drug-induced autoimmune liver disease:a diagnostic dilemma of an increasingly reported disease

The aetiology of autoimmune hepatitis(AIH) is uncer-tain but the disease can be triggered in susceptible patients by external factors such as viruses or drugs.AIH usually develops in individuals with a genetic back-ground mainly consisting of some risk alleles of the major histocompatibility complex(HLA).Many drugs have been linked to AIH phenotypes,which sometimes persist after drug discontinuation,suggesting that they awaken latent autoimmunity.At least three clini-cal scenarios have been proposed that refers to drug- induced autoimmune liver disease(DIAILD):AIH with drug-induced liver injury(DILI); drug induced-AIH(DI-AIH); and immune mediated DILI(IM-DILI).In addi-tion,there are instances showing mixed features of DI-AIH and IM-DILI,as well as DILI cases with positive autoantibodies.Histologically distinguishing DILI from AIH remains a challenge.Even more challenging is the differentiation of AIH from DI-AIH mainly relying in histological features; however,a detailed standard-ised histologic evaluation of large cohorts of AIH and DI-AIH patients would probably render more subtle features that could be of help in the differential diag-nosis between both entities.Growing information on the relationship of drugs and AIH is being available,being drugs like statins and biologic agents more fre-quently involved in cases of DIAILD.In addition,there is some evidence on the fact that patients diagnosed with DIAILD may have had a previous episode of hepa-totoxicity.Further collaborative studies in DIAILD will strengthen the knowledge and understanding of this intriguing and complex disorder which might represent different phenotypes across the spectrum of

Carbimazole Drug-Induced Hepatitis during Treatment of Graves’ Disease: About Four Cases at Dakar Teaching Hospital

Introduction: Mostly reported common side effects of carbimazole are cutaneous allergies and severe agranulocytosis. However, hepatotoxicity is rarely described. Thus, we report four observations of carbimazole drug-induced hepatitis during the treatment of Graves’ disease, which imputability is likely and probably an immuno-allergic mechanism. Observations: They were four women whose average age was 43 years, with extreme ages of 32 and 54. Patients were monitored and treated with carbimazole in doses contained between 40 mg and 60 mg per day. Clinical manifestations of liver injury were mainly dominated by cholestatic jaundice, found in 100% of our patients. A painful sensitivity of the right hypochondrium was concomitant with jaundice for two patients. The jaundice time to onset after the beginning of treatment with carbimazole varies between 1 month and 6 months. They all had acute hepatitis. The biological assays used to determine the type of liver injury showed, in all cases, a mixed, cholestatic and cytolytic hepatitis. Therapeutically, in all patients, carbimazole was stopped as soon as the suspicion of its incrimination in the occurrence of liver damage was set up. They all had a substitution of carbimazole with benzylthiouracil. Evolution was favorable for all patients, after therapeutic substitution. It was marked by disappearance of jaundice and normalization of the liver biological parameters within a maximum delay of two months after stopping carbimazole use. Conclusion: Treatment with synthetic antithyroid drugs, particularly carbimazole that is most widely used in our regions, requires clinical and biological monitoring. This surveillance, which is often difficult in Africa because of the limited economic resources, can lead to the occurrence of side effects such as potentially serious drug-induced hepatitis, but which has been favorable in our observations.

Current remarks and future directions on the interactions between metabolic dysfunction-associated fatty liver disease and COVID-19

During the outbreak of the coronavirus disease 2019(COVID-19)pandemic,particular interest rose regarding the interaction between metabolic dysfunctionassociated fatty liver disease(MAFLD)and the COVID-19 infection.Several studies highlighted the fact that individuals with MAFLD had higher probability of severe acute respiratory syndrome coronavirus 2 infection and more severe adverse clinical outcomes.One of the proposed mechanisms is the inflammatory response pathway,especially the one involving cytokines,such as interleukin 6,which appeared particularly elevated in those patients and was deemed responsible for additional insult to the already damaged liver.This should increase our vigilance in terms of early detection,close follow up and early treatment for individuals with MAFLD and COVID-19 infection.In the direction of early diagnosis,biomarkers such as cytokeratin-18 and scoring systems such as Fibrosis-4 index score are proposed.COVID-19 is a newly described entity,expected to be of concern for the years to come,and MAFLD is a condition with an ever-increasing impact.Delineating the interaction between these two entities should be brought into the focus of research.Reducing morbidity and mortality of patients with COVID-19 and MAFLD should be the ultimate objective,and the optimal way to achieve this is by designing evidence-based prevention and treatment policies.

