[This corrects the article DOI: 10.3389/fneur.2018.00412.].

Oxidative stress is a pathophysiological condition resulting in neurotoxicity, which is possibly associated with neurodegenerative disorders. In this study, the antioxidative effects of the antioxidant astaxanthin (AXT) in combination with huperzine A (HupA), which is used as a cholinesterase inhibitor for the treatment of Alzheimer's disease, were investigated. PC12 cells were treated with either tert‑butyl hydroperoxide (TBHP), or with the toxic version of β‑amyloid, Aβ25‑35, to induce oxidative stress and neurotoxicity. Cell viability, morphology, lactate dehydrogenase (LDH) release, intracellular accumulation of reactive oxygen species (ROS), superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were determined, while neuroprotection was also monitored using an MTT assay. It was found that combining AXT with HupA significantly increased the viability of PC12 cells, prevented membrane damage (as measured by LDH release), attenuated intracellular ROS formation, increased SOD activity and decreased the level of MDA after TBHP exposure when compared to these drugs administered alone. Pretreatment with HupA and AXT decreased toxic damage produced by Aβ25‑35. These data indicated that combining an antioxidant with a cholinesterase inhibitor increases the degree of neuroprotection; with future investigation this could be a potential therapy used to decrease neurotoxicity in the brain.

Recent studies have demonstrated circular RNAs (circRNAs) to be widely expressed and to have important physiological functions. However, the expression, regulation, and function of circRNAs in neuroglial cells are unknown. Herein, we characterized the expression, regulation, and function of circRNAs in astrocytes. Astrocyte circRNAs were identified by computational analysis of newborn SD rat primary astrocytes cultured with 20 g/L D-galactose. In this manner, 7376 circRNAs were identified, among which most circRNAs (5754) were derived from annot_exons, whereas 27 were antisense, 853 were exon/intron, 329 were intergenic, 41 were intronic, and 372 were one exon. Among these, circNF1-419 was demonstrated to regulate autophagy, in over-expressing circNF1-419 transfected astrocytes, through the PI3K-I/Akt-AMPK-mTOR and PI3K-I/Akt-mTOR signaling pathways. An adenovirus associated virus packaging system (virus titer 1 ×1012), over-expressing circNF1-419 and injected into mouse cerebral cortex, showed autophagy enhancing activity by binding the proteins Dynamin-1 and Adaptor protein 2 B1 (AP2B1). This binding regulated aging markers (p21, p35/25, and p16) and inflammatory factors (TNF-α and NF-κB), and reduced the expression of Alzheimer's disease marker proteins (Tau, p-Tau, Aβ1-42, and APOE), which delayed senile dementia. Transcriptome analysis of the brain showed that circNF1-419 improved other signaling pathways, especially those related to the synapses of SAMP8 mice. These findings provide novel insights into circNF1-419 and its potential usefulness for the diagnosis and treatment of dementia by regulating Dynamin-1 and AP2B1 mediated autophagy.

Context: Bajijiasu (BJJS), a main bioactive compound from Morinda officinalis F.C. How. (Rubiaceae), is widely administered concomitantly with other drugs for treating male impotence, female infertility, fatigue, chronic rheumatism, depression, etc.Objective: This study investigates the regulation of P-glycoprotein (P-gp) by BJJS in vitro and in vivo.Material and methods: HepG2 cells were incubated with BJJS (10, 20 or 40 μM) for 48 h. C57 mice were orally treated with BJJS (25, 50 or 100 mg/kg) for 2 weeks. The protein and mRNA levels of P-gp were measured by using Western blot and real-time PCR, respectively. siNrf2 RNA was used to explore the mediation effects of Nrf2 on the P-gp expression. The efflux activity of P-gp was tested via a flow cytometry.Results: Incubation of HepG2 cells with BJJS at 10, 20, and 40 μM up-regulated the P-gp protein expression by 12.3%, 82.9%, and 134.3%, respectively. Treatment of C57 mice with BJJS at 25, 50 and 100 mg/kg increased the P-gp protein expression by 49.3%, 75.8% and 106.0%, respectively. Incubation of the cells with BJJS at 10, 20 and 40 μM up-regulated the total Nrf2 protein levels by 34.3%, 93.1% and 118.6%, respectively, and also increased the nuclear Nrf2 protein levels by 14.8%, 44.4% and 59.25%, respectively. The total Nrf2 protein levels were increased by 46.3%, 66.5%, and 87.4%, respectively, in the mice exposed to BJJS at 25, 50, and 100 mg/kg. Inhibition of Nrf2 by siRNA diminished the P-gp induction by 25.0%, 33.4%, and 38.7%, respectively, in the cells. In addition, BJJS enhanced the efflux activity of P-gp by 9.6%, 37.1%, and 48.1%, respectively, in the cells.Conclusions: BJJS activates Nrf2 to induce P-gp expression, and enhanced the efflux activity of P-gp. The possibility of potential herb–drug interactions when BJJS is co-administered with other P-gp substrate drugs should be carefully monitored.

