DOCSLIB.ORG

The Exposome in Human Evolution: from Dust to Diesel

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
The Exposome in Human Evolution: from Dust to Diesel Volume 94, No. 4 December 2019 THE QUARTERLY REVIEW of Biology THE EXPOSOME IN HUMAN EVOLUTION: FROM DUST TO DIESEL Benjamin C. Trumble School of Human Evolution & Social Change and Center for Evolution and Medicine, Arizona State University Tempe, Arizona 85287 USA e-mail: [email protected] Caleb E. Finch Leonard Davis School of Gerontology and Dornsife College, University of Southern California Los Angeles, California 90089-0191 USA e-mail: cefi[email protected] keywords exposome, human evolution, genes, toxins, infections abstract Global exposures to air pollution and cigarette smoke are novel in human evolutionary history and are associated with at least 12 million premature deaths per year. We investigate the history of the human exposome for relationships between novel environmental toxins and genetic changes during human evo- lution in six phases. Phase I: With increased walking on savannas, early human ancestors inhaled crustal dust, fecal aerosols, and spores; carrion scavenging introduced new infectious pathogens. Phase II: Domestic fire exposed early Homo to novel toxins from smoke and cooking. Phases III and IV: Neolithic to preindustrial Homo sapiens incurred infectious pathogens from domestic animals and dense com- munities with limited sanitation. Phase V: Industrialization introduced novel toxins from fossil fuels, industrial chemicals, and tobacco at the same time infectious pathogens were diminishing. Thereby, pathogen-driven causes of mortality were replaced by chronic diseases driven by sterile inflammogens, exog- enous and endogenous. Phase VI: Considers future health during global warming with increased air pol- lution and infections. We hypothesize that adaptation to some ancient toxins persists in genetic variations associated with inflammation and longevity. The Quarterly Review of Biology, December 2019, Vol. 94, No. 4 Copyright © 2019 by The University of Chicago Press. All rights reserved. 0033-5770/2019/9404-0001$15.00 333 This content downloaded from 128.230.234.162 on November 23, 2019 12:00:33 PM All use subject to University of Chicago Press Terms and Conditions (http://www.journals.uchicago.edu/t-and-c). 334 THE QUARTERLY REVIEW OF BIOLOGY Volume 94 Introduction miologic approaches that characterized indi- vidual factors, “one by one” and has become S human ancestors diverged from great widely adapted to approach interactions of A apes, they encountered additional envi- multiple exogenous and endogenous toxins ronmental hazards: increased savanna min- across the lifetime (National Academies of eral dust and fecal aerosols; pathogens from Sciences, Engineering, and Medicine 2017). decaying carrion; smoke from domestic fire; Wild (2012) identified three domains: the ex- new pathogens from domesticated animals ogenous macrolevel (rural versus urban; social in the Neolithic; and, in the Industrial Age, stratification); the exogenous individual (diet, airborne toxins from fossil fuels and tobacco. infections); and the endogenous (biomes, fat During these phases, humans also evolved depots, injuries). The exposome includes all larger brains and extended life histories with stages of life history, from prefertilization prolonged maturation and longer life spans, gametes to development and later life. We as discussed below. Genetic adaptations ac- focus on genes of host defense and brain de- quired during these six million years are velopment during the evolution of the long analyzed in terms of the novel toxins from human life span with its uniquely prolonged exogenous and endogenous sources. Table 1 postreproductive phase. and Figure 1 outline sequential phases of the Evolutionary inquiry of the human expo- expanding human exposome, in which new some illuminates unexplored domains of in- environmental hazards are cumulatively added flammatory processes in the evolution of the to those from prior phases. These new expo- lungs and brain that may inform the future sures need not have occurred at the same of human health and longevity during global time in all human populations, and should warming. Inflammatory responses are near not be considered as hard boundaries for ubiquitous in human adaptations to these the phases. exposures. Many inflammatory responses to The exposome concept was introduced airborne toxins from cigarettes and fossil fu- by Wild (2005, 2012) for comprehensive anal- els are shared with the pathophysiology of ysis of environmental and lifestyle factors in chronic diseases associated with modern air cancer. The exposome extends prior epide- pollution. We hypothesize that adaptation to TABLE 1 Phases in the human exposome Exposome phase, species/ Exposome cumulative progression Chemistry life expectancy, age IA. Pre-Homo/25 y 5–2.5 MYA Dust (mineral), pollen; endotoxins from herd Iron and other toxic metals animals; increased carrion pathogens IB. Early Homo/30 y 2.5–1 MYA II. Early Homo/30 y 1–0.3 MYA Dust, pollen, endotoxins, carrion pathogens; Toxic metals; plus PAH plus domestic biomass smoke and charred meat III. H. sapiens/35–45 y Paleo- to pre- Dust, feces, endotoxins, smoke, charred meat; Toxic metals, PAH; plus endotoxins, infections Neolithic 0.3 MYA-10,000 BP plus human feces IV. H. sapiens/35–45 y Neolithic Dust, smoke, charred meat, human feces; Toxic metals, PAH; plus new endotoxins, 10,000–200 YA plus high-density populations, domestic animal antigens feces, new infections – V. H sapiens/50 85 y Industrial Dust, smoke, charred meat, human and Toxic metals, NH4, PAH, endotoxins, – 1820 2020 animal feces, infections; plus fossil fuels, infections; plus adiposity, CO, O3, NOx, SOx industrial toxins, sugar, tobacco – VI. Future 21st 22nd centuries H. Dust, smoke, charred meat, feces, infections, Transition metals, PAH, NH4, endotoxins, – sapiens/35 90 y global warming fossil fuels, industrial toxins; plus higher O3, infections, O3, NOx, SOx; plus increased and coastal inundation crustal dust, insect-borne infections, migrations, O3, glycoxidation, PAH, temperature water shortages New factors in each phase are italicized. This content downloaded from 128.230.234.162 on November 23, 2019 12:00:33 PM All use subject to University of Chicago Press Terms and Conditions (http://www.journals.uchicago.edu/t-and-c). December 2019 THE EXPOSOME IN HUMAN EVOLUTION 335 ancient airborne toxins may be recognized in diverse environments near the southern in modern genetic variations, including the edge of the Sahara, showed early evidence genotypes of cigarette survivors who may of bipedalism (Brunet et al. 2002). Later hom- have genetic resistance to cigarette aerosols. inins, including Ardipithicus ramidus (ap- Inflammation has become an environmen- proximately 4.4 MYA), inhabited a primarily tal byword because inflammatory responses forest and wooded grassland paleoecology are broadly stimulated by molecular damage. (White et al. 2009). We discriminate two broad classes of inflam- Major aridification in East Africa during matory stimulae: pathogen-driven inflammation the last three million years has particular rel- from infectious viruses, microbes, and para- evance to the emergence of Homo (Finch sites versus sterile inflammation from noninfec- 2012). Early habitats gradually shifted from tious toxins and stressors such as cigarette closed canopy forest to open grass- and shrub- smoke or fat depots (Crimmins and Finch land savannas (Feakins et al. 2005; Bonnefille 2006; Finch and Kulminski 2019; Phase V). 2010; Cerling et al. 2011). Savanna grasses Some inflammatory responses are shared generally rely on wind pollination, and thus by infectious pathogenic and sterile inflam- produced more pollen than tropical trees that mogens, as in the toll-like receptor (TLR4) rely on insect or animal pollination (Dupont pathway responses to bacterial lipopolysac- and Wyputta 2003). Thus, novel sources of charides (LPSs) and urban air pollution par- pollen exposure may have increased as grass- ticles (Woodward et al. 2017). The many lands expanded. Arid areas are also major TLR pathways are critical to innate immune sources of dust (Prospero et al. 2002). The ari- responses (“911 standby”), but also to the dification the East African hominin sites is am- slower adaptive immune responses target- ply documented by an increase in windblown ing specific antigens. Innate immune genes dust reaching marine sediments (deMenocal are prominent among the evolved genetic ac- 1995) and by the carbon isotope ratios in pa- commodations in the context of adaptive re- leosols that distinguish woodlands and grass- sistance to pathogens and survival of injury. lands (Sikes 1994; Cerling et al. 2011; Rowan Furthermore, neurodevelopmental processes and Reed 2015; Lüdecke et al. 2018). These employ innate immune mechanisms during changes in foliage were complex and region- brain maturation. Building from these estab- ally diverse, involving Southern Africa and lished findings, we suggest how evolved im- the upper Rift Valley (Levin et al. 2011). Most mune genes may have interacted with new hominid sites were within extensive wood- brain genes. lands (approximately 40%; Reed 1997; Cerling et al. 2011; Rowan and Reed 2015). Poor pres- Exposome Phase I: Savanna Aerosols ervation of bones in forests limits knowledge expanding exposure to dust, pollen, of our early ancestors and their environmen- endotoxins, and carrion pathogens tal conditions. After 3 MYA in the Rift Valley, hominins The African environment has undergone were exposed to seasonal surges in airborne major changes in the last 10 million years dust and pollen (Wood and Lonergan 2008;
Load more

Recommended publications
  • A Spongiform Encephalopathy Outbreak: Anthropophagy Or Not?