Hepatic complications induced by immunosuppressants and biologics in inflammatory bowel disease

The incidence of inflammatory bowel diseases(IBD)is rising worldwide.The therapeutic options for IBD are expanding,and the number of drugs with new targets will rapidly increase in coming years.A rapid step-up approach with close monitoring of intestinal inflammation is extensively used.The fear of side effects represents one the most limiting factor of their use.Despite a widespread use for years,drug induced liver injury(DILI)management remains a challenging situation with Azathioprine and Methotrexate.DILI seems less frequent with anti-tumor necrosis factor agents and new biologic therapies.The aim of this review is to report incidence,physiopathology and practical guidelines in case of DILI occurrence with the armamentarium of old and new drugs in the field of IBD.

Role of non-steroidal anti-inflammatory drugs on intestinal permeability and nonalcoholic fatty liver disease

The use of non-steroidal anti-inflammatory drugs(NSAIDs) is widespread worldwide thanks to their analgesic, anti-inflammatory and antipyretic effects. However, even more attention is placed upon the recurrence of digestive system complications in the course of their use. Recent data suggests that the complications of the lower gastro-intestinal tract may be as frequent and severe as those of the upper tract. NSAIDs enteropathy is due to enterohepatic recycling of the drugs resulting in a prolonged and repeated exposure of the intestinal mucosa to the compound and its metabolites. Thus leading to so-called topical effects, which, in turn, lead to an impairment of the intestinal barrier. This process determines bacterial translocation and toxic substances of intestinal origin in the portal circulation, leading to an endotoxaemia. This condition could determine a liver inflammatory response and might promote the development of nonalcoholic steatohepatitis, mostly in patients with risk factors such as obesity, metabolic syndrome and a high fat diet, which may induce a small intestinal bacterial overgrowth and dysbiosis. This alteration of gut microbiota may contribute to nonalcoholic fatty liver disease and its related disorders in two ways: firstly causing a malfunction of the tight junctions that play a critical role in the increase of intestinal permeability, and then secondly leading to the development of insulin resistance, body weight gain, lipogenesis, fibrogenesis and hepatic oxidative stress.

Familial Alzheimer's disease modelling using induced pluripotent stem cell technology

Alzheimer’s disease(AD)is a progressive neurodegenerative disease in which patients exhibit gradual loss of memory that impairs their ability to learn or carry out daily tasks.Diagnosis of AD is difficult,particularly in early stages of the disease,and largely consists of cognitive assessments,with only one in four patients being correctly diagnosed.Development of novel therapeutics for the treatment of AD has proved to be a lengthy,costly and relatively unproductive process with attrition rates of】90%.As a result,there are no cures for AD and few treatment options available for patients.Therefore,there is a pressing need for drug discovery platforms that can accurately and reproducibly mimic the AD phenotype and be amenable to high content screening applications.Here,we discuss the use of induced pluripotent stem cells(iPSCs),which can be derived from adult cells,as a method of recapitulation of AD phenotype in vitro.We assess their potential use in high content screening assays and the barriers that exist to realising their full potential in predictive efficacy,toxicology and disease modelling.At present,a number of limitations need to be addressed before the use of iPSC technology can be fully realised in AD therapeutic applications.However,whilst the use of AD-derived iPSCs in drug discovery remains a fledgling field,it is one with immense potential that is likely to reach fruition within the next few years.

Rituximab Induced Interstitial Lung Disease Diagnosis, Treatment Outcome, and Risk’s Factor, a Place for Transbronchial Pulmonary Cryobiopsy

Rituximab (RTX) is a mouse/human chimeric anti-CD20 IgG1 monoclonal antibody, approved in late 1998 by the FDA. Effectively used as a single agent or combined with a chemotherapy regimen to treat lymphoma, RTX is a significant step forward in the arsenal treatment of idiopathic thrombocytopenic purpura, systemic lupus erythematous, rheumatoid arthritis, and autoimmune hemolytic anemia. Side effects of RTX are commonly seen during the first infusion in up to 50% of patients and include fever, chills, and rigors. These side effects are generally transient and related to the tumor burden, probably due to a greater degree of complement activation and proinflammatory cytokine release. Severe lung toxicity like cryptogenic organizing pneumonia, pneumonitis, and interstitial lung diseases are infrequent, with most of the knowledge coming from case reports.

