行逐步法多重线性回归分析.结果 轻度AD患者ADAS-cog量表12项条目池中,144例全部出现"单词辨认"异常,其他异常条目出现频次较高的依次为单词回忆、回忆测验、定向力、注意力;评分较高的异常分项为单词辨认、单词回忆、定向力.患者ADL主要以工具性ADL(IADL)异常为主.认知功能与ADL最相关异常分项为定向力和单词回忆.结论 轻度AD主要以近期记忆力、定向力及IADL减退为主;患者ADL减退与近期记忆力、定向力的损害最为密切.