多奈哌齐合并复方海蛇胶囊治疗阿尔茨海默病性痴呆患者对照研究

目的:探讨多奈哌齐合并复方海蛇胶囊对阿尔茨海默病(AD)患者认知功能和行为能力的改善作用。方法:90例AD患者随机分为3组:联合治疗组(给予多奈哌齐合并复方海蛇胶囊治疗)30例、多奈哌齐治疗组(单用多奈哌齐治疗)30例、对照组(仅予常规治疗,不予痴呆药物)30例。观察3个月。分别在治疗前和治疗3个月后采用简易精神状态检查量表(MMSE)及日常生活能力量表(ADL)测评3组患者的认知功能和生活能力。结果:治疗3个月,联合治疗组MMSE减分值明显高于多奈哌齐治疗组(t=5.09,P0.01)和对照组(t=7.71,P0.01);多奈哌齐治疗组减分值明显高于对照组(t=3.10,P0.01)。联合治疗组ADL评分减分值明显高于多奈哌齐治疗组(t=-2.33,P=0.02)和对照组(t=-6.88,P0.01);多奈哌齐治疗组减分值明显高于对照组(t=-5.50,P0.01)。结论:多奈哌齐和复方海蛇胶囊联合治疗对AD患者的认知功能及行为能力有显著的改善作用。     

多奈哌齐联合尼莫地平治疗中重度阿尔茨海默病的疗效及安全性

目的：观察多奈哌齐联合尼莫地平治疗中、重度阿尔茨海默病（AD）的疗效及安全性。方法：32例中、重度AD患者随机分为多奈哌齐组及多奈哌齐＋尼莫地平（联用尼莫地平）组。采用简易精神状态量表（MMSE）、临床痴呆评定量表（CDR）歧全面衰退量表（GDS）评定疗效。结果：多奈哌齐组MMSE和CDR评分较治疗前明显改善；联用尼莫地平组3种量表评分较治疗前均显著改善。两组均无严重不良反应。结论：多奈哌齐联用尼莫地平较单用多奈哌齐可能更显著改善中、重度AD的认知功能，两种药物安全性俱佳。     

VitB12及叶酸对伴高同型半胱氨酸血症的AD患者血清神经递质、细胞因子水平及认知功能的影响

目的 探讨VitB12及叶酸对伴高同型半胱氨酸血症的阿尔茨海默病(AD)患者血清神经递质、细胞因子水平及认知功能的影响。方法 选取2018年2月-2019年2月在本院收治的伴高同型半胱氨酸血症的AD患者90例为研究对象,并将其随机分为2组,即对照组和研究组,各45例; 对照组采用盐酸多奈哌齐+盐酸美金刚进行治疗,研究组采用VitB12+叶酸+盐酸多奈哌齐+盐酸美金刚治疗; 比较2组患者治疗后的血清神经递质、细胞因子水平以及认知功能。结果 2组治疗前血清IFN-r、IL-6、VEGF、BDNF水平比较无明显差异(P>0.05); 2组治疗后血清IL-6、IFN-r、Hcy水平与治疗前比较明显降低(P<0.05),且组间比较有明显差异(P<0.05); 研究组治疗6个月后Hcy水平较治疗前明显降低(P<0.05),而对照组则治疗前后无明显变化(P>0.05),2组治疗6个月后Hcy水平比较,有明显差异(P<0.05)。2组治疗后血清BDNF和VEGF水平与治疗前比较明显升高(P<0.05),且组间比较也有明显差异(P<0.05)。2组治疗前血清5-HT、β-EP、DA水平比较无明显差异(P>0.05); 2组治疗后血清5-HT、β-EP、DA水平与治疗前比较明显升高(P<0.05),且组间比较有明显差异(P<0.05)。治疗6个月后研究组的认知功能评分明显高于对照组(P<0.05)。结论 采用VitB12结合叶酸可以降低伴高同型半胱氨酸血症的AD患者的同型半胱氨酸水平,并且还可有效改善患者血清神经递质、细胞因子水平以及认知功能。     