Thinking outside the liver: Induced pluripotent stem cells for hepatic applications

The discovery of induced pluripotent stem cells (iPSCs) unraveled a mystery in stem cell research, after identification of four re-programming factors for generating pluripotent stem cells without the need of embryos. This breakthrough in generating iPSCs from somatic cells has overcome the ethical issues and immune rejection involved in the use of human embryonic stem cells. Hence, iPSCs form a great potential source for developing disease models, drug toxicity screening and cell-based therapies. These cells have the potential to differentiate into desired cell types, including hepatocytes, under in vitro as well as under in vivo conditions given the proper microenvironment. iPSC-derived hepatocytes could be useful as an unlimited source, which can be utilized in disease modeling, drug toxicity testing and producing autologous cell therapies that would avoid immune rejection and enable correction of gene defects prior to cell transplantation. In this review, we discuss the induction methods, role of reprogramming factors, and characterization of iPSCs, along with hepatocyte differentiation from iPSCs and potential applications. Further, we discuss the location and detection of liver stem cells and their role in liver regeneration. Although tumor formation and genetic mutations are a cause of concern, iPSCs still form a promising source for clinical applications.

Hepatobiliary manifestations in inflammatory bowel disease: The gut,the drugs and the liver

Abnormal liver biochemical tests are present in up to30%of patients with inflammatory bowel disease(IBD),and therefore become a diagnostic challenge.Liver and biliary tract diseases are common extraintestinal manifestations for both Crohn’s disease and ulcerative colitis(UC),and typically do not correlate with intestinal activity.Primary sclerosing cholangitis(PSC)is the most common hepatobiliary manifestation of IBD,and is more prevalent in UC.Approximately 5%of patients with UC develop PSC,with the prevalence reaching up to 90%.Cholangiocarcinoma and colon cancer risks are increased in these patients.Less common disorders include autoimmune hepatitis/PSC overlap syndrome,IgG4-associated cholangiopathy,primary biliary cirrhosis,hepatic amyloidosis,granulomatous hepatitis,cholelithiasis,portal vein thrombosis,liver abscess,and non-alcoholic fatty liver disease.Hepatitis B reactivation during immunosuppressive therapy is a major concern,with screening and vaccination being recommended in serologically negative cases for patients with IBD.Reactivation prophylaxis with entecavir or tenofovir for 6to 12 mo after the end of immunosuppressive therapy is mandatory in patients showing as hepatitis B surface antigen(HBsAg)positive,independently from viral load.HBsAg negative and anti-HBc positive patients,with or without anti-HBs,should be closely monitored,measuring alanine aminotransferase and hepatitis B virus DNA within 12 mo after the end of therapy,and should be treated if the viral load increases.On the other hand,immunosuppressive therapy does not seem to promote reactivation of hepatitis C,and hepatitis C antiviral treatment does not influence IBD natural history either.Most of the drugs used for IBD treatment may induce hepatotoxicity,although the incidence of serious adverse events is low.Abnormalities in liver biochemical tests associated with aminosalicylates are uncommon and are usually not clinically relevant.Methotrexaterelated hepatotoxicity has been described in 14%of patients with IBD,in a dose-dependent manner.Liver biopsy is not routinely recommended.Biologics-related hepatotoxicity is rare,but has been shown most frequently in patients treated with infliximab.Thiopurines have been associated with veno-occlusive disease,regenerative nodular hyperplasia,and liver peliosis.Routine liver biochemical tests are recommended,especially during the first month of treatment.All these conditions should be considered in IBD patients with clinical or biochemical features suggestive of hepatobiliary involvement.Diagnosis and management of these disorders usually involve hepatologists and gastroenterologists due to its complexity.

