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      Indoor incense burning impacts cognitive functions and brain functional connectivity in community older adults

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          Abstract

          To investigate (1) the effects of indoor incense burning upon cognition over 3 years; (2) the associations between indoor incense burning with the brain’s structure and functional connectivity of the default mode network (DMN); and (3) the interactions between indoor incense burning and vascular disease markers upon cognitive functions. Community older adults without stroke or dementia were recruited (n = 515). Indoor incense use was self-reported as having burnt incense at home ≥ weekly basis over the past 5 years. Detailed neuropsychological battery was administered at baseline (n = 227) and the Montreal Cognitive Assessment at baseline and year 3 (n = 515). MRI structural measures and functional connectivity of the DMN were recorded at baseline. Demographic and vascular risk factors and levels of outdoor pollutants were treated as covariates. Indoor incense burning was associated with reduced performance across multiple cognitive domains at baseline and year 3 as well as decreased connectivity in the DMN. It interacted with diabetes mellitus, hyperlipidemia and white matter hyperintensities to predict poorer cognitive performance. Indoor incense burning is (1) associated with poorer cognitive performance over 3 years; (2) related to decreased brain connectivity; and (3) it interacts with vascular disease to predispose poor cognitive performance.

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          Airborne particulate matter and human health: toxicological assessment and importance of size and composition of particles for oxidative damage and carcinogenic mechanisms.

          Air pollution has been considered a hazard to human health. In the past decades, many studies highlighted the role of ambient airborne particulate matter (PM) as an important environmental pollutant for many different cardiopulmonary diseases and lung cancer. Numerous epidemiological studies in the past 30 years found a strong exposure-response relationship between PM for short-term effects (premature mortality, hospital admissions) and long-term or cumulative health effects (morbidity, lung cancer, cardiovascular and cardiopulmonary diseases, etc). Current research on airborne particle-induced health effects investigates the critical characteristics of particulate matter that determine their biological effects. Several independent groups of investigators have shown that the size of the airborne particles and their surface area determine the potential to elicit inflammatory injury, oxidative damage, and other biological effects. These effects are stronger for fine and ultrafine particles because they can penetrate deeper into the airways of the respiratory tract and can reach the alveoli in which 50% are retained in the lung parenchyma. Composition of the PM varies greatly and depends on many factors. The major components of PM are transition metals, ions (sulfate, nitrate), organic compound, quinoid stable radicals of carbonaceous material, minerals, reactive gases, and materials of biologic origin. Results from toxicological research have shown that PM have several mechanisms of adverse cellular effects, such as cytotoxicity through oxidative stress mechanisms, oxygen-free radical-generating activity, DNA oxidative damage, mutagenicity, and stimulation of proinflammatory factors. In this review, the results of the most recent epidemiological and toxicological studies are summarized. In general, the evaluation of most of these studies shows that the smaller the size of PM the higher the toxicity through mechanisms of oxidative stress and inflammation. Some studies showed that the extractable organic compounds (a variety of chemicals with mutagenic and cytotoxic properties) contribute to various mechanisms of cytotoxicity; in addition, the water-soluble faction (mainly transition metals with redox potential) play an important role in the initiation of oxidative DNA damage and membrane lipid peroxidation. Associations between chemical compositions and particle toxicity tend to be stronger for the fine and ultrafine PM size fractions. Vehicular exhaust particles are found to be most responsible for small-sized airborne PM air pollution in urban areas. With these aspects in mind, future research should aim at establishing a cleared picture of the cytotoxic and carcinogenic mechanisms of PM in the lungs, as well as mechanisms of formation during internal engine combustion processes and other sources of airborne fine particles of air pollution.
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            Air pollution, cognitive deficits and brain abnormalities: a pilot study with children and dogs.