盐酸美金刚与盐酸多奈哌齐治疗阿尔茨海默病疗效对比

目的比较盐酸美金刚与盐酸多奈哌齐治疗阿尔茨海默病(AD)的有效性和安全性。方法将72例AD患者随机分为2组:美金刚组36例给予盐酸美金刚片20mg/d,多奈哌齐组36例给予盐酸多奈哌齐10mg/d,2组疗程均为6个月。2组患者治疗前和治疗3个月、6个月后均采用简易智能精神状态检查量表(MMSE)和AD评定量表的认知次级量表(ADAS-cog)评价患者认知功能、精神行为及痴呆严重程度。结果经治疗3个月、6个月后,2组患者MMSE、ADAS-cog评分均较治疗前明显好转(P<0.05或P<0.01);治疗3个月、6个月后,2组患者MMSE、ADAS-cog评分比较差异无统计学意义(均P>0.05);美金刚组的不良反应发生率低于多奈哌齐组(χ2=4.5714,P>0.05)。结论盐酸美金刚与盐酸多奈哌齐均能显著改善AD患者的认知功能、日常生活能力和人格情感障碍,两药疗效无明显差异,且盐酸美金刚具有良好的安全性。     

黄连解毒汤对APP/PS1双转基因阿尔茨海默病小鼠脑组织自由基代谢及IL-6、IL-1β含量的影响

目的观察黄连解毒汤(HLJDT)对阿尔茨海默病(Alzhemer’s disease,AD)模型小鼠自由基代谢及炎性细胞因子(IL-6,IL-1β)含量的影响,并探讨其可能治疗机制。方法采用APP/PS1双转基因AD小鼠模型,并随机分为模型对照组(CMC组)、阳性对照组(盐酸多奈哌齐组)、HLJDT大中小剂量组,每日予以相应药物灌胃治疗后检测脑组织中自由基代谢指标(SOD、MDA),并应用ELISA法检测炎性细胞因子(IL-6,IL-1β)含量。结果 HLJDT各剂量组均能明显提高SOD活性,降低MDA含量(P<0.01);盐酸多奈哌齐组及HLJDT各剂量组均显著降低IL-6含量(P<0.01);HLJDT小剂量组IL-1β含量低于CMC组,但HLJDT各剂量组及盐酸多奈哌齐组与模型对照组(CMC组)比较均无统计学差别(P>0.05)。结论 HLJDT治疗AD的机制可能与提高抗氧化能力,减轻炎症反应有关。     

黄芪甲苷Ⅳ通过激活PPAR-γ抑制NF-κB介导的炎症反应减少AD大鼠脑中淀粉样蛋白沉淀

目的探讨黄芪甲苷IV对阿尔茨海默病(AD)大鼠脑中β淀粉样蛋白和学习记忆功能的影响及其机制。方法将72只老年雄性SD大鼠随机分为6组,对照组、模型组、多奈哌齐组、黄芪甲苷低剂量组、黄芪甲苷高剂量组、黄芪甲苷高剂量+抑制剂组,每组12只。利用A β_(1-42)脑室注射与AlCl3连续灌胃建立AD模型,造模期间持续使用黄芪甲苷或多奈哌齐进行治疗,水迷宫结束后检测大脑组织中A β_(1-42)、APP及炎症因子表达,Western blot检测PPAR-γ及炎症相关蛋白表达。结果黄芪甲苷Ⅳ与多奈哌齐疗效一致,能够显著改善大鼠学习认知能力,抑制脑中APP水解成A β_(1-42),减少脑中炎症因子IL-1β、TNF-α、IL-6表达。黄芪甲苷Ⅳ能够有效升高PPAR-γ蛋白表达,减少NLRP3炎性小体的表达。此外,PPAR-γ抑制剂则逆转黄芪甲苷Ⅳ改善大鼠认知功能的作用,造成大鼠脑中炎症因子含量升高,促进APP水解生成A β_(1-42)。结论黄芪甲苷通过增加PPAR-γ蛋白表达,抑制大鼠脑中炎症因子表达,减少APP水解生成A β_(1-42),改善大鼠认知学习能力降低。     

多奈哌齐治疗阿尔茨海默病临床疗效分析

目的 探讨多奈哌齐对阿尔茨海默病治疗的有效性及安全性。方法 采用分组对照，治疗组给予多奈哌齐及脑复康治疗16周，对照组只给予脑复康治疗。治疗前后采用AD评定量表的认知次级量表(ADAS-cog)和简易智能精神状态检查量表(MMSE)评价患者认知功能、精神行为及痴呆严重程度结果多奈哌齐治疗组患者较对照组患者ADAS-cog及MMSE评分改善明显，而对照组患者评分无明显改变。治疗患者无明显药物副作用。结论 多奈哌齐可以安全地用于治疗阿尔茨海默病。     

