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  • 1
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    A population-specific HTR2B stop codon predisposes to severe impulsivity (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-24
    Description: Impulsivity, describing action without foresight, is an important feature of several psychiatric diseases, suicidality and violent behaviour. The complex origins of impulsivity hinder identification of the genes influencing it and the diseases with which it is associated. Here we perform exon-focused sequencing of impulsive individuals in a founder population, targeting fourteen genes belonging to the serotonin and dopamine domain. A stop codon in HTR2B was identified that is common (minor allele frequency 〉 1%) but exclusive to Finnish people. Expression of the gene in the human brain was assessed, as well as the molecular functionality of the stop codon, which was associated with psychiatric diseases marked by impulsivity in both population and family-based analyses. Knockout of Htr2b increased impulsive behaviours in mice, indicative of predictive validity. Our study shows the potential for identifying and tracing effects of rare alleles in complex behavioural phenotypes using founder populations, and indicates a role for HTR2B in impulsivity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3183507/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3183507/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bevilacqua, Laura -- Doly, Stephane -- Kaprio, Jaakko -- Yuan, Qiaoping -- Tikkanen, Roope -- Paunio, Tiina -- Zhou, Zhifeng -- Wedenoja, Juho -- Maroteaux, Luc -- Diaz, Silvina -- Belmer, Arnaud -- Hodgkinson, Colin A -- Dell'osso, Liliana -- Suvisaari, Jaana -- Coccaro, Emil -- Rose, Richard J -- Peltonen, Leena -- Virkkunen, Matti -- Goldman, David -- AA-09203/AA/NIAAA NIH HHS/ -- AA-12502/AA/NIAAA NIH HHS/ -- Z01 AA000301-09/Intramural NIH HHS/ -- Z01 AA000301-10/Intramural NIH HHS/ -- Z99 AA999999/Intramural NIH HHS/ -- England -- Nature. 2010 Dec 23;468(7327):1061-6. doi: 10.1038/nature09629.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, NIH, Rockville, Maryland 20852, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179162" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism ; Case-Control Studies ; Cell Line ; Female ; Finland ; Founder Effect ; Gene Expression Regulation ; Gene Knockout Techniques ; Genotype ; Humans ; Impulsive Behavior/*genetics ; Male ; Mental Disorders/genetics ; Mice ; Mice, 129 Strain ; Mice, Knockout ; Pedigree ; Polymorphism, Single Nucleotide/genetics ; Receptor, Serotonin, 5-HT2B/*genetics/*metabolism ; Testosterone/blood/cerebrospinal fluid
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    A bizarre Jurassic maniraptoran from China with elongate ribbon-like feathers (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-10-25
    Description: Recent coelurosaurian discoveries have greatly enriched our knowledge of the transition from dinosaurs to birds, but all reported taxa close to this transition are from relatively well known coelurosaurian groups. Here we report a new basal avialan, Epidexipteryx hui gen. et sp. nov., from the Middle to Late Jurassic of Inner Mongolia, China. This new species is characterized by an unexpected combination of characters seen in several different theropod groups, particularly the Oviraptorosauria. Phylogenetic analysis shows it to be the sister taxon to Epidendrosaurus, forming a new clade at the base of Avialae. Epidexipteryx also possesses two pairs of elongate ribbon-like tail feathers, and its limbs lack contour feathers for flight. This finding shows that a member of the avialan lineage experimented with integumentary ornamentation as early as the Middle to Late Jurassic, and provides further evidence relating to this aspect of the transition from non-avian theropods to birds.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Fucheng -- Zhou, Zhonghe -- Xu, Xing -- Wang, Xiaolin -- Sullivan, Corwin -- England -- Nature. 2008 Oct 23;455(7216):1105-8. doi: 10.1038/nature07447.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Evolutionary Systematics of Vertebrates, Institute of Vertebrate Paleontology and Paleoanthropology, Chinese Academy of Sciences, PO Box 643, Beijing 100044, China. zhangfucheng@ivpp.ac.cn〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18948955" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; China ; Dinosaurs/*anatomy & histology/*classification ; Feathers/*anatomy & histology ; *Fossils ; History, Ancient ; Phylogeny
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    Genetic variation in human NPY expression affects stress response and emotion (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-04-04