The gut microbiota is considered an important factor in the progression of Alzheimer's disease (AD). Active research on the association between the metabolome and the gut microbiome is ongoing and can provide a large amount of beneficial information about the interactions between the microbiome and the metabolome. Previous studies have shown that the oligosaccharides from Morinda officinalis (OMO) can delay the progress of AD in model animals by regulating the diversity of the gut microbiome and metabolic components, and the correlation between the gut microbiome and metabolic components still needs to be further verified. This study applied a new two-level strategy to investigate and ensure the accuracy and consistency of the results. This strategy can be used to determine the association between the gut microbiome and serum metabolome in APP/PS1 transgenic mice and C57BL/6J male mice. The "4C0d-2 spp.-Cholesterol," "CW040 spp.-L-valine," "CW040 spp.-L-acetylcarnitine," "RF39 spp.-L-valine," "TM7-3 spp.-L-valine," and "TM7-3 spp.-L-acetylcarnitine" associations among specific "microbiota-metabolite" pairs were further identified based on univariate and multivariate correlation analyses and functional analyses. The key relevant pairs were verified by an independent oligosaccharide intervention study, and the gut microbiome and serum metabolome of the OMO intervention group were similar to those of the normal group. The results indicate that OMO can significantly suppress Alzheimer's disease by regulating the key microbiota-metabolite pairs. Therefore, this two-level strategy is effective in identifying the principal correlations in large datasets obtained from combinations of multiomic studies and further enhancing our understanding of the correlation between the brain and gut in patients with AD.

Alzheimer's disease (AD), a progressive neurodegenerative disorder, lacks preclinical diagnostic biomarkers and therapeutic drugs. Thus, earlier intervention in AD is a top priority. Studies have shown that the gut microbiota influences central nervous system disorders and that prebiotics can improve the cognition of hosts with AD, but these effects are not well understood. Preliminary research has shown that oligosaccharides from Morinda officinalis (OMO) are a useful prebiotic and cause substantial memory improvements in animal models of AD; however, the mechanism is still unclear. Therefore, this study was conducted to investigate whether OMO are clinically effective in alleviating AD by improving gut microbiota. OMO were administered to APP/PS1 transgenic mice, and potential clinical biomarkers of AD were identified with metabolomics and bioinformatics. Behavioral experiments demonstrated that OMO significantly ameliorated the memory of the AD animal model. Histological changes indicated that OMO ameliorated brain tissue swelling and neuronal apoptosis and downregulated the expression of the intracellular AD marker Aβ1-42. 16S rRNA sequencing analyses indicated that OMO maintained the diversity and stability of the microbial community. The data also indicated that OMO are an efficacious prebiotic in an animal model of AD, regulating the composition and metabolism of the gut microbiota. A serum metabolomics assay was performed using UHPLC-LTQ Orbitrap mass spectrometry to delineate the metabolic changes and potential early biomarkers in APP/PS1 transgenic mice. Multivariate statistical analysis showed that 14 metabolites were significantly upregulated, and 8 metabolites were downregulated in the model animals compared to the normal controls. Thus, key metabolites represent early indicators of the development of AD. Overall, we report a drug and signaling pathway with therapeutic potential, including proteins associated with cognitive deficits in normal mice or gene mutations that cause AD.