多奈哌齐联合养血清脑颗粒改善轻度认知功能障碍的效应

目的评价多奈哌齐联合养血清脑颗粒对轻度认知功能障碍患者的疗效。方法30例轻度认知功能障碍患者随机分为多奈哌齐组14例;多奈哌齐联合养血清脑颗粒16例,共服用16周。分别测定两组治疗前后简易智力状态量表(MMSE)总分及成人韦氏记忆测验记忆商(MQ);经颅多普勒(TCD)检查评估两组治疗前后的脑血流参数改变。结果(1)治疗前多奈哌齐组及多奈哌齐联合养血清脑颗粒治疗组在MMSE的亚项记忆力和回忆力无显著差别(P>0.05);治疗16周后多奈哌齐组及多奈哌齐联合养血清脑颗粒治疗组在MMSE的亚项记忆力和回忆力上较治疗前有显著差别(P<0.05);(2)治疗前多奈哌齐组及多奈哌齐联合养血清脑颗粒治疗组在MQ的亚项图片回忆、再认及背数方面上无显著差别,治疗后多奈哌齐组及多奈哌齐联合养血清脑颗粒治疗组在亚项图片回忆、再认及背数方面较治疗前均有提高;联合治疗组更为显著。(3)治疗前TCD检测两组患者均可显示双侧脑血流不对称、血管阻力指数增高,治疗后自身对照脑血流趋于对称,血管阻力指数降低,多奈哌齐联合养血清脑颗粒组改变明显(P<0.05),多奈哌齐组无显著改善(P>0.05)。结论多奈哌齐联合养血清脑颗粒对改善轻度认知功能障碍患者的记忆力及脑血流改善有明显疗效。     

多奈哌齐与法舒地尔联合心理疏导对血管性认知障碍患者的负性情绪及对血清炎性因子的影响

目的探讨多奈哌齐与法舒地尔联合心理疏导对血管性认知障碍(VCI)患者负性情绪及血清炎性因子水平的影响。方法选取68例VCI患者随机分为观察组与对照组,各34例。对照组应用多奈哌齐治疗和心理疏导,观察组在对照组基础上加用法舒地尔。比较两组治疗前后简易精神状态检查量表(MMSE)、Barthel指数(BI)、汉密尔顿焦虑量表(HAMA)和汉密尔顿抑郁量表(HAMD)评分,检测血清超敏C反应蛋白(hs-CRP)、白介素-6(IL-6)和肿瘤坏死因子α(TNF-α)水平。结果观察组治疗后MMSE、BI评分显著高于对照组,HAMA、HAMD评分显著低于对照组(P0.05);观察组治疗后血清hs-CRP、IL-6及TNF-α水平显著低于对照组(P0.05)。结论多奈哌齐与法舒地尔联合心理疏导有利于改善VCI患者的认知功能与日常生活活动能力,减轻负性情绪,并可下调促炎因子水平。     

多奈哌齐联合鼠神经生长因子治疗阿尔茨海默病48例临床观察

目的：探讨多奈哌齐联合鼠神经生长因子联合治疗阿尔茨海默病的临床疗效。方法48例患者随机分为2组，分别接受多奈哌齐或多奈哌齐联合鼠神经生长因子治疗，总疗程12周，根据MMSE、ADL、ADAS‐cog量表评价2组治疗前后认知功能及生活能力变化。结果2组在日常生活能力及缓解认知功能的减退方面，显示有效；且联合治疗组较单纯使用多奈哌齐组在MMSE和ADL评分上改善更为显著。结论多奈哌齐联合鼠神经生长因子治疗能有效改善AD患者的认知、行为能力，并且具有良好安全性。     

Elevated interleukin-6 levels in cerebrospinal fluid of vascular dementia patients

OBJECTIVES: To investigate a possible implication of inflammatory processes in the development of dementia in cerebrovascular disease. PATIENTS AND METHODS: We examined the levels of interleukin-6 (IL-6) in the cerebrospinal fluid (CSF) of patients with Alzheimer's disease (AD) (n = 26), ischemic cerebrovascular disease without dementia (CVD) (n = 11), vascular dementia (VD) (n = 11), and other neurological disorders (n = 21) using sensitive enzyme-linked immunosorbent assay. RESULTS: The CSF concentrations of IL-6 were significantly elevated in patients with VD compared with those of patients with AD or CVD. CONCLUSION: The CSF IL-6 levels are increased in patients with VD, suggesting that inflammatory mechanisms may be involved in the development of cognitive decline in some patients with cerebrovascular disease. CSF IL-6 may be a biological marker for dementia in cerebrovascular disease.     