            Exposure to air pollution is associated with neuroinflammation in healthy children and dogs in Mexico City. Comparative studies were carried out in healthy children and young dogs similarly exposed to ambient pollution in Mexico City. Children from Mexico City (n: 55) and a low polluted city (n:18) underwent psychometric testing and brain magnetic resonance imaging MRI. Seven healthy young dogs with similar exposure to Mexico City air pollution had brain MRI, measurement of mRNA abundance of two inflammatory genes cyclooxygenase-2, and interleukin 1 beta in target brain areas, and histopathological evaluation of brain tissue. Children with no known risk factors for neurological or cognitive disorders residing in a polluted urban environment exhibited significant deficits in a combination of fluid and crystallized cognition tasks. Fifty-six percent of Mexico City children tested showed prefrontal white matter hyperintense lesions and similar lesions were observed in dogs (57%). Exposed dogs had frontal lesions with vascular subcortical pathology associated with neuroinflammation, enlarged Virchow-Robin spaces, gliosis, and ultrafine particulate matter deposition. Based on the MRI findings, the prefrontal cortex was a target anatomical region in Mexico City children and its damage could have contributed to their cognitive dysfunction. The present work presents a groundbreaking, interdisciplinary methodology for addressing relationships between environmental pollution, structural brain alterations by MRI, and cognitive deficits/delays in healthy children.
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              The Default Mode Network in Autism.

              Autism spectrum disorder (ASD) is characterized by deficits in social communication and interaction. Since its discovery as a major functional brain system, the default mode network (DMN) has been implicated in a number of psychiatric disorders, including ASD. Here we review converging multimodal evidence for DMN dysfunction in the context of specific components of social cognitive dysfunction in ASD: 'self-referential processing' - the ability to process social information relative to oneself and 'theory of mind' or 'mentalizing' - the ability to infer the mental states such as beliefs, intentions, and emotions of others. We show that altered functional and structural organization of the DMN, and its atypical developmental trajectory, are prominent neurobiological features of ASD. We integrate findings on atypical cytoarchitectonic organization and imbalance in excitatory-inhibitory circuits, which alter local and global brain signaling, to scrutinize putative mechanisms underlying DMN dysfunction in ASD. Our synthesis of the extant literature suggests that aberrancies in key nodes of the DMN and their dynamic functional interactions contribute to atypical integration of information about the self in relation to 'other', as well as impairments in the ability to flexibly attend to socially relevant stimuli. We conclude by highlighting open questions for future research.
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                Author and article information

                Contributors
                vctmok@cuhk.edu.hk
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                27 April 2020
                27 April 2020
                2020
                : 10
                : 7090
                Affiliations
                [1 ]ISNI 0000 0004 1937 0482, GRID grid.10784.3a, Department of Medicine and Therapeutics, , The Chinese University of Hong Kong, ; Hong Kong SAR, China
                [2 ]ISNI 0000 0004 1937 0482, GRID grid.10784.3a, Therese Pei Fong Chow Research Centre for Prevention of Dementia, , The Chinese University of Hong Kong, ; Hong Kong SAR, China
                [3 ]ISNI 0000 0004 1937 0482, GRID grid.10784.3a, Gerald Choa Neuroscience Centre, Lui Che Woo Institute of Innovative Medicine, , The Chinese University of Hong Kong, ; Hong Kong SAR, China
                [4 ]ISNI 0000 0004 1937 0482, GRID grid.10784.3a, Department of Imaging and Interventional Radiology, , The Chinese University of Hong Kong, ; Hong Kong SAR, China
                [5 ]ISNI 0000 0004 1937 0482, GRID grid.10784.3a, The Jockey Club School of Public Health and Primary Care, , The Chinese University of Hong Kong, ; Hong Kong SAR, China
                [6 ]ISNI 0000 0004 1937 0482, GRID grid.10784.3a, Department of Psychiatry, Faculty of Medicine, , The Chinese University of Hong Kong, ; Hong Kong SAR, China
                [7 ]ISNI 0000 0001 2216 9681, GRID grid.36425.36, Stony Brook University School of Medicine, Stony Brook, ; New York, United States
                Article
                63568
                10.1038/s41598-020-63568-6
                7184605
                31913322
                27c23c6b-e0a8-4632-9c7b-e93add7d2bd4
                © The Author(s) 2020

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 20 December 2019
                : 13 February 2020
                Categories
                Article
                Custom metadata
                © The Author(s) 2020

                Uncategorized
                cerebrovascular disorders,neurodegenerative diseases,white matter disease,risk factors,diseases of the nervous system

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