目的 探讨精神分裂症患者 CYP2D6*10 基因多态性与利培酮( RISP)稳态血药浓度的相关性.方法 以质谱分析法检测99例连续服用RISP达稳态的精神分裂症患者血液中RISP及其代谢产物9羟基-利培酮(9-OH-RISP)的浓度,根据9-OH-RISP/RISP比值,将受检者分为3组,分别为A组35例(比值＜5)、B组26例(比值5~10)和C组38例(比值＞10).以实时荧光PCR分别检测所有受检对象CYP2D6*10等位基因多态性,同时抽取部分样本进行DNA测序,统计分析不同9-OH-RISP/RISP比值与CYP2D6*10基因多态性的相关性.结果 A组35例患者中,CYP2D6*10基因多态性为C/C 4例(11.43%),C/T 6例(17.14%),T/T 25例(71.43%);B 组26 例患者中,C/C 8 例(30.77%),C/T 14 例(53.85%),T/T 4 例(15.38%);C组38例患者中,C/C 17例(44.74%),C/T 21例(55.26%),T/T为0例.不同组别CYP2D6*10等位基因分布差异有统计学意义(P＜0.001).按照基因型进行分类,C/C 基因型组9-OH -RISP/RISP为14.21 ±1.37,C/T基因型组9 -OH -RISP/RISP 为12.31 ±1.15,T/T 基因型组 9 -OH -RISP/RISP 为3.14 ±1.36. T/T组的9-OH-RISP/RISP比值显著低于 C/C 组和 C/T组(P ＜0.000 1),而 C/T组的9 -OH-RISP/RISP比值略低于C/C组,但差异无统计学意义( P=0.87).结论 个体稳态血药浓度9 -OH-RISP/RISP相对比较恒定,且该比值与CYP2D6*10等位基因多态性存在显著的相关性;CYP2D6*10纯合突变对RISP代谢的影响非常明显,而杂合突变型个体对RISP代谢的影响非常小.

Objective To investigate the polymorphism of CYP2C19 gene and the distribution of metabolic phenotypes in bipolar disorder patients of Han nationality in Southern China ,and the relationship between sex and CYP2C19 gene polymorphism will be explored .Methods DNA microarray was used to detect the CYP2C19 gene polymorphism and metabolic phenotype in 1043 bipolar disorder patients ,gene counting meth-ods were used to calculate the genotype frequency and allele frequency ,and the relationship between different gender and the frequency of genetic polymorphism was analyzed .Results Six detected genotype(CYP2C191/1 ,1/2 ,1/3 ,2/2 ,2/3 ,3 /3 ) f requency w ere 40 .6％ ,40 .5％ ,5 .2％ ,9 .9％ ,3 .4％ , 0 .5％ ,the frequency of 3 metabolic phenotypes(extensive metabolizer ,intermediate metabolizer ,poor metabo-lizer) were 40 .5％ ,45 .8％ ,13 .7％ respectively .There was no significant difference in CYP2C19 genotype and metabolic phenotype between different gender groups .Conclusion 1/1 and 1/2 are the main poly-morphism of CYP2C19 in bipolar disorder patients of Han nationality ,681 loci′s mutation frequency is higher than that of 636 ,detection of the CYP2C19 gene polymorphism and metabolic phenotypes contribute to the clinical reasonable medication .

目的证实PS-1环状RNA（Cir-PS1-615）的存在,建立Cir-PS1-615的检测方法,并对其与AD的关系进行初步研究。方法采用反向PCR后克隆测序的方法,在人神经母细胞瘤SY5Y细胞对PS1基因的十二个外显子设计引物分别检测,发现可能存在的环状RNA,并对30例AD患者及对照组全血进行RT-qPCR检测。结果证实了PS1基因第2-5外显子有环状RNA的存在（Cir-PS1-615）,对AD患者与对照组血液进行检测,发现AD患者与对照组血液Cir-PS1-615有差异表达。结论 PS1环状RNA Cir-PS1-615可能成为AD新的临床诊断标志物。

目的:探讨华南地区汉族精神分裂症患者CYP2C19基因多态性及代谢表型的分布,并分析性别与CYP2C 19基因多态性的关系.方法:以DNA微阵列技术检测1562例精神分裂症患者的CYP2C19基因多态性及代谢表型,用基因计数法计算基因型频率和等位基因频率,同时分析基因多态性发生频率与性别的相关性.结果:6种CYP2C19基因型(CYP2C19*1/*1,*1/*2,*1/*3,*2/*2,*2/*3,*3/*3)频率分别为:38.7％、41.9％、6.5％、9.2％、3.5％、0.3％;快代谢型、中等代谢型、慢代谢型所占比例分别为:38.9％、48.2％、12.9％;不同性别间CYP2C 19基因型及代谢表型比较,差异无统计学意义(P＞0.05).结论:华南地区汉族精神分裂症患者CYP2C19基因多态性以*1/*1及*1/*2为主,其分布与性别无关.

