ABSTRACT:Hypertension is a primary risk factor for the progression of cognitive impairment caused by cerebral small vessel disease, the most common cerebrovascular disease. However, the causal relationship between hypertension and cerebral small vessel disease remains unclear. Hypertension has substantial negative impacts on brain health and is recognized as a risk factor for cerebrovascular disease. Chronic hypertension and lifestyle factors are associated with risks for stroke and dementia, and cerebral small vessel disease can cause dementia and stroke. Hypertension is the main driver of cerebral small vessel disease, which changes the structure and function of cerebral vessels via various mechanisms and leads to lacunar infarction, leukoaraiosis, white matter lesions, and intracerebral hemorrhage, ultimately resulting in cognitive decline and demonstrating that the brain is the target organ of hypertension. This review updates our understanding of the pathogenesis of hypertension-induced cerebral small vessel disease and the resulting changes in brain structure and function and declines in cognitive ability. We also discuss drugs to treat cerebral small vessel disease and cognitive impairment.

目的 探索胶原交联术后4 周角膜基质弹性模量与基质深度的定量关系,为交联术前个性化手术设计和术后效果评估提供理论基础.方法 选取健康7 月龄新西兰白兔 7 只,任选 1 只做空白对照组,其余 6 只左眼行角膜交联术,为实验组,右眼作自身对照.术后4 周,取眼球制作角膜基质冷冻切片,沿角膜基质深度方向选取 3～4 个 50 μm×50 μm的区域进行原子力显微镜压痕实验,使用Sneddon接触模型对压痕曲线进行拟合,获得弹性模量,研究角膜基质弹性模量与基质深度的定量关系.结果 胶原交联术后4 周,角膜基质弹性模量是其自身对照眼弹性模量的 1.59 倍.实验组相对弹性模量(E)与基质深度(x)的关系为E=0.66+6.05 e(-x/77.50),拟合优度为0.97.有效的交联深度为190 μm±41 μm.结论 胶原交联术后4 周角膜基质的弹性模量随基质深度仍存在指数衰减的规律.本文方法可获得角膜的有效交联深度,为相关的实验提供参考.

本研究应用可视化角膜生物力学分析仪,于角膜胶原交联术前与术后3月内不同时间对兔眼角膜实施测试,探讨角膜胶原交联后,角膜动态响应参数随术后时间的变化,并计算角膜弹性模量,分析生物力学参数与中央角膜厚度、生物力学矫正眼压的相关性.研究发现,术后1周内角膜动态响应参数变化明显,术后2～3月开始趋于稳定.交联后4周角膜弹性模量增加78.7％,交联效果较好.生物力学参数与中央角膜厚度、生物力学矫正眼压均有相关性,评估角膜生物力学性质同时要关注角膜厚度与眼压的影响.本研究探讨角膜胶原交联后生物力学特性的变化,为交联处置术式的个性化和评估交联手术术后效果提供参考.