    Description: Understanding inter-individual differences in stress response requires the explanation of genetic influences at multiple phenotypic levels, including complex behaviours and the metabolic responses of brain regions to emotional stimuli. Neuropeptide Y (NPY) is anxiolytic and its release is induced by stress. NPY is abundantly expressed in regions of the limbic system that are implicated in arousal and in the assignment of emotional valences to stimuli and memories. Here we show that haplotype-driven NPY expression predicts brain responses to emotional and stress challenges and also inversely correlates with trait anxiety. NPY haplotypes predicted levels of NPY messenger RNA in post-mortem brain and lymphoblasts, and levels of plasma NPY. Lower haplotype-driven NPY expression predicted higher emotion-induced activation of the amygdala, as well as diminished resiliency as assessed by pain/stress-induced activations of endogenous opioid neurotransmission in various brain regions. A single nucleotide polymorphism (SNP rs16147) located in the promoter region alters NPY expression in vitro and seems to account for more than half of the variation in expression in vivo. These convergent findings are consistent with the function of NPY as an anxiolytic peptide and help to explain inter-individual variation in resiliency to stress, a risk factor for many diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2715959/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2715959/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Zhifeng -- Zhu, Guanshan -- Hariri, Ahmad R -- Enoch, Mary-Anne -- Scott, David -- Sinha, Rajita -- Virkkunen, Matti -- Mash, Deborah C -- Lipsky, Robert H -- Hu, Xian-Zhang -- Hodgkinson, Colin A -- Xu, Ke -- Buzas, Beata -- Yuan, Qiaoping -- Shen, Pei-Hong -- Ferrell, Robert E -- Manuck, Stephen B -- Brown, Sarah M -- Hauger, Richard L -- Stohler, Christian S -- Zubieta, Jon-Kar -- Goldman, David -- K01 MH072837/MH/NIMH NIH HHS/ -- K02-DA17232/DA/NIDA NIH HHS/ -- P01 HL040962/HL/NHLBI NIH HHS/ -- P50-DA16556/DA/NIDA NIH HHS/ -- PL1 DA024859/DA/NIDA NIH HHS/ -- PL1 DA024859-02/DA/NIDA NIH HHS/ -- R01 DA 016423/DA/NIDA NIH HHS/ -- R01 DE 15396/DE/NIDCR NIH HHS/ -- R01 HL065137/HL/NHLBI NIH HHS/ -- R01 MH074697/MH/NIMH NIH HHS/ -- R01 MH074697-04A1/MH/NIMH NIH HHS/ -- R01-AA13892/AA/NIAAA NIH HHS/ -- Z01 AA000301-09/Intramural NIH HHS/ -- Z99 AA999999/Intramural NIH HHS/ -- England -- Nature. 2008 Apr 24;452(7190):997-1001. doi: 10.1038/nature06858. Epub 2008 Apr 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Neurogenetics, NIAAA, NIH, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18385673" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Anxiety/genetics ; Anxiety Disorders/genetics ; Brain/*metabolism/physiology/physiopathology ; *Emotions ; European Continental Ancestry Group/genetics ; Facial Expression ; Finland/ethnology ; Gene Expression Regulation/*genetics ; Genetic Variation/*genetics ; Haplotypes/genetics ; Humans ; Lymphocytes/metabolism ; Magnetic Resonance Imaging ; Male ; Neuropeptide Y/blood/*genetics ; Opioid Peptides/metabolism ; Pain/genetics ; Polymorphism, Single Nucleotide/genetics ; RNA, Messenger/genetics/metabolism ; Stress, Physiological/*genetics/psychology ; United States/ethnology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Solubility trapping in formation water as dominant CO(2) sink in natural gas fields (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-04-03
    Description: Injecting CO(2) into deep geological strata is proposed as a safe and economically favourable means of storing CO(2) captured from industrial point sources. It is difficult, however, to assess the long-term consequences of CO(2) flooding in the subsurface from decadal observations of existing disposal sites. Both the site design and long-term safety modelling critically depend on how and where CO(2) will be stored in the site over its lifetime. Within a geological storage site, the injected CO(2) can dissolve in solution or precipitate as carbonate minerals. Here we identify and quantify the principal mechanism of CO(2) fluid phase removal in nine natural gas fields in North America, China and Europe, using noble gas and carbon isotope tracers. The natural gas fields investigated in our study are dominated by a CO(2) phase and provide a natural analogue for assessing the geological storage of anthropogenic CO(2) over millennial timescales. We find that in seven gas fields with siliciclastic or carbonate-dominated reservoir lithologies, dissolution in formation water at a pH of 5-5.8 is the sole major sink for CO(2). In two fields with siliciclastic reservoir lithologies, some CO(2) loss through precipitation as carbonate minerals cannot be ruled out, but can account for a maximum of 18 per cent of the loss of emplaced CO(2). In view of our findings that geological mineral fixation is a minor CO(2) trapping mechanism in natural gas fields, we suggest that long-term anthropogenic CO