Objective To investigate the polymorphism of CYP2C19 gene and the distribution of metabolic phenotypes in dementia patients of Han nationality,and the relationship between sex and CYP2C19 gene polymorphism was explored. Methods DNA microarray was used to detect the CYP2C19 gene polymorphism and metabolic phenotype in 327 dementia patients,and the relationship between different gender and the frequency of genetic polymorphism was analyzed. Results The frequencies of the six detected genotype CYP2C19 *1/*1,*1/*2,*1/*3,*2/*2,*2/*3,and *3/*3 were 37.3%,41.6%, 8.6%,9.5%,2.4%,and 0.6%,respectively;the frequencies of 3 metabolic phenotypes extensive metabolizer,intermediate metabolizer,and poor metabolizer were 38.2%,49.2%,and 12.5%,respectively. There was no significant difference in CYP2C19 genotype and metabolic phenotype between different gender groups. Conclusion The polymorphism of CYP2C19 gene and the distribution of metabolic phenotype in dementia patients of Han nationality in Southern China were consistent with those in other regions of China. Relationship between the CYP2C19 gene polymorphisms and gender was not found.

Objective To investigate the relationship of apolipoprotein E (ApoE) allelic frequency and serum lipid levels in patients with Alzheimer′s disease (AD). Methods DNA microarray was used to detect the ApoE genotypes of AD patients (n = 200) and age-matched non-demented elderly control subjects (n = 159). Serum lipid levels was measured by Immunoturbidimetric assay at the same time. We analyzed the ApoE genotype distribution and the relationship of apolipoprotein E ( ApoE ) allelic frequency and serum lipid levels . Results The ApoE ε4 allelic frequencies (25.5%) in AD group is higher than that of the control group (7.9%) (P < 0.05). The ε2 allele was associated with a higher ApoE concentration, whereas with a mediate concentration in ε3 and the lowest concentration ( P < 0 . 05 ) in ε4 . Serum concentrations of ApoE showed no significant difference between AD patients and the healthy population who were with the same genotype (P > 0.05). Conclusion The ApoE levels are negatively related to ApoE ε4 allele frequency and have no significant differences with the same genotype in AD and the control group,which suggests that lower serum ApoE levels in AD patients is caused by higher ApoE ε4 allelic frequency in AD than in healthy population.

Objective To explore the plasma levels of soluble CD40 (sCD40) and soluble CD40 ligand (sCD40L) in the patients with Alzheimer’s disease (AD) and those with amnestic mild cognitive impairment (aMCI). Methods The levels of plasma sCD40 and sCD40L were measured in 20 patients with AD, 35 patients with aMCI, and 32 cognitively normal controls (NC) using commercially available ELISAs. The cognitive function of AD and aMCI patients was mea?sured by mini-mental state examination (MMSE). Results There were significant differences in plasma sCD40 among AD, aMCI and NC groups (P<0.05) as the medians (the upper and lower quartiles) of plasma levels were 123.3 (97.4, 149.5) pg/mL, 102.9 (63.6, 124.0) pg/mL and 70.66 (51.0, 90.8) pg/mL, respectively. There were significant differences in plasma sCD40L among AD, aMCI and NC groups (P<0.05) as plasma levels were 537.0 (316.0, 1134.0) pg/mL, 316.0&nbsp;(190.0,546.0) pg/mL and 167.0 (107.5,478.0) pg/mL. A negative correlation between the plasma concentrations of sCD40L and the MMSE scores was found in aMCI patients (r=-0.736, P<0.001). Conclusions There are relevant chang?es of plasma sCD40 and sCD40L levels in patients with AD and aMCI. The present results suggest that plasma levels of sCD40 and sCD40L may be appropriate biomarkers for AD patients and indicate that CD40-CD40L signaling may be in?volved in AD pathophysiology.