Objective:To investigate the efficacy of adalimumab (ADA) on refractory Behcet′s uveitis (BU).Methods:Ten patients (20 eyes) diagnosised with refractory BU at the Eye Center of Beijing Tongren Hospital affiliated to Capital Medical University from May 2020 to October 2021 and treated with ADA were collected. Among them, there were 8 males (16 eyes) and 2 females (4 eyes) with an average age of (37.0 ± 14.2) years (ranged from 22 to 62 years). The initial treatment was glucocorticoids combined with immunosuppressants. Methylprednisolone tablets as glucocorticoids, were used an initial dose of 1 mg·kg-1·d-1, then gradually reduced after the inflammation was controlled. If the inflammation recurred during the follow-up, the dose of glucocorticoid was restored to the dosage at the last reduction. Among immunosuppressants, one of cyclosporine (3 mg·kg-1·d-1), azathioprine (2 mg·kg-1·d-1) or mycophenolate (750 mg, twice a day) has to be chosen. Before ADA treatment, the general condition of patients were checked. If they were up to standards, then ADA treated by subcutaneous injection was used to therapy for recurrent patients or patients with poor response to traditional treatment. The initial dosage of ADA for treatment was 80 mg, followed by subcutaneous injection of 40 mg every two weeks. After the patient′s inflammation was reduced, oral glucocorticoids and immunosuppressants were gradually reduced. Patients were treated by local prednisolone acetate eye drops and retrohemispheric injection of 20 mg methylprednisolone sodium succinate or 20 mg triamcinolone acetonide injection according to the inflammation of the anterior segment. Atropine sulfate eye drops or compound tropicamide eye drops were used for mydriasis. Before and after treatment, the best corrected visual acuity, intraocular pressure, anterior segment inflammation, vitreous inflammation and retinal inflammation of the affected eyes were examined; the macular morphology was evaluated by optical coherence tomography, and the occurrence of complications was recorded and described by frequency and percentage.Results:The course of ten patients (20 eyes) diagnosed as BU was 2 to 22 years with an average of (8.9 ± 6.6) years. After ADA treatment for 6 months, uveitis was reduced in all patients. The vitreous inflammation was transferred from 3+ ~ 4+ to 0 ~ 1+ . Following up for 6 months, they had no recurrence of uveitis. there were 4 cases (8 eyes) with visual acuity improvement ≥ 2 lines, accounting for 40% (8/20); 2 cases (4 eyes) with visual acuity improved ≥ 1 line, accounting for 20% (4/20); 2 cases (3 eyes) with no change in visual acuity, accounting for 15% (3/20); 3 cases (5 eyes) with visual acuity decreased ( 2 eyes with no light perception), accounting for 25% (5/20). The macular edema of 10 patients (20 eyes), was reduced or subsided after ADA treatment. There were 5 patients (8 eyes) with the thickness of macular neuroepithelial edema was reduced to less than 200 μm, accounting for 40% (8/20). There were 4 patients (6 eyes) with epiretinal membrane, accounting for 30% (6/20). After treating patients using ADA, the inflammation was reduced. Then there were 5 cases (10 eyes) with discontinued methylprednisolone tablets, accounting for 50% (5/10); 5 cases (10 eyes) with reduced to 16 mg methylprednisolone tablets. There were 1 case (2 eyes) with discontinued immunosuppressant, accounting for 10% (1/10); 9 cases (18 eyes) with reduced dosage of immunosuppressant, accounting for 90% (9/10). During ADA treatment, there were 3 cases (6 eyes) with skin injection site pain or rash, accounting for 30% (3/10). There were no found other systemic side effects.Conclusions:ADA is safe, effective and well tolerated in the treatment of refractory BU, which could reduce the demand dose for systemic glucocorticoids and immunosuppressants.

目的 评价中国健康受试者空腹和餐后状态下单次口服盐酸二甲双胍缓释片的生物等效性.方法 采用单剂量、随机、开放、两制剂、两周期、交叉对照的试验设计,健康受试者每周期在空腹或餐后状态下口服盐酸二甲双胍缓释片受试制剂和参比制剂500 mg.采用经验证的液相色谱-串联质谱(LC-MS/MS)法测定二甲双胍的血浆浓度,使用Phoenix WinNonlin 8.0计算药动学参数并用SAS 9.4软件进行生物等效性评价.结果 空腹状态下,受试制剂和参比制剂中二甲双胍Cmax分别为(733.00±178.25)、(665.80±146.58) ng·mL-1,AUC0-t分别为(4848.60±1204.80)、(4743.00±1104.34)h·ng·mL-1,AUC0～∞分别为(4940.70±1219.48)、(4832.58±1093.55)h·ng·mL-1.餐后状态下,受试制剂和参比制剂中二甲双胍Cmax分别为(519.10±92.55)、(475.50±65.88) ng·mL-1,AUC0～t分别为(5989.20±1112.01)、(5946.50±1094.81) h·ng·mL-1,AUC0～∞分别为(6052.20±1118.35)、(6049.80±1062.28) h·ng·mL-1.受试制剂和参比制剂二甲双胍Cmax、 AUC0～t和AUC0～∞几何均值比的90％置信区间均在80.00％～125.00％的生物等效性范围内.结论 盐酸二甲双胍缓释片受试制剂和参比制剂在空腹和餐后状态下均具有生物等效性.

