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      Lactonase Activity and Lipoprotein-Phospholipase A 2 as Possible Novel Serum Biomarkers for the Differential Diagnosis of Autism Spectrum Disorders and Rett Syndrome: Results from a Pilot Study

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          Abstract

          Rett syndrome (RTT) and autism spectrum disorders (ASDs) are not merely expression of brain dysfunction but also reflect the perturbation of physiological/metabolic homeostasis. Accordingly, both disorders appear to be associated with increased vulnerability to toxicants produced by redox imbalance, inflammation, and pollution, and impairment of systemic-detoxifying agents could play a role in the exacerbation of these detrimental processes. To check this hypothesis, the activities of two mechanistically related blood-based enzymes, paraoxonase-1 (arylesterase, paraoxonase, and lactonase), and lipoprotein-associated phospholipase A 2 (Lp-PLA 2) were measured in the serum of 79 ASD and 95 RTT patients, and 77 controls. Lactonase and Lp-PLA 2 showed a similar trend characterized by significantly lower levels of both activities in ASD compared to controls and RTT ( p < 0.001 for all pairwise comparisons). Noteworthy, receiving operator curve (ROC) analysis revealed that lactonase and, mostly, Lp-PLA 2 were able to discriminate between ASD and controls (lactonase: area under curve, AUC = 0.660; Lp-PLA 2, AUC = 0.780), and, considering only females, between ASD and RTT (lactonase, AUC = 0.714; Lp-PLA 2, AUC = 0.881). These results suggest that lactonase and, especially, Lp-PLA 2 activities might represent novel candidate biomarkers for ASD.

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          Rett syndrome: revised diagnostic criteria and nomenclature.

          Jeffrey Neul, Walter Kaufmann, Daniel G. Glaze … (2010)
          Rett syndrome (RTT) is a severe neurodevelopmental disease that affects approximately 1 in 10,000 live female births and is often caused by mutations in Methyl-CpG-binding protein 2 (MECP2). Despite distinct clinical features, the accumulation of clinical and molecular information in recent years has generated considerable confusion regarding the diagnosis of RTT. The purpose of this work was to revise and clarify 2002 consensus criteria for the diagnosis of RTT in anticipation of treatment trials. RettSearch members, representing the majority of the international clinical RTT specialists, participated in an iterative process to come to a consensus on a revised and simplified clinical diagnostic criteria for RTT. The clinical criteria required for the diagnosis of classic and atypical RTT were clarified and simplified. Guidelines for the diagnosis and molecular evaluation of specific variant forms of RTT were developed. These revised criteria provide clarity regarding the key features required for the diagnosis of RTT and reinforce the concept that RTT is a clinical diagnosis based on distinct clinical criteria, independent of molecular findings. We recommend that these criteria and guidelines be utilized in any proposed clinical research.
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            Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism.

            S. Jill James, Paul Cutler, Stepan Melnyk … (2004)
            Autism is a complex neurodevelopmental disorder that usually presents in early childhood and that is thought to be influenced by genetic and environmental factors. Although abnormal metabolism of methionine and homocysteine has been associated with other neurologic diseases, these pathways have not been evaluated in persons with autism. The purpose of this study was to evaluate plasma concentrations of metabolites in the methionine transmethylation and transsulfuration pathways in children diagnosed with autism. Plasma concentrations of methionine, S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), adenosine, homocysteine, cystathionine, cysteine, and oxidized and reduced glutathione were measured in 20 children with autism and in 33 control children. On the basis of the abnormal metabolic profile, a targeted nutritional intervention trial with folinic acid, betaine, and methylcobalamin was initiated in a subset of the autistic children. Relative to the control children, the children with autism had significantly lower baseline plasma concentrations of methionine, SAM, homocysteine, cystathionine, cysteine, and total glutathione and significantly higher concentrations of SAH, adenosine, and oxidized glutathione. This metabolic profile is consistent with impaired capacity for methylation (significantly lower ratio of SAM to SAH) and increased oxidative stress (significantly lower redox ratio of reduced glutathione to oxidized glutathione) in children with autism. The intervention trial was effective in normalizing the metabolic imbalance in the autistic children. An increased vulnerability to oxidative stress and a decreased capacity for methylation may contribute to the development and clinical manifestation of autism.
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              Lipoprotein-associated phospholipase A2 and risk of coronary disease, stroke, and mortality: collaborative analysis of 32 prospective studies