    A SPONGIFORM ENCEPHALOPATHY OUTBREAK: ANTHROPOPHAGY OR NOT? Mani Vessal A thesis submitted to the Faculty of Graduate Studies and Research in partial fulfilmrnt of the requirements for the degree of Master of Arts Department of Anthropology Carleton University Ottawa, Ontario June 281 1 999 copyright 1999, Mani Vessal National Library Bibliothèque nationale ($1 of Canada du Canada Acquisitions and Acquisitions et Bibliographie Services seMces bibliographiques 395 Wellington Street 395, rue Wellington Ottawa ON KIA ON4 Otiawa ON KiA OF14 Canada Canada Your fi& Vorre refamœ Our IW Notre feWrI)Ree The author has granted a non- L'auteur a accordé une licence non exclusive Licence allowing the exclusive permettant à la National Library of Canada to Bibliothèque nationale du Canada de reproduce, loan, distribute or sel1 reproduire, prêter, distribuer ou copies of ths thesis in rnicroform, vendre des copies de cette thèse sous paper or electronic formats. la forme de rnicrofiche/fd.m, de reproduction sur papier ou sur format électronique. The author retains ownership of the L'auteur conserve la propriété du copyright in this thesis. Neither the droit d'auteur qui protège cette thèse. thesis nor substantial extracts fiom it Ni la thèse ni des extraits substantiels may be p~tedor otherwike de celle-ci ne doivent être imprimés reproduced without the author's ou autrement reproduits sans son permission. autorisation. Abstract Since the Kum endemic among the Fore Papua New Guinea, there have ken numerous theories proposed to explain the mode of transmission of the agent responsible for the spread of this fatal neurodegenerative disorder. The "cannibaiism" theory proposed by S.
    [Show full text]
  • Balancing Selection at the Prion Protein Gene Consistent with Prehistoric Kurulike Epidemics Simon Mead,1 Michael P
    Balancing Selection at the Prion Protein Gene Consistent with Prehistoric Kurulike Epidemics Simon Mead,1 Michael P. H. Stumpf,2 Jerome Whitfield,1,3 Jonathan A. Beck,1 Mark Poulter,1 Tracy Campbell,1 James Uphill,1 David Goldstein,2 Michael Alpers,1,3,4 Elizabeth M. C. Fisher,1 John Collinge1* 1Medical Research Council, Prion Unit, and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK. 2Department of Biology (Galton Laboratory), University College London, Gower Street, London WC1E 6BT, UK. 3Institute of Medical Research, Goroka, EHP, Papua New Guinea. 4Curtin University of Technology, Perth, WA, Australia. *To whom correspondence should be addressed. E-mail: [email protected] Kuru is an acquired prion disease largely restricted to the cannibalism imposed by the Australian authorities in the mid- Fore linguistic group of the Papua New Guinea Highlands 1950s led to a decline in kuru incidence, and although rare which was transmitted during endocannibalistic feasts. cases still occur these are all in older individuals and reflect Heterozygosity for a common polymorphism in the the long incubation periods possible in human prion human prion protein gene (PRNP) confers relative diseasekuru has not been recorded in any individual born after the late 1950s (4). resistance to prion diseases. Elderly survivors of the kuru A coding polymorphism at codon 129 of PRNP is a strong epidemic, who had multiple exposures at mortuary feasts, susceptibility factor for human prion diseases. Methionine are, in marked contrast to younger unexposed Fore, homozygotes comprise 37% of the UK population whereas predominantly PRNP 129 heterozygotes.