Soluble interleukin-1 receptor type II levels are elevated in cerebrospinal fluid in Alzheimer's disease patients

Evidence from epidemiological, clinical and experimental studies favour the hypothesis that inflammatory events are part of the neuropathology in Alzheimer's disease. Proinflammatory cytokines such as interleukin-1 (IL-1), interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha) have been found in activated microglia in the vicinity of amyloid plaques in Alzheimer's disease brain. In the present study, the levels of soluble IL-1 receptor type II (sIL-1R type II), IL-1 receptor antagonist (IL-1ra), IL-1beta, IL-6 and TNF-alpha were analyzed in cerebrospinal fluid (CSF) samples from Alzheimer's disease patients and control subjects. The levels of sIL-1R type II were significantly higher in CSF from Alzheimer's disease patients than in CSF samples from control subjects (38.5+/-8 pg/ml (mean+/-S.E.M.) vs. 7.9+/-4 pg/ml, p<0.05). Measurements of the proinflammatory cytokines IL-6 and TNF-alpha showed no significant difference between the two groups, and the levels of IL-1beta and IL-1ra in the present material were too low to permit detection. The increased levels of sIL-1R type II may reflect a compensatory mechanism to balance an increased release of IL-1 receptor agonists in the Alzheimer's disease brain.     

Serum interleukin-6 levels correlate with the severity of dementia in Down syndrome and in Alzheimer's disease

Introduction - Inflammatory processes are suspected in the pathomechanism of Alzheimer's dementia (AD) but the serum and cerebrospinal fluid (CSF) levels of inflammatory cytokines are not yet determined in the different forms of the disorder. Subjects and methods - Interleukin-6 (IL-6) levels were examined in the sera and CSF of patients with mild-moderate and severe stage of late onset sporadic type of AD and in the sera of demented Down syndrome (DS) probands with similar stages of AD and compared with data of age-matched healthy controls. Results - Normal serum IL-6 levels were found in the mild-moderate stage, but significantly increased levels were found in the severe stage of both dementia groups. The CSF concentrations remained within the normal range in all groups. Positive correlations between the serum IL-6 levels and age and the severity of the disease were present. Conclusion - These findings suggest a disease stage dependent general activation of the immune system both in sporadic AD and in DS with AD.     

Intra vitam lumbar and post mortem ventricular cerebrospinal fluid immunoreactive interleukin-6 in Alzheimer's disease patients

OBJECTIVES: In view of contradictory findings in previous studies, to examine the diagnostic value of interleukin-6 measurements in cerebrospinal fluid (CSF) of Alzheimer's disease patients. MATERIAL AND METHODS: Interleukin-6-immunoreactivity (IL-6-IR) was measured in 169 intra vitam lumbar and 21 post mortem ventricular CSF samples of patients with probable and neuropathologically confirmed Alzheimer's disease (AD), non-AD dementias (NAD), neurological disorders without cognitive impairment (OND) and controls (CON) using a specific sandwich enzyme immunoassay. RESULTS: Intra vitam lumbar samples had significantly elevated (P < 0.03) IL-6-IR not only in the AD, but also in the NAD and OND group compared with controls. AD patients with late onset (> 65 years) had slightly (P > 0.05) higher values than patients with early onset (< 65 years). In post mortem ventricular fluid, differences among groups did not reach significance (P > 0.05). CONCLUSION: We conclude that elevations of CSF IL-6-IR can not serve as a diagnostic marker of the disease, but, hypothetically, could reflect presence or activity of IL-6 mediated immunological phenomena in single AD patients.     