Induced pluripotent stem cells for modeling neurological disorders

Several diseases have been successfully modeled since the development of induced pluripotent stem cell(i PSC) technology in 2006. Since then, methods for increased reprogramming efficiency and cell culture maintenance have been optimized and many protocols for differentiating stem cell lines have been successfully developed, allowing the generation of several cellular subtypes in vitro. Gene editing technologies have also greatly advanced lately, enhancing disease-specific phenotypes by creating isogenic cell lines, allowing mutations to be corrected in affected samples or inserted in control lines. Neurological disorders have benefited the most from i PSC-disease modeling for its capability for generating disease-relevant cell types in vitro from the central nervous system, such as neurons and glial cells, otherwise only available from post-mortem samples. Patient-specific i PSC-derived neural cells can recapitulate the phenotypes of these diseases and therefore, considerably enrich our understanding of pathogenesis, disease mechanism and facilitate the development of drug screening platforms for novel therapeutic targets. Here, we review the accomplishments and the current progress in human neurological disorders by using i PSC modeling for Alzheimer's disease, Parkinson's disease, Huntington's disease, spinal muscular atrophy, amyotrophic lateral sclerosis, duchenne muscular dystrophy, schizophrenia and autism spectrum disorders, which include Timothy syndrome, Fragile X syndrome, Angelman syndrome, Prader-Willi syndrome, PhelanMc Dermid, Rett syndrome as well as Nonsyndromic Autism.

Nrf2-ARE信号通路参与肝脏疾病病理机制研究进展

核因子NF-E2相关因子2(Nrf2)是细胞抵御氧化应激的一个重要转录因子,它能够在活性氧或亲电试剂的刺激下,转位进入细胞核,并与抗氧化反应元件(ARE)相互作用,从而诱导下游保护性Ⅱ相解毒酶和抗氧化酶的表达,达到细胞保护的作用。氧化应激是诸多肝脏疾病共同的发病机制,而Nrf2-ARE是体内一条极为重要的抗氧化应激信号通路,该通路在肝脏疾病的发生、发展及预防过程中起着非常重要的作用,Nrf2或将成为肝脏疾病治疗的新靶点。该文综述了Nrf2-ARE信号通路参与肝脏疾病病理机制的最新研究进展,以期为日后相关研究提供参考。

S-腺苷蛋氨酸治疗药物性胆汁淤积性肝病伴抑郁/焦虑患者的研究

目的研究S-腺苷蛋氨酸对药物性胆汁淤积性肝病伴抑郁/焦虑患者的治疗作用。方法 38例不同病因的药物性胆汁淤积性肝病并抑郁/焦虑患者予S-腺苷蛋氨酸治疗,应用SDS/SAS量表分别评估、比较治疗前后各组患者抑郁/焦虑情况。结果 S-腺苷蛋氨酸治疗后,中草药致药物性肝病伴抑郁/焦虑患者以及抗生素、他汀类药物致药物性肝病伴抑郁患者胆汁淤积明显改善,抑郁/焦虑症状改善有显著差异(P值分别为0.001、0.011、0.018),而在抗肿瘤药物致药物性肝病患者中无显著性差异。结论 S-腺苷蛋氨酸在中草药以及抗生素、他汀类药物性胆汁淤积性肝病并抑郁/焦虑患者中具有保肝及抗抑郁的双重作用,这将为人类"生理-心理"疾病的全面治疗奠定基础。

老年药物性肝损伤患者临床特征分析

目的分析老年药物性肝损伤(DILI)患者的临床特征,以为临床干预提供依据。方法2018年12月~2024年2月我院老年医学科诊治的老年多种疾病患者181例,常规行临床分型和疾病程度分度。应用单因素和多因素Logistic回归分析影响DILI病情严重程度的危险因素。结果在181例老年患者中,发现DILI者44例(24.3%),其中肝细胞损伤型28例,胆汁淤积型12例,混合型4例;轻度25例,中度10例,重度8例,死亡1例;可疑药物为中草药占27.3%,保健类药物占22.7%,内分泌系统疾病用药占13.6%,心脑血管疾病用药占11.4%,等;DILI组年龄为72(66,76)岁,显著大于非DILI组【67(65,69),P<0.05】,多种疾病、饮酒、脂肪肝和高脂血症占比分别为79.6%、27.3%、56.8%和84.1%,显著高于非DILI组(分别为11.7%、3.6%、12.4%和8.7%,均P<0.05);9例≥3级肝损伤患者年龄为73(67,75)岁,显著大于35例≤2级肝损伤者【67(66,70)岁,P<0.05】,饮酒、多种疾病和合并脂肪肝占比分别为88.9%、100.0%和88.9%,均显著大于≤2级肝损伤者(分别为11.4%,74.3%和48.6%,均P<0.05),多因素Logistic回归分析表明,高龄【OR:1.67,95%CI:1.26~3.05】、饮酒【OR:2.43,95%CI:1.35~3.17】和脂肪肝【OR:2.14,95%CI:1.50~4.75】均是影响老年DILI患者病情严重程度的独立危险因素(P<0.05)。结论中草药、保健类药物、内分泌和心脑血管系统疾病用药容易导致老年基础疾病多的患者发生DILI,戒酒、降低脂肪肝程度和控制好疾病发作可能减轻DILI严重程度,值得临床深入研究。