目的 探索联合角膜形态学与生物力学特性诊断顿挫期圆锥角膜的其他组合方式,以发掘更多的潜在敏感参数.设计诊断试验.研究对象顿挫期圆锥角膜患者50例(50眼),同期欲行角膜屈光手术术前患者50例(50眼).方法 绘制受试者工作特征(receiver operating characteristic,ROC)曲线分析各纳入参数对顿挫期圆锥角膜的诊断效率并进行Delong检验.将ROC曲线下面积(the area under the ROC curve,AUC)＞0.70的参数作为自变量,用前向逐步法建立Logistic回归模型对顿挫期圆锥角膜的诊断进行多因素分析.主要指标角膜最薄点厚度(TP)、角膜断层摄影和生物力学指数(TBI)及在体角膜弹性模量(E).结果 除Km F、Astig F、KmaxF、A1V、A2T、A2V、HCT、PD、bIOP外,其余参数的组间比较均存在统计学差异.在所纳入参数中,TP对顿挫期圆锥角膜的诊断效率最高(AUC=0.810).对AUC＞0.7的参数进行Logistic回归,结果显示TP和弹性模量E是顿挫期圆锥角膜确诊的独立危险因素:CP=eβ/(1+eβ)(β=-0.063 ×TP-42.158×E+45.919).ROC曲线分析显示,该模型预测值的AUC为0.916,可显著提高对于顿挫期圆锥角膜的诊断能力(CP与TP比较,Z=2.796,P=0.0052).结论 角膜最薄点厚度对顿挫期圆锥角膜的诊断效率与TBI无统计学差异;在圆锥角膜发病早期,虽然角膜中央3 mm区域内总平均曲率几乎无改变,但其下上方曲率差值呈现增大趋势;角膜弹性模量在顿挫期圆锥角膜诊断中的作用值得被关注,可作为补充参数用于疾病评估.

目的:通过非靶向代谢组学等研究方法探讨二苯乙烯苷(tetrahydroxy stilbene glucoside,TSG)对乙酰氨基酚(acetaminophen,APAP)造成急性肝损伤的保护作用.方法:采用随机分组方式将SPF级C57BL/6小鼠分为APAP模型组和TSG干预组,每组15只.灌胃给予小鼠TSG连续7 d后,一次性腹腔注射APAP进行造模,6 h后取肝脏组织.结果:H&E染色、MDA和SOD检测表明单次APAP注射会造成肝脏损伤,TSG干预会降低肝脏受损程度.代谢产物检测结果显示,与APAP模型组相比,TSG组的ABC转运体、胆碱代谢、中心碳代谢、半乳糖、丙氨酸类氨基酸代谢等变化显著.结论:TSG通过改善脂质过氧化和能量代谢紊乱等过程抵御APAP导致的急性肝损伤.

目的 基于处方数据初步评价试点带量采购的左乙拉西坦片(LEV)吉易克与原研LEV片开浦兰临床应用的一致性.方法 回顾性分析带量政策实施前(2018年3月至2019年1月)和带量政策实施后(2019年3月至2020年1月)首都医科大学宣武医院门诊使用吉易克和开浦兰的患者处方数据,按1:1最邻近匹配法匹配后统计药物持有率、持续单药使用率、3、6、9个月药物持续治疗率、持续治疗剂量异常上调率、初诊后持续使用率指标,并比较二者的药物更换情况.比较带量政策实施后开浦兰和吉易克的药品费用及带量政策实施前后LEV药物费用.结果 吉易克组和开浦兰组≥80％药物持有率患者比例比较,差异无统计学意义(P>0.05).开浦兰组持续治疗3、6、9个月患者比例高于吉易克组(P<0.05).开浦兰组持续治疗剂量异常上调率、持续单药使用率明显高于吉易克组(P<0.05).两组之间初诊后持续使用率比较,差异无统计学意义(P>0.05).吉易克组和开浦兰组药物更换情况比较,差异无统计学意义(P>0.05).吉易克组药品人均年费用低于开浦兰组,差异有统计学意义(P<0.05).带量政策实施后LEV人均年费用显著低于带量政策实施前,差异有统计学意义(P<0.05).结论 吉易克与开浦兰的临床应用情况基本一致,同时可较大程度的减轻患者经济负担.

左乙拉西坦(levetiracetam,LEV)是第2代新型抗癫痫药物,具有抗癫痫谱广、不良反应少、耐受性好和安全性高等优点,说明书推荐适应证为控制癫痫部分性发作.越来越多的临床证据显示其对癫痫全身强直痉挛发作、肌阵挛发作、难治性癫痫、癫痫持续状态等方面也有较好疗效,给癫痫的临床治疗提供了更多选择;且在偏头痛的替代治疗、脑胶质瘤及神经保护方面也具有一定潜力.本文结合近5年来左乙拉西坦临床应用的最新研究进展进行综述,为左乙拉西坦新的、更合理的临床应用提供参考.