              (2010)
              Summary Background Lipoprotein-associated phospholipase A2 (Lp-PLA2), an inflammatory enzyme expressed in atherosclerotic plaques, is a therapeutic target being assessed in trials of vascular disease prevention. We investigated associations of circulating Lp-PLA2 mass and activity with risk of coronary heart disease, stroke, and mortality under different circumstances. Methods With use of individual records from 79 036 participants in 32 prospective studies (yielding 17 722 incident fatal or non-fatal outcomes during 474 976 person-years at risk), we did a meta-analysis of within-study regressions to calculate risk ratios (RRs) per 1 SD higher value of Lp-PLA2 or other risk factor. The primary outcome was coronary heart disease. Findings Lp-PLA2 activity and mass were associated with each other (r=0·51, 95% CI 0·47–0·56) and proatherogenic lipids. We noted roughly log-linear associations of Lp-PLA2 activity and mass with risk of coronary heart disease and vascular death. RRs, adjusted for conventional risk factors, were: 1·10 (95% CI 1·05–1·16) with Lp-PLA2 activity and 1·11 (1·07–1·16) with Lp-PLA2 mass for coronary heart disease; 1·08 (0·97–1·20) and 1·14 (1·02–1·27) for ischaemic stroke; 1·16 (1·09–1·24) and 1·13 (1·05–1·22) for vascular mortality; and 1·10 (1·04–1·17) and 1·10 (1·03–1·18) for non-vascular mortality, respectively. RRs with Lp-PLA2 did not differ significantly in people with and without initial stable vascular disease, apart from for vascular death with Lp-PLA2 mass. Adjusted RRs for coronary heart disease were 1·10 (1·02–1·18) with non-HDL cholesterol and 1·10 (1·00–1·21) with systolic blood pressure. Interpretation Lp-PLA2 activity and mass each show continuous associations with risk of coronary heart disease, similar in magnitude to that with non-HDL cholesterol or systolic blood pressure in this population. Associations of Lp-PLA2 mass and activity are not exclusive to vascular outcomes, and the vascular associations depend at least partly on lipids. Funding UK Medical Research Council, GlaxoSmithKline, and British Heart Foundation.
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                Author and article information

                Contributors
                Carlo Cervellati:
                ORCID: http://orcid.org/0000-0003-4777-6300
                Journal
                Journal ID (nlm-ta): Oxid Med Cell Longev
                Journal ID (iso-abbrev): Oxid Med Cell Longev
                Journal ID (publisher-id): OMCL
                Title: Oxidative Medicine and Cellular Longevity
                Publisher: Hindawi
                ISSN (Print): 1942-0900
                ISSN (Electronic): 1942-0994
                Publication date (Print): 2017
                Publication date (Electronic): 28 November 2017
                Volume: 2017
                Electronic Location Identifier: 5694058
                Affiliations
                1Child Neuropsychiatry Unit, University General Hospital, Azienda Ospedaliera Universitaria Senese, Viale M. Bracci 16, 53100 Siena, Italy
                2Department of Biomedical and Specialist Surgical Sciences, University of Ferrara, Via Luigi Borsari 46, 44121 Ferrara, Italy
                3Department of Life Sciences and Biotechnology, University of Ferrara, Via Luigi Borsari 46, 44121 Ferrara, Italy
                4Plants for Human Health Institute, Animal Science Department, NC Research Campus, NC State University, 600 Laureate Way, Kannapolis, NC 28081, USA
                Author notes

                Academic Editor: Serafina Perrone

                Author information
                http://orcid.org/0000-0003-4777-6300
                http://orcid.org/0000-0002-8792-0947
                Article
                DOI: 10.1155/2017/5694058
                PMC ID: 5727786
                SO-VID: e00f9654-7a82-4378-b34a-619ae3dc9d65
                Copyright © Copyright © 2017 Joussef Hayek et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 16 August 2017
                Date revision received : 27 October 2017
                Date accepted : 5 November 2017
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Molecular medicine
                Data availability:
                ScienceOpen disciplines: Molecular medicine

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