Objective To investigate the application value of apolipoprotein E (ApoE) genotyping by DNA microarray technology and the relationship between ApoE allelic frequency and serum ApoE levels in both healthy individuals and patients with Alzheimer ′s disease (AD).Methods This research is case-control study.DNA microarray was used to detect the ApoE genotypes of AD patients (n =280) and age-matched non-demented elderly control subjects ( n =230) .The cases and controls were collected in Guangzhou Huiai Hospital during July 2014 to September 2015.The accuracy of genotype results was verified by DNA sequencing.Serum ApoE levels were measured by immunoturbidimetric assay .The ApoE genotype distribution and the relationship between ApoE allelic frequency and serum ApoE levels were analyzed.The “t” test was used to compare the ApoE levels of AD patients and controls , variance analysis was used to analyze ApoE levels in the persons with different genotype .Results DNA microarray technology genotyping results were completely consistent with the results of DNA sequencing .In AD group, the ApoE genotype distribution were 2.9%(8 /280) for ε2ε3, 1.8% (5/280) for ε2ε4, 46.8% (131/280)for ε3ε3,45.4%(127 /280) for ε3ε4 and 3.1%(9 /280) for ε4ε4.While in the control group, the ApoE genotype distribution were 0.9%(2 /230) for ε2ε2, 12.6% (29/230)for ε2ε3, 1.3%(3 /230) forε2ε4, 70.0% (161 /230) for ε3ε3 and 15.2% (35 /230) for ε3ε4.The average serum concentrations of ApoE were (33.29 ±10.87)mg/L in AD patients and (41.28 ±10.95)mg/L in the controls.Among all participants, the average serum levels of ApoE were (50.86 ±6.21) mg/L for ε2 carriers, (38.78 ± 12.07)mg/L for ε3 carriers and (30.47 ±7.68)mg/L for ε4 carriers.In AD group,ApoE level of ε2, ε3,ε4 carriers is (50.31 ±9.08)mg/L, (38.30 ±7.60) mg/L and (32.86 ±5.93)mg/L respectively.In the control group, the ApoE level of ε2, ε3, ε4 carriers is (51.00 ±5.53)mg/L, (41.01 ±10.09)mg/L and (32.86 ±5.93)mg/L respectively.The ApoE levels of persons with different ApoE alleles are ε2 >ε3 >ε4. The difference is significant (F =89.6, P <0.05).However, the ApoE levels in persons with the same ApoE genotype between healthy individuals and AD patients have no significant difference ( t =0.981, 2.878 and 1.732 respectively, P >0.05) .Conclusions DNA microarray technology possesses high efficiency and favorable accuracy.The ε2 allele is associated with a higher ApoE concentration , ε3 allele with a mediate concentration and ε4 allele with a lowest concentration.Serum concentrations of ApoE showed no significant difference between AD patients and the healthy groups who have the same genotype .The primary cause of the low serum ApoE levels in AD patients is that the ApoE ε4 allelic frequencies of them are higher than that of the healthy persons.

Objective To investigate the association between cognitive impairment and levels of serum cortisol in patients with late - life depression(LLD). Methods We included 35 LLD patients with cognitive impairment,14 LLD patients without cognitive impairment and 25 normal controls. The Hamilton Depression Scale - 17 item( HAMD - 17)and Mini Mental State Examination (MMSE)were used to assess the severity of depressive symptoms and the cognitive function,respectively. Serum cortisol levels were measured by radioimmunoassay. Results Serum cortisol levels in LLD patients with cognitive impairment were significantly higher than those in LLD patients without cognitive impairment and normal controls(All P < 0. 01). LLD patients with cognitive impairment in episode stage and those in remitted stage showed significantly higher serum cortisol levels than LLD patients without cognitive impairment in remitted stage and normal controls(All P < 0. 05). Conclusion The findings suggest that,in both episode and remitted stages,LLD patients with cognitive impairment show increased serum cortisol levels. High cortisol level might be associated with impaired cognitive function in LLD patients.

目的 检测不同水平同型半胱氨酸(HCY)患者5,10-亚甲基四氢叶酸还原酶(MTHFR)基因第677核苷酸的突变频率,探讨MTHFR基因多态性与不同HCY水平的相关性.方法 以HCY大于15 μmol/L的受检者(435例)作为实验组,将实验组按照HCY水平分成4组:15 μmol/L＜ HCY≤20 μmol/L为第一组;20 μmol/L＜HCY≤25 μmol/L为第2组;25 μmol/L＜ HCY≤30μmol/L为第3组;HCY＞ 30 μmol/L为第4组,同时以HCY≤15 μmol/L的人群(229例)为对照组.用DNA微阵列技术检测实验组和对照组MTHFR基因第677核苷酸的突变,统计分析各组MTHFR基因型及等位基因频率分布.结果 MTHFR基因677位核苷酸由C变异为T与HCY水平显著相关(x2=180.16,P＜0.0001),且随着HCY水平升高T等位基因频率呈增大趋势,经线性趋势检验有统计意义(x2=156.67,P＜0.0001);同时,单独一组与对照组比较,MTHFR基因型和等位基因频率分布没有显著差异(x2=0.031,P＞0.05).结论 MTHFR 677位等位基因由C突变为T是导致HCY水平明显升高的重要原因,而且是导致HCY＞ 30 μmol/L的主要原因;而HCY轻度升高(15 μmol/L＜ HCY≤20 μmol/L)可能为其它原因所致,并非MTHFR基因突变引起.