Esophageal squamous cell cancer (ESCC) is the eighth most common cancer around the world. Several reports have focused on somatic mutations and common germline mutations in ESCC. However, the contributions of pathogenic germline alterations in cancer susceptibility genes (CSGs), highly frequently mutated CSGs, and pathogenically mutated CSG-related pathways in ESCC remain unclear. We obtained data on 571 ESCC cases from public databases and East Asian from the 1000 Genomes Project database and the China Metabolic Analytics Project database to characterize pathogenic mutations. We detected 157 mutations in 75 CSGs, accounting for 25.0% (143/571) of ESCC cases. Six genes had more than five mutations: TP53 (n = 15 mutations), GJB2 (n = 8), BRCA2 (n = 6), RECQL4 (n = 6), MUTYH (n = 6), and PMS2 (n = 5). Our results identified significant differences in pathogenic germline mutations of TP53, BRCA2, and RECQL4 between the ESCC and control cohorts. Moreover, we identified 84 double-hit events (16 germline/somatic double-hit events and 68 somatic/somatic double-hit events) occurring in 18 tumor suppressor genes from 83 patients. Patients who had ESCC with germline/somatic double-hit events were diagnosed at younger ages than patients with the somatic/somatic double-hit events, though the correlation was not significant. Fanconi anemia was the most enriched pathway of pathogenically mutated CSGs, and it appeared to be a primary pathway for ESCC predisposition. The results of this study identified the underlying roles that pathogenic germline mutations in CSGs play in ESCC pathogenesis, increased our awareness about the genetic basis of ESCC, and provided suggestions for using highly mutated CSGs and double-hit features in the early discovery, prevention, and genetic counseling of ESCC.

Alzheimer's disease (AD), also defined as a tauopathology, is a common neurodegenerative disease. Hyper-phosphorylation, cleavage or truncation, and aggregation of tau contribute to AD. Thus, targeting the post-translational modifications on tau may be a therapeutic strategy to treat AD. This study understood how cornel iridoid glycoside (CIG) affects tau post-translational modifications and synaptic abnormalities. The 10-month old P301S tau transgenic mice were given CIG at 100 and 200 mg/kg every day orally for 1 month. Hyperphosphorylated and truncated tau, synapse-associated proteins and glutamatergic receptors were all detected using Western blotting. The interactions between Morroniside (MOR) or Loganin (LOG) and tau were detected using Autodock and Surface Plasmon Resonance (SPR). The effects of CIG on the aggregation of tau were investigated using a cell-free system. CIG attenuated tau hyperphosphorylation at Thr205, Ser212, Ser262, Thr231 and Ser235 (AT180), but had no effect on tau truncation in the brains of 10-month old P301S mice. Binding free energies and interactions revealed that MOR and LOG bound with tau. We also found that CIG upregulated synapse-associated proteins such as PSD-95, syntaxin1A and synaptotagmin. In addition, CIG restored N-methyl-D-aspartic acid receptor and glutamate receptor levels. CIG improves post-translational modification of tau as well as synaptic abnormalities. The data presented here reveal that CIG may be used in the treatment of AD.

目的 探索基于原子力显微镜(atomic force microscope,AFM)压痕技术确定大鼠小梁网组织弹性模量的方法,为揭示小梁网组织力学特性与小梁网通道房水外流阻力之间的关系等研究奠定基础.方法 首先利用大鼠眼球组织切片获取大鼠小梁网组织与毗邻组织之间的距离信息和结构信息;其次利用AFM压痕实验获取角膜-角巩膜缘-小梁网-巩膜方向的弹性模量与相对位置的关系;最后综合对比以确定小梁网组织测试区域.结果 探索了一种基于原子力显微镜压痕实验定位小梁网组织并获取该组织弹性模量的方法,利用该方法获取了大鼠眼球鼻侧、颞侧、上侧、下侧4个位置处的小梁网组织弹性模量范围为300～600 Pa.结论 本研究给出了一种基于AFM压痕技术确定大鼠小梁网组织弹性模量的方法,该方法提供了AFM测试环境下小梁网组织区域的位置参考,优势在于可快速定位到大鼠小梁网组织区域.