    [Show full text]
  • Kuru: the Neurodegenerative Disorder; Roles of Prpc and Prpsc in Infection, Effects in Blocking Neural Synapses and Its Comprehensive Observation
    ISSN: 2641-1911 DOI: 10.33552/ANN.2021.09.000717 Archives in Neurology & Neuroscience Research Article Copyright © All rights are reserved by Ahnaf Ilman Kuru: The Neurodegenerative Disorder; Roles of PrPC and PrPSc in infection, Effects in Blocking Neural Synapses and its Comprehensive Observation Ahnaf Ilman1* and Md. Abu Syed2 1Department of Science, Dhaka Residential Model College, Bangladesh 2Department of English, Dhaka Residential Model College, Bangladesh *Corresponding author: Ahnaf Ilman, Founder & President, Organization for Received Date: December 10, 2020 Natural Science Research; Department of Science, Dhaka Residential Model College, Dhaka, Bangladesh. Published Date: January 08, 2021 Abstract Kuru is a rare and neurodegenerative disorder-creating disease that effectively and principally affects Neural Synapses and the Central Nervous System. For this reason, brain cells and tissues started to be damaged and deceased. Microbials step out to act against the dangerous deceased cells of the human brain, and spongiform encephalopathy gets created. Thus, the Axon-Dendron of Neuron that contains the human brain gets blocked. In the mid of 19s, Kuru has been revealed as a complicated and a suspected pandemic creating disease. Although most of the diseases are caused protein. Human body also bears protein, but that is a normal and not dangerous protein, and it is regarded as Cellular Prion Protein, also known as PrPby differentC. That protein types ofdonates virus, itselfbacteria, for thefungus betterment etc., Kuru of isthe the human first human body. But transmitted the Scrapie disease Prion that Protein has beenalso known caused as by PrPS a complicatedc is the Prion and Protein misfolded that causes Kuru Disease and acts against the Brain and Immune System.
    [Show full text]
  • Kuru: Its Ramifications After Fifty Years P.P
    Kuru: its ramifications after fifty years P.P. Liberski, P. Brown To cite this version: P.P. Liberski, P. Brown. Kuru: its ramifications after fifty years. Experimental Gerontology, Elsevier, 2008, 44 (1-2), pp.63. 10.1016/j.exger.2008.05.010. hal-00499057 HAL Id: hal-00499057 https://hal.archives-ouvertes.fr/hal-00499057 Submitted on 9 Jul 2010 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Accepted Manuscript Kuru: its ramifications after fifty years P.P. Liberski, P. Brown PII: S0531-5565(08)00134-4 DOI: 10.1016/j.exger.2008.05.010 Reference: EXG 8488 To appear in: Experimental Gerontology Received Date: 21 April 2008 Revised Date: 5 May 2008 Accepted Date: 6 May 2008 Please cite this article as: Liberski, P.P., Brown, P., Kuru: its ramifications after fifty years, Experimental Gerontology (2008), doi: 10.1016/j.exger.2008.05.010 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form.
    [Show full text]
  • Mortuary Practices, Genetics and Other Factors Relevant to the Transmission of Kuru in Papua New Guinea
    Mortuary practices, genetics and other factors relevant to the transmission of kuru in Papua New Guinea Mr Jerome T Whitfield University College London PhD in Neurology 1 ‘I, Mr Jerome T Whitfield, confirm that the work presented in this thesis is my own. Where information has been derived from other sources, I confirm that this has been indicated in the thesis.’ ................................................................... 2 Table of Contents Title page..............................................................................................1 Table of Contents .............................................................................. 3 List of Tables and Figures ............................................................... 36 Abstract ........................................................................................... 41 Introduction ..................................................................................... 44 Chapter 1: Prion diseases of humans and animals ........................ 49 Introduction .................................................................................... 49 Prion diseases of animals ............................................................... 53 Scrapie ......................................................................................... 54 Transmissible mink encephalopathy ......................................... 56 Chronic wasting disease in North American cervids ................ 58 Prion diseases of humans ..............................................................