目的 探讨DNA微阵列技术检测CYP2C19基因多态性的应用价值.方法 用PCR结合DNA微列阵技术检测300例精神疾病患者的CYP2C19基因型,并用DNA测序法验证DNA微列阵技术检测结果的可靠性.结果 CYP2C19基因型检测结果分别为快代谢型109例(36.3％),中等代谢型158例(52.7％),慢代谢型33例(11.0％);DAN微阵列技术检测结果与DNA测序法结果完全一致;患者性别之间基因型和表型所占比例差异均无统计学意义(P均＞0.05).结论 DNA微阵列技术检测CYP2C19基因多态性具有快速、准确的特点,可替代DNA测序法用于个体化医疗.

Immunohistochemical studies have revealed that cystatin C (CysC) co-localizes with amyloid-β (Αβ) in amyloid-laden vascular walls and in the senile plaque cores of amyloid. In vitro and in vivo animal studies suggest that CysC protects against neurodegeneration by inhibition of cysteine proteases, inhibition of Αβ aggregation, induction of autophagy and induction of cell division. CysC levels may be altered and may have a potential link with cerebrospinal fluid (CSF) Aβ levels in various types of dementia with characteristic amyloid deposits, such as Alzheimer's disease (AD), dementia with Lewy bodies (DLB) and the atrophic form of general paresis (AF-GP). We assessed the serum and CSF levels of CysC and the CSF levels of Aβ40 and Aβ42 in patients with AD (n = 51), DLB (n = 26) and AF-GP (n = 43) and normal controls (n = 30). Using these samples, we explored the correlation between CSF CysC and CSF Aβ levels. We found that in comparison to the normal control group, both CSF CysC and CSF Aβ42 levels were significantly lower in all three dementia groups (all p<0.001); serum CysC levels were the same in the AD and DLB groups, and were lower in the AF-GP group (p = 0.008). The CSF CysC levels were positively correlated with both the CSF Aβ40 and Aβ42 levels in the AD, AF-GP and normal control groups (r = 0.306∼0.657, all p<0.05). Lower CSF CysC levels might be a common feature in dementia with characteristic amyloid deposits. Our results provide evidence for the potential role of CysC involvement in Aβ metabolism and suggest that modulation of the CysC level in the brain might produce a disease-modifying effect in dementia with characteristic amyloid deposits.

Objective To determine the microRNA(miRNA) expression profile of in CSF in AD patients. Methods miRNA microarrays were performed to detect the expression profile of miRNAs in 10 cases of CSF in AD patients and the healthy control persons. Preliminary bioinformatic analysis was conducted. The microarray results were confirmed by real-time PCR assay. Results miRNA microarray results revealed that 128 miRNAs were dysregulated in AD patients and the corresponding healthy controls. Sixty-three miRNAs were significantly up-regulated, and 65 miRNAs were significantly down-regulated. Real-time PCR results demonstrated that up-regulation of miR-125b and miR-132 was consistent with that based on microarray array. Conclusion Specific miRNA expression profile was determined in CSF in AD patients, and the differentially expressed miRNAs may be used as potential biomarkers of AD.

目的建立定量检测α-synuclein的ELISA夹心法。方法采用抗人α-synuclein单抗包被酶标板,以兔抗人α-synuclein多抗为夹心抗体、HRP标记羊抗兔IgG为检测抗体、重组人α-synuclein为标准品,建立检测α-synuclein的间接ELISA法,并对36例正常对照、27例路易体痴呆患者脑脊液样本进行了检测。结果建立的夹心ELISA法检测α-synuclein的线性范围为1.56～200 ng/ml,批内、批间变异系数分别为为7.51%和13.7%,36例正常对照、27例路易体痴呆患者脑脊液α-synuclein的含量比较差异有统计学意义（P〈0.05）。结论成功建立了一种检测α-synuclein的夹心ELISA法。