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CSF tau and amyloid β<sub>42</sub>levels in Alzheimer’s disease—A meta-analysis

Advances in Alzheimer's Disease 2012年第3期1卷 30-44页

作者： Rachna Agarwal Neelam Chhillar Vijay Nath Mishra Chandra Bhushan Tripathi Department of Biostatistics Institute of Human Behaviour & Allied Sciences Delhi India Department of Neurochemistry Institute of Human Behaviour & Allied Sciences Delhi India Department of Neurology Institute of Medical Sciences Banaras Hindu University Varanasi India

Alzheimer’s disease International (ADI) estimates that there are currently 30 million people with dementia in the world. The main objective was to perform meta-analysis of studies of CSF tau and Amyloid β42 (Aβ42) levels in Alzheimer’s disease (AD) patients and controls. In the present study MEDLINE was reviewed from 1995 to 2009, supplemented by citation analysis from retrieved articles to select case control studies. Descriptive statistics showed that median effect size (raw mean difference) of CSF tau and Aβ42 levels were 301 pg/ml (Range: 22 to 614 pg/ml) and –352 pg/ml (Range: –969 to 203 pg/ml) respectively. The pooled effect size CSF tau and Aβ42 was 289.14 pg/ml (95% CI 253.278 to 325.013 pg/ml) and –329.02 pg/ml (95% CI –387.740 to –270.445 pg/ml) respectively. Heterogeneity in effect size of selected studies was present for both parameters (CSF tau: Q statistics = 1816.596, DF = 40, P = 0.000 and CSF Aβ42: Q-statistics = 1259.358, DF = 24, p 42 levels in AD and controls may be considered as potential biomarker along with the clinical phenotype to perform them during high quality diagnostic testing in dementia.

关键词： Alzheimer’s Disease Dementia CSF Amyloid β42 CSF Tau Meta-Analysis

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Protective effect of carnosine on amyloid - β42 - induced neurotoxicity in differentiated rat PC12 cells is independent of histamine pathway

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中国药理通讯 2006年第4期23卷 33-33页

作者： Fu Qiu-Li Dai Hai-Bin Shen Yao Hu Wei-wei Chen Zhong Department of Pharmacology School of Medicine Zhejiang University Hangzhou 310058

Considerable circumstantial evidence suggests that amyloid -β42 is the initiating molecule in Alzheimer's disease (AD) pathogenesis。Carnosine, a ROS scavenger, has been implicated to inverse or partially inverse the excitotoxic neuronal cell death through histamine/H1 receptor pathway in NMDA -induced impairment。However, in our studies this was not the case at all。Amyloid -β42 caused dose - dependent and time - dependent loss of viability in nerve growth factor differentiated rat phaeochromocytoma (PC12) cells。Pretreatment with carnosine alone followed by perfusion with amyloid-β42 can partially inverse the amyloid -β42 -induced impairment, but it can not be antagonized by either H1 receptor antagonist diphenhydramine or H2 receptor antagonist zolatidime。Meanwhile,α- fluoromethylhistidine (α- FMH), an irreversible inhibitor of histidine decarboxylase which induces a reduction in histamine synthesis, also has no effect in this issue。Additionally, elevation of glutamate but not histamine or histidine induced by amyloid -β42 can be inversed by carnosine。Our results indicate that sorts of pathway are existed in the protective effect of carnosine in the excitotoxic neuronal cell death。

关键词：肌肽 β淀粉样多肽- β42 诱发神经毒性大鼠PC12分化细胞保护作用组胺通路

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