Inflammatory markers in matched plasma and cerebrospinal fluid from patients with Alzheimer's disease

It has been suggested that a number of molecules associated with inflammation are involved in the pathogenesis of Alzheimer's disease (AD). We measured the levels of alpha(1)-antichymotrypsin (ACT), alpha(1)-antitrypsin (AAT), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1) and oxidised low-density lipoprotein (oxLDL) in matched cerebrospinal fluid (CSF) and plasma of 141 patients with probable AD. We found a significant relationship between CSF and plasma levels of ACT (r = 0.4, p < 0.001), IL-6 (r = 0.74, p < 0.001), MCP-1 (r = 0.71, p < 0.001), and a borderline relationship between CSF and plasma oxLDL (r = 0.22, p < 0.05). In addition, linear regression analysis revealed a positive correlation between levels of CSF-ACT and oxLDL (p < 0.001), but an inverse relation between levels of CSF ACT, CSF AAT and MCP-1 (p < 0.001). A significant correlation was also found between levels of CSF ACT, oxLDL and the ratio of CSF to serum albumin, which is used as a measure of the blood-brain barrier function. Our data extend previous reports regarding the inflammatory markers in the plasma and CSF of patients with AD and provide good evidence that levels of ACT, IL-6, MCP-1 and oxLDL in plasma and CSF might be candidates as biomarkers for monitoring the inflammatory process in AD.     

Interleukin-12 is reduced in cerebrospinal fluid of patients with Alzheimer's disease and frontotemporal dementia

Interleukin-12 is a heterodimeric cytokine produced by activated blood monocytes, macrophages and glial cells. It enhances differentiation and proliferation of T cells and increases production of proinflammatory cytokines, such as Interferon-gamma and Tumor Necrosis Factor-alpha. There is little information about the involvement of IL-12 in the pathophysiology of Alzheimer's disease (AD) and other tauopathies. OBJECTIVES: The objective of our study was to assess the role of IL-12 as a potential marker of immune reactions in patients with AD and frontotemporal dementia (FTD). PATIENTS AND METHODS: We measured by immunoassay cerebrospinal fluid (CSF) IL-12 levels in 19 patients with AD and 7 patients with FTD in comparison with CSF IL-12 levels in 30 patients with non-inflammatory neurological diseases served as neurological control patients (NCTRL). IL-12 levels were correlated with age, age of disease onset, disease duration, MMSE score, and rate of dementia progression. Abeta42 and Total tau (tau(T)) levels in CSF were also measured. RESULTS: Patients with AD had significantly lower CSF IL-12 levels compared with NCTRL patients (p<0.001). Patients with FTD had also lower CSF IL-12 levels compared with NCTRL patients (p<0.05). Age, sex, disease duration and MMSE score did not affect IL-12 levels in any of the groups. In AD a significant positive correlation was noted between IL-12 levels and tau(T) levels (Rs=0.46, p=0.048). CONCLUSIONS: Our findings may suggest a reduced inflammatory reaction during the course of AD and FTD. A neurotrophic role of IL-12 and other proinflammatory cytokines cannot be excluded.     

Open-label, multicenter, phase 3 extension study of the safety and efficacy of donepezil in patients with Alzheimer disease

BACKGROUND: Donepezil hydrochloride is a selective acetylcholinesterase inhibitor approved for the symptomatic treatment of mild to moderately severe Alzheimer disease (AD). Controlled clinical trials of up to 24 weeks have demonstrated that donepezil treatment (5 and 10 mg/d) significantly improves cognition and global function. OBJECTIVE: To investigate the long-term benefits of donepezil treatment in patients with AD. DESIGN: Multicenter, open-label, 144-week extension of 2 US phase 3, double-blind, placebo-controlled clinical trials: a 15-week study (12 weeks of treatment followed by a 3-week placebo washout) and a 30-week study (24 weeks of treatment followed by a 6-week placebo washout). INTERVENTIONS: All patients (N = 763) initially received donepezil, 5 mg/d, for 6 weeks, after which an increase to 10 mg/d was encouraged. MEASURES: Primary efficacy measures were the Alzheimer's Disease Assessment Scale-cognitive subscale and the Clinical Dementia Rating-Sum of the Boxes. RESULTS: After the shorter 3-week placebo washout, donepezil-associated benefits remained above original baseline values for an additional 24 weeks of open-label treatment. Benefits on Alzheimer's Disease Assessment Scale-cognitive subscale scores for patients who received 10 mg/d in the double-blind study were evident compared with the other groups for 108 weeks of open-label treatment. In contrast, donepezil-associated benefits were lost after the 6-week placebo washout, and scores decreased below original baseline values for all patient groups. Although scores improved relative to the new open-label study baseline scores after drug use was restarted, patients remained below original baseline values. The most common adverse events were associated with the nervous and digestive systems and were generally mild and transient; 17% of patient discontinuations were associated with adverse events. CONCLUSIONS: Donepezil is an effective and safe drug for the long-term symptomatic treatment of mild to moderately severe AD for up to 144 weeks (2.8 years), and sustained treatment may confer some advantages.     