    [Show full text]
  • Creutzfeldt-Jakob Disease
    TREATMENTOFHEMOPHILIA APRIL 2009 • NO 49 CREUTZFELDT-JAKOB DISEASE James W. Ironside National Creutzfeldt-Jakob Disease Surveillance Unit School of Molecular and Clinical Medicine, University of Edinburgh Western General Hospital United Kingdom Published by the World Federation of Hemophilia (WFH), 2009 © World Federation of Hemophilia, 2009 The WFH encourages redistribution of its publications for educational purposes by not-for-profit hemo- philia organizations. In order to obtain permission to reprint, redistribute, or translate this publication, please contact the Communications Department at the address below. This publication is accessible from the World Federation of Hemophilia’s website at www.wfh.org. Additional copies are also available from the WFH at: World Federation of Hemophilia 1425 René Lévesque Boulevard West, Suite 1010 Montréal, Québec H3G 1T7 CANADA Tel. : (514) 875-7944 Fax : (514) 875-8916 E-mail: [email protected] Internet: www.wfh.org The Treatment of Hemophilia series is intended to provide general information on the treatment and man- agement of hemophilia. The World Federation of Hemophilia does not engage in the practice of medi- cine and under no circumstances recommends particular treatment for specific individuals. Dose sched- ules and other treatment regimes are continually revised and new side effects recognized. WFH makes no representation, express or implied, that drug doses or other treatment recommendations in this publi- cation are correct. For these reasons it is strongly recommended that individuals seek the advice of a medical adviser and/or consult printed instructions provided by the pharmaceutical company before administering any of the drugs referred to in this monograph. Statements and opinions expressed here do not necessarily represent the opinions, policies, or recom- mendations of the World Federation of Hemophilia, its Executive Committee, or its staff.
    [Show full text]
  • Kuru in the 21St Century—An Acquired Human Prion Disease with Very Long Incubation Periods
    Articles Kuru in the 21st century—an acquired human prion disease with very long incubation periods John Collinge, Jerome Whitfi eld, Edward McKintosh, John Beck, Simon Mead, Dafydd J Thomas, Michael P Alpers Summary Lancet 2006; 367: 2068–74 Background Kuru provides the principal experience of epidemic human prion disease. Its incidence has steadily fallen MRC Prion Unit and after the abrupt cessation of its route of transmission (endocannibalism) in Papua New Guinea in the 1950s. The Department of onset of variant Creutzfeldt-Jakob disease (vCJD), and the unknown prevalence of infection after the extensive dietary Neurodegenerative Disease, exposure to bovine spongiform encephalopathy (BSE) prions in the UK, has led to renewed interest in kuru. We Institute of Neurology, University College London, investigated possible incubation periods, pathogenesis, and genetic susceptibility factors in kuru patients in Papua London WC1N 3BG, UK New Guinea. (Prof J Collinge FRS, J Whitfi eld MSc, Methods We strengthened active kuru surveillance in 1996 with an expanded fi eld team to investigate all suspected E McKintosh MRCS, J Beck BSc, S Mead MRCP, D J Thomas FRCP, patients. Detailed histories of residence and exposure to mortuary feasts were obtained together with serial neurological M P Alpers FTWAS); Papua New examination, if possible. Guinea Institute of Medical Research, Goroka, EHP, Papua Findings We identifi ed 11 patients with kuru from July, 1996, to June, 2004, all living in the South Fore. All patients New Guinea (J Whitfi eld); and Centre for International were born before the cessation of cannibalism in the late 1950s. The minimum estimated incubation periods ranged Health, Curtin University, from 34 to 41 years.
    [Show full text]
  • Seiter Timothy 2019URD.Pdf (3.760Mb)
    KARANKAWAS: REEXAMINING TEXAS GULF COAST CANNIBALISM _______________ An Honors Thesis Presented to The Faculty of the Department of History University of Houston _______________ In Partial Fulfillment Of the Requirements for the Degree of Bachelor of Arts with Honors in Major _______________ By Timothy F. Seiter May, 2019 i KARANKAWAS: REEXAMINING TEXAS GULF COAST CANNIBALISM ______________________________ Timothy F. Seiter APPROVED: ______________________________ David Rainbow, Ph.D. Committee Chair ______________________________ Matthew J. Clavin, Ph.D. ______________________________ Andrew Joseph Pegoda, Ph.D. ______________________________ Mark A. Goldberg, Ph.D. ______________________________ Antonio D. Tillis, Ph.D. Dean, College of Liberal Arts and Social Sciences Department of Hispanic Studies ii KARANKAWAS: REEXAMINING TEXAS GULF COAST CANNIBALISM _______________ An Abstract of An Honors Thesis Presented to The Faculty of the Department of History University of Houston _______________ In Partial Fulfillment Of the Requirements for the Degree of Bachelor of Arts with Honors in Major _______________ By Timothy F. Seiter May, 2019 iii ABSTRACT In 1688, the Karankawa Peoples abducted and adopted an eight-year-old Jean-Baptiste Talon from a French fort on the Texas Gulf Coast. Talon lived with these Native Americans for roughly two and a half years and related an eye-witness account of their cannibalism. Despite his testimony, some present-day scholars reject the Karankawas’ cannibalism. Because of an abundance of farfetched and grisly accounts made by Spanish priests, bellicose Texans, and sensationalist historians, these academics believe the custom of anthropophagy is a colonial fabrication. Facing a sea of outrageously prejudicial sources, these scholars have either drowned in them or found no reason to wade deeper.