To investigate the relationship between non-coding RNAs [especially circular RNAs (circRNAs)] and docetaxel resistance in breast cancer, and to find potential predictive biomarkers for taxane-containing therapies, we have performed transcriptome and microRNA (miRNA) sequencing for two established docetaxel-resistant breast cancer (DRBC) cell lines and their docetaxel-sensitive parental cell lines. Our analyses revealed differences between circRNA signatures in the docetaxel-resistant and -sensitive breast cancer cells, and discovered circRNAs generated by multidrug-resistance genes in taxane-resistant cancer cells. In DRBC cells, circABCB1 was identified and validated as a circRNA that is strongly up-regulated, whereas circEPHA3.1 and circEPHA3.2 are strongly down-regulated. Furthermore, we investigated the potential functions of these circRNAs by bioinformatics analysis, and miRNA analysis was performed to uncover potential interactions between circRNAs and miRNAs. Our data showed that circABCB1, circEPHA3.1 and circEPHA3.2 may sponge up eight significantly differentially expressed miRNAs that are associated with chemotherapy and contribute to docetaxel resistance via the PI3K-Akt and AGE-RAGE signaling pathways. We also integrated differential expression data of mRNA, long non-coding RNA, circRNA, and miRNA to gain a global profile of multi-level RNA changes in DRBC cells, and compared them with changes in DNA copy numbers in the same cell lines. We found that Chromosome 7 q21.12-q21.2 was a common region dominated by multi-level RNA overexpression and DNA amplification, indicating that overexpression of the RNA molecules transcribed from this region may result from DNA amplification during stepwise exposure to docetaxel. These findings may help to further our understanding of the mechanisms underlying docetaxel resistance in breast cancer.

目的 原子力显微镜(atomic force microscope,AFM)可提供多种扫描模式及测试方法,而细胞弹性模量的获得方法目前尚未统一,本研究拟探讨通过AFM力曲线阵列模式(force volume)获得细胞弹性模量的方法.方法 首先通过酶消化法提取正常兔眼角膜基质细胞,进行培养并通过波形蛋白(vimentin)免疫荧光染色进行鉴定.通过AFM力曲线阵列测试,选定9个100×100μm2区域,获得每个区域均匀分布的1024点的力-压痕深度曲线,利用Snedden模型拟合曲线获得相应测试点弹性模量.结果 波形蛋白(vimentin)免疫荧光染色鉴定结果证实,提取细胞免疫荧光波形蛋白鉴定阳性,确定细胞为角膜基质细胞.通过原子力显微镜测试得到每个区域约有3～5个完整细胞,拟合得到细胞的弹性模量中央与边缘处略有差别.细胞中央处拟合得弹性模量为53.1 kPa±6.35 kPa.结论 AFM力曲线阵列模式可以较为简易方便地获得众多细胞数据,更为细致地获得细胞整体力学特性,有效避免了实验操作与压入点不同带来的误差.

目的 探究痘苗病毒致炎兔皮提取物(AGC)对大鼠脑缺血再灌注损伤的保护作用及机制.方法 Sprague-Dawley大鼠61只分为假手术组(n=11)、假手术给药组(n=11)、模型组(n=20)和模型给药组(n=19).模型组和模型给药组线栓法脑缺血1.5 h后恢复灌注.模型组和模型给药组各有2只造模不成功.再灌注3 h后,假手术给药组和模型给药组尾静脉每天注射AGC 20 U/kg,假手术组和模型组尾静脉注射等体积生理盐水.给药48 h后每组取4只大鼠Western blotting方法检测脑组织热休克蛋白(HSP70)、Bcl-2和Bax表达;给药7 d后,行抓握牵引实验;各组取4只大鼠,免疫组化法观察离子钙结合蛋白(Iba1)阳性和胶质纤维酸性蛋白(GFAP)阳性表达.结果 与模型组相比,模型给药组抓握时间明显延长(P<0.01),HSP70和Bcl-2表达明显升高(P<0.01),Iba1阳性和GFAP阳性面积下降(P<0.05).结论 AGC能促进脑缺血再灌注损伤大鼠运动功能恢复,可能与抑制细胞凋亡和神经炎症反应有关.