组织病理、免疫组化及荧光在自身免疫性肝病诊断及鉴别诊断中的应用探究

目的 以自身免疫性肝炎(autoimmune hepatitis,AIH)、原发性胆汁性胆管炎(primary biliary cholangitis,PBC)、AIH-PBC重叠综合征(overlap syndrome,OS)和药物诱发性自身免疫样肝炎(drug-induced autoimmune-like hepatitis,DI-AILH)为研究对象,结合临床特征、组织病理、免疫组织化学染色和免疫荧光染色展开多方面研究,以探寻有助于鉴别诊断它们的临床病理特征。方法 对各组患者的肝穿刺标本进行HE、免疫组化和免疫荧光染色,结合判读结果量化分析AIH、PBC和OS之间及AIH和DI-AILH之间的组织学、免疫组织化学和免疫荧光差异;并针对DI-AILH和AIH之间显著性差异因子建立Logistic回归模型。结果 组织学评估中,AIH出现显著的界面性肝炎、Rosette花环形成、界板处成簇的浆细胞浸润;PBC出现汇管区浆细胞浸润、明显的淋巴细胞性小叶间胆管炎;OS出现更高的汇管区和肝小叶内炎症分级。免疫组化和免疫荧光半定量评分显示,AIH和PBC在汇管区和界板处阳性细胞有显著性差异、AIH出现IgG小叶内和汇管区沉积、PBC出现IgA沿小叶间胆管线状沉积。DI-AILH和AIH浆细胞、中性粒细胞浸润和界板处炎症差异明显,Logistic回归模型曲线下面积>0.80。结论 尽管在临床病理特点方面存在重叠,AIH、PBC和AIH-PBC OS仍存在有助于各自诊断的组织学、免疫组化及荧光特点,根据肝组织损伤模型,病理医师也可以给出关于AIH和DI-AILH较为准确的诊断。

阿托伐他汀药物性肝损伤的临床特征分析

背景药物性肝损伤是常见的药物不良反应之一,阿托伐他汀是临床上广泛应用的他汀类降脂药物之一,易引发肝损伤,目前对其所导致的药物性肝损伤的临床特征研究数据较少。目的探讨阿托伐他汀药物性肝损伤的临床特征,以提高临床医生对阿托伐他汀药物性肝损伤的认识。方法选取广西医科大学第一附属医院2012年1月—2022年8月住院且使用阿托伐他汀治疗,出现肝损伤且经Roussel Uclaf因果关系评估法评估为阿托伐他汀药物性肝损伤的患者,分析其临床特征。结果经Roussel Uclaf因果关系评估法评估,共确诊84例阿托伐他汀药物性肝损伤。阿托伐他汀药物性肝损伤患者中男性较多(72.6%),平均年龄为(60.2±11.5)岁,且均合并基础疾病(100.0%);达到中度肝损伤2例(2.4%),经治疗治愈或好转率达到100.0%。根据病程分型,主要表现为急性病程(100.0%);根据受损靶细胞分型以混合型最多(60.7%),其次是胆汁淤积型(26.2%)、肝细胞型(11.9%)。78.6%的患者服用阿托伐他汀发生肝损伤的时间在3个月内,且以第1~2周内居多;81.0%的患者在累积服用阿托伐他汀80个药物限定日剂量时发生肝损伤。结论阿托伐他汀药物性肝损伤多发生于男性、中老年、合并基础疾病的患者,多为轻度肝损伤,预后较好;临床分型以混合型、胆汁淤积型居多;肝损伤发生时间主要在3个月内,且阿托伐他汀药物性肝损伤的发生有一定剂量依赖性。

《伤寒论》方佐药组方规律理论研究《伤寒论》方佐药组方规律理论研究(正文见847-850页)图1佐药药物类别统计图图2佐药补虚药统计图图3佐药解表药统计图图4佐药四气统计图图5佐药归经统计图图6佐药规律统计图