    [Show full text]
  • Disclaimer: the Opinions Expressed Herein Are Those of the Author and Not of His Employer Or Any Other Federal Agency
    Christy G. Turner, II, Jacqueline A. Turner. Man Corn: Cannibalism and Violence in the Prehistoric American Southwest. Salt Lake City: Utah State University Press, 1999. v + 547 pp. $60.00, cloth, ISBN 978-0-87480-566-6. Reviewed by Charles C. Kolb Published on H-NEXA (October, 1999) The American Southwest Revisited: Violence who are debating the hottest issue in the prehis‐ and Cannibalism, and the Anasazi and Toltecs of toric American Southwest explications of warfare, Mesoamerica witchcraft, ritual executions, and cannibalism. Introduction Even in the most dire, life-threatening cir‐ The topic of cannibalism is an emotionally cumstances, the consumption of the fesh of the charged issue that may engage humanistic or an‐ affiliates of one's own species or sociocultural thropological terms (endocannibalism and exo‐ group, whether the members of the stranded Don‐ cannibalism, or example), suggestions of human ner Party (Hardesty 1997) or sports team airplane sacrifice, or near starvation resulting in emergen‐ crash survivors in the Andes (Read 1974) is re‐ cy or survival cannibalism. These and psychoana‐ garded by a majority of outside observers as be‐ lytical phrases such as social pathology and "Han‐ haviorally inappropriate and, even as a criminal nibalistic" (Silence of the Lambs) behaviors, may or anti-religious act. Neurological disease vectors bring vivid, perhaps Stephen King-like or Dracula- aside (kuru, for example), the consumption of the like imagery to the minds of laypersons and scien‐ body parts or fesh of an enemy or of an ancestor tists alike. Add to this the potential for institution‐ is in some cultures considered appropriate, if not alized violence or warfare, witchcraft or sorcery, mandatory, behavior.
    [Show full text]
  • Review Article Transmissible Spongiform Encephalopathies Affecting Humans
    Hindawi Publishing Corporation ISRN Infectious Diseases Volume 2013, Article ID 387925, 11 pages http://dx.doi.org/10.5402/2013/387925 Review Article Transmissible Spongiform Encephalopathies Affecting Humans Dudhatra G. B., Avinash Kumar, Modi C. M., Awale M. M., Patel H. B., and Mody S. K. Department of Pharmacology & Toxicology, College of Veterinary Science & Animal Husbandry, Sardarkrushinagar Dantiwada Agricultural University, Sardarkrushinagar 385506, Gujarat, India Correspondence should be addressed to Dudhatra G. B.; [email protected] Received 2 April 2012; Accepted 5 May 2012 Academic Editors: A. Carvalho, K. Peoc’H, and T. A. Rupprecht Copyright © 2013 Dudhatra G. B. et al. is 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. Transmissible spongiform encephalopathies (TSEs) or prion diseases are group of rare and rapidly progressive fatal neurologic diseases. e agents responsible for human prion diseases are abnormal proteins or prion that can trigger chain reactions causing normal proteins in the brain to change to the abnormal protein. ese abnormal proteins are resistant to enzymatic breakdown, and they accumulate in the brain, leading to damage. TSEs have long incubation periods followed by chronic neurological disease and fatal outcomes, have similar pathology limited to the CNS including convulsions, dementia, ataxia, and behavioral or personality changes, and are experimentally transmissible to some other species. 1. Introduction 129, 51 are heterozygous, and 11 are homozygous for V [1]. Human transmissible spongiform encephalopathies (TSEs Methionine% homozygotes (codon% 129MM) are at a higher or prion diseases) include Creutzfeldt-Jakob disease (CJD), risk of developing prion disease, which may be explained Gerstmann-Straussler-Scheinker disease (GSS), fatal familial by the increased propensity of PrP to form PrPSc-like insomnia (FFI), kuru, and variant CJD (vCJD).