Tumor necrosis factor-alpha, interleukin-1beta and interleukin-6 in the cerebrospinal fluid of newborn with meningitis

OBJECTIVE: To analyze the usefulness of determining the cerebrospinal fluid (CSF) levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) for the early diagnosis and evaluation of the prognosis of neonatal meningitis. METHOD: We studied 54 newborn that underwent lumbar puncture. Thirty patients had meningitis and 24 were the control group. CSF and sera were obtained at the moment of suspicion of meningitis and stored at -70 degrees C. Cytokines were performed by enzyme-linked immunosorbent assay method. RESULTS: CSF cytokines were detected in all the newborn with meningitis. TNF-alpha was detected in the CSF in 63.3% of the neonates, IL-1beta in 73.3% and IL-6 in 96.6%. The CSF levels were significantly higher than serum in neonates with meningitis. There was no correlation between the CSF levels of cytokines and neurologic complications. CONCLUSION: The detection of TNF-alpha, IL-1beta and IL-6 in the CSF is of great value in order to achieve a early diagnosis of neonatal meningitis. Among the three cytokines analyzed, IL-6 was the best indicator of meningeal inflammation.     

Cerebral pattern of pro- and anti-inflammatory cytokines in dementias

The knowledge regarding putative inflammatory component(s) participating in Alzheimer's disease (AD) and vascular dementia (VAD) is scarce. Recently, we have demonstrated the presence of certain inflammatory cytokines in the cerebrospinal fluid (CSF) of demented patients. Although the initial event(s) triggering the neurodegenerative processes in AD versus VAD may be different and lead to different neuropathological changes, it may initiate a similar cascade of cytokine production in response to neuronal injury. The cytokines released in the central nervous system (CNS) may, in turn, act in a similar manner in both diseases, amplifying some pathological changes such as amyloidogenesis and white matter lesions or on the contrary acting as neuroprotective molecules. This review will focus on the intracerebral production of the pro- and anti-inflammatory cytokines interleukin IL-1beta, IL-1 receptor antagonist (IL-1ra), IL-6 and TNF-alpha in dementia, and their relation to gene polymorphism, to cerebral neuronal damage, apoptosis, and to clinical variables of dementia. Our results, which show for the first time strikingly increased CSF levels of TNF-alpha but not of TNF-beta, IL-1beta or IL-6 in AD and VAD, may form a conceptual framework for further studies of neuroprotective mechanisms in dementias.     

Discriminant power of combined cerebrospinal fluid tau protein and of the soluble interleukin-6 receptor complex in the diagnosis of Alzheimer's disease

Alzheimer's disease (AD) still can only be definitively diagnosed with certainty by examination of brain tissue. There is a great need for a noninvasive, sensitive and specific in vivo test for AD. We combined cerebrospinal fluid analyses of tau protein (levels were significantly increased in AD patients [p=0.0001]), a putative marker of neuronal degeneration, with components of the soluble interleukin-6 receptor complex (sIL-6RC: IL-6, soluble IL-6 receptor and soluble gp130), putative markers of neuroregulatory and inflammatory processes in the brain. A stepwise multivariate discriminant analysis revealed that tau protein and soluble gp130 (levels were significantly reduced in AD subjects [p=0.007]), the affinity converting and signal-transducing receptor of neuropoietic cytokines, maximized separation between the investigated groups. The discriminant function predicted 23 of 25 clinically diagnosed AD patients (sensitivity 92%) with mild to moderate dementia correctly as having AD. Furthermore, 17 of 19 physically and cognitively healthy age-matched control subjects (specificity 90%) were accurately distinguished by this test. Later predicting with the jackknife procedure each case in turn through the remaining patient group, the discriminant function remained stable. Our data suggest that multivariate discriminant analysis of combined CSF tau protein and sIL-6RC components may add more certainty to the diagnosis of AD, however, the method will need to be extended to an independent group of patients, comparisons and control subjects to assess the true applicability.