建立《伤寒论》方剂数据库,统计112首方剂的佐药药物类别、四气、五味、归经、毒性,总结佐药的组方规律,认为佐药的规律是偏于扶正。

药物性肝病患者中医体质分布和临床特点分析

目的:分析药物性肝病患者的性别、年龄、中医体质、中医证型等分布规律。方法:选取2020年8月至2022年8月解放军总医院第五医学中心中医肝病科收治的药物性肝病患者368例,收集患者相关临床资料,分析药物性肝病患者的性别、年龄、中医体质、中医证型等分布规律和临床特征。结果:药物性肝病患者中医体质分布以气郁质(19.02%)最为多见,其次依次为阴虚质(18.21%)、湿热质(15.22%)、阳虚质(13.32%)、血瘀质(11.14%)、平和质(7.61%)、痰湿质(6.25%)、气虚质(5.16%)、特禀质(4.08%)。药物性肝病患者中医体质在性别、年龄等方面均具有差异性,男性以湿热质、阴虚质为多见;女性以气郁质、阴虚质为多见,而阴虚质在男性、女性均多见;青年中以气郁质和湿热质较多见,中年中以痰湿质较多见、老年以血瘀质较多见。药物性肝病患者在中医证型分布中主要为湿热内蕴证125例(34%),其次分别为肝郁脾虚证98例(27%)、肝肾阴虚证56例(15%)、气滞血瘀证46例(12%)、寒湿中阻证43例(12%);药物性肝病患者在体质与证型存在相关性,体质类型决定了该病证型的易感性。结论:根据药物性肝病患者的中医体质以及证型的分布特点以及相关临床特征,提示可以通过调节情志、合理饮食以及药物防治等方面做到“未病先防”“既病防变”,做到“辨体”“辨证”“辨病”的有机结合。

湿润烧伤膏保留灌肠治愈混合痔经肛门直肠黏膜环切术后药物性肠病1例报告

给予2019年4月湖北省中医院收治的1例混合痔经肛门直肠黏膜环切术后药物性肠病患者在常规中药辨证口服治疗的基础上行湿润烧伤膏保留灌肠治疗,治疗1个月后,溃疡创面完全愈合,愈后黏膜无瘢痕增生,肠腔无狭窄。

TNF-α在对乙酰氨基酚所致大鼠药物性肝损伤中的作用

目的探讨TNF-α在对乙酰氨基酚所致大鼠急性药物性肝损伤中的作用。方法 40只SD大鼠随机分成空白对照组、益赛普对照组、对乙酰氨基酚组、对乙酰氨基酚+益赛普组,每组10只。单次给药,24 h后采集血液测定生化指标,之后处死大鼠,取肝脏组织做病理检查以及应用ELISA试剂盒检测血清TNF-α。结果对乙酰氨基酚组肝损伤明显,阻断TNF-α后肝损伤减轻。对乙酰氨基酚组肝功生化值及TNF-α水平较空白对照组升高,差异有统计学意义(P<0.05),对乙酰氨基酚+益赛普组肝功生化值及TNF-α水平较对乙酰氨基酚组下降,差异有统计学意义(P<0.05)。结论 TNF-α的表达在对乙酰氨基酚所致大鼠急性肝损伤肝组织中明显升高,阻断TNF-α后肝损伤减轻,TNF-α可能参与对乙酰氨基酚所致肝损伤。

Current status and future prospects of stem cell therapy in Alzheimer’s disease

Alzheimer’s disease is a common progressive neurodegenerative disorder, pathologically characterized by the presence of β-amyloid plaques and neurofibrillary tangles. Current treatment approaches using drugs only alleviate the symptoms without curing the disease, which is a serious issue and influences the quality of life of the patients and their caregivers. In recent years, stem cell technology has provided new insights into the treatment of neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Currently, the main sources of stem cells include neural stem cells, embryonic stem cells, mesenchymal stem cells, and induced pluripotent stem cells. In this review, we discuss the pathophysiology and general treatment of Alzheimer’s disease, and the current state of stem cell transplantation in the treatment of Alzheimer’s disease. We also assess future challenges in the clinical application and drug development of stem cell transplantation as a treatment for Alzheimer’s disease.