    [Show full text]
  • The Exposome in Human Evolution: from Dust to Diesel
    Volume 94, No. 4 December 2019 THE QUARTERLY REVIEW of Biology THE EXPOSOME IN HUMAN EVOLUTION: FROM DUST TO DIESEL Benjamin C. Trumble School of Human Evolution & Social Change and Center for Evolution and Medicine, Arizona State University Tempe, Arizona 85287 USA e-mail: [email protected] Caleb E. Finch Leonard Davis School of Gerontology and Dornsife College, University of Southern California Los Angeles, California 90089-0191 USA e-mail: cefi[email protected] keywords exposome, human evolution, genes, toxins, infections abstract Global exposures to air pollution and cigarette smoke are novel in human evolutionary history and are associated with at least 12 million premature deaths per year. We investigate the history of the human exposome for relationships between novel environmental toxins and genetic changes during human evo- lution in six phases. Phase I: With increased walking on savannas, early human ancestors inhaled crustal dust, fecal aerosols, and spores; carrion scavenging introduced new infectious pathogens. Phase II: Domestic fire exposed early Homo to novel toxins from smoke and cooking. Phases III and IV: Neolithic to preindustrial Homo sapiens incurred infectious pathogens from domestic animals and dense com- munities with limited sanitation. Phase V: Industrialization introduced novel toxins from fossil fuels, industrial chemicals, and tobacco at the same time infectious pathogens were diminishing. Thereby, pathogen-driven causes of mortality were replaced by chronic diseases driven by sterile inflammogens, exog- enous and endogenous. Phase VI: Considers future health during global warming with increased air pol- lution and infections. We hypothesize that adaptation to some ancient toxins persists in genetic variations associated with inflammation and longevity.
    [Show full text]
  • Kuru: a Journey Back in Time from Papua New Guinea to the Neanderthals’ Extinction
    Pathogens 2013, 2, 472-505; doi:10.3390/pathogens2030472 OPEN ACCESS pathogens ISSN 2076-0817 www.mdpi.com/journal/pathogens Review Kuru: A Journey Back in Time from Papua New Guinea to the Neanderthals’ Extinction Pawel P. Liberski Department of Molecular Pathology and Neuropathology, Medical University of Lodz, Kosciuszki st. 4, Lodz 90-419, Poland; E-Mail: [email protected]; Tel./Fax: +48-42-679-14-77 Received: 19 June 2013; in revised form: 4 July 2013 / Accepted: 12 July 2013 / Published: 18 July 2013 Abstract: Kuru, the first human transmissible spongiform encephalopathy was transmitted to chimpanzees by D. Carleton Gajdusek (1923–2008). In this review, I briefly summarize the history of this seminal discovery along its epidemiology, clinical picture, neuropathology and molecular genetics. The discovery of kuru opened new windows into the realms of human medicine and was instrumental in the later transmission of Creutzfeldt-Jakob disease and Gerstmann-Sträussler-Scheinker disease as well as the relevance that bovine spongiform encephalopathy had for transmission to humans. The transmission of kuru was one of the greatest contributions to biomedical sciences of the 20th century. Keywords: kuru; prion diseases; neuropathology; D. Carleton Gajdusek 1. Introduction Kuru is a disease that will forever be linked with the name of D. Carleton Gajdusek [1–11]. It was the first human prion disease transmitted to chimpanzees and subsequently classified as a transmissible spongiform encephalopathy (TSE), or slow unconventional virus disease. It was first reported in Western medicine in 1957 by Gajdusek and Vincent Zigas (Figure 1) [12,13]. The recognition of kuru as a neurodegenerative disease that is transmissible (i.e., infectious is a microbiological term) [14–18] and subsequent transmission of Creutzfeldt-Jakob disease (CJD) [19] not only proved that kuru is not merely an exotic disease caused by cannibalism on a remote island, but it represents a novel class of diseases caused by a novel class of pathogens.
    [Show full text]