目的探讨不同月龄APP/PS1/tau三转基因（3×Tg）小鼠脑内突触相关蛋白及其影响因素的变化,为选择合适时程的3×Tg小鼠进行阿尔茨海默病（Alzheimer’s disease,AD）研究提供参考数据;并且研究山茱萸环烯醚萜苷（cornel iridoid glycoside,CIG）对模型小鼠脑内突触相关蛋白的影响,从而明确其对不同月龄的模型动物的作用特点,为阐明CIG改善AD样认知障碍机制提供实验依据。方法 7月龄小鼠3×Tg小鼠给予200 mg/kg CIG至9月龄,16月龄3×Tg小鼠给予100或200 mg·kg -1 ·d -1 CIG至18月龄;采用新物体识别实验检测CIG对学习记忆的影响;采用Western blotting方法检测突触相关蛋白synapsin-1、synaptophysin和synaptotagmin的表达,淀粉样前体蛋白（amyloid precurson protein,APP）及相关代谢酶α分泌酶（recombinant a disintegrin and metalloprotease 10, ADAM10）、β分泌酶（β-site APP-cleaving enzyme 1, BACE1）、早老素1（presenilin-1,PS1）、胰岛素降解酶（insulin degrading enzyme, IDE）的表达,tau蛋白在pSer404及pSer199/202位点的磷酸化水平。结果 7月龄3×Tg模型小鼠与对照组小鼠相比,物体识别分辨指数无明显变化,主要突触相关蛋白synapsin-1、synaptophysin和synaptotagmin的表达没有差异,CIG给药未对3×Tg模型小鼠分辨指数及脑内突触相关蛋白产生影响;16月龄3×Tg小鼠物体识别分辨指数明显降低,synapsin-1在脑内表达水平均相比对照组下降,而给予CIG治疗后不仅能够提高转基因小鼠的分辨指数,而且明显提升synapsin-1的表达。7月龄3×Tg小鼠模型与对照组全长APP、ADAM10、BACE1、PS1、IDE及tau蛋白磷酸化水平比较,差异均无统计学意义（P＞0.05）。结论突触相关蛋白在不同月龄3×Tg小鼠脑内表达差异较大,CIG对不同月龄3×Tg小鼠脑内突触相关蛋白的表达及认知功能存在不同作用特点。

牛痘疫苗接种家兔炎症皮肤提取物(neurotropin,NTP)是一种非蛋白小分子生物制品,早期在临床上多应用在镇痛方面,近年来发现其在免疫调节和神经保护方面也有重要作用,被认为有扩大适应症的潜能.本文综述该药在治疗神经源性疼痛、恶性肿瘤和缺血性脑卒中等疾病中的临床应用及其在镇痛、神经保护和免疫调节等药理学作用机制方面的研究进展.

以首都医科大学临床医学一系七年制学生为调查对象,就学生医学英语基础、对医学英语的认知、医学英语学习动机及需求进行调查.调查结果显示,七年制临床医学专业学生具有较好的公共及医学英语基础,他们认为学习医学英语对于将来专业课学习或从事的工作很重要,他们对医学英语的教学需求从提升阅读写作能力转变为提升听说能力,更注重实际应用.医学英语教学应明确教学目标,调整教学内容,完善教学评价体系,提高临床长学制医学生医学英语水平,培养高层次医学英语交流型人才.

Objective To observe the effects of 2,3,5,4'-tetrahydroxy-stilbene-2-O-β-D-glycoside (TSG) on formation of senile plaques and beta amyloid (Aβ), as well as activation of microglia and astrocytes, in cortex and hippocampus of APP/PS1 double transgenic mice. Methods A total of 64 five-month-old APP/PS1 mice were randomly divided into model group (n=16), low-dose TSG (0.05 g/kg) group (n=16), high-dose TSG (0.1 g/kg) group (n=16), and donepezil group (n=16); other 32 same age wild type (WT) mice were randomly divided into normal control group (n=16) and high-dose TSG (0.1 g/kg) WT group (n=16). The normal control group and model group were given distilled water, and the other groups were given the corresponding drugs intragastrically. The mice were tested with object recognition test, the deposi-tion of plaques in brain was detected with Congo red staining, and the expression of Aβ40/42, ionized calcium bind-ing adapter molecule 1 (Iba1) and glial fibrillary acidic protein (GFAP) with immunohistochemistry after seven months of treatment (twelve-month-old). Results Compared with the model group, the discrimination index significantly increased (P<0.01), the deposition of plaques decreased in brain (P<0.05), and the expression of Aβ40/42, Iba1 and GFAP all significantly decreased in each treatment group (P<0.05). Conclusion TSG can improve learning and memory of APP/PS1 transgenic mice, reduce Aβ deposition and senile plaques, and reduce the inflammatory response, even in low-dose, which is similar to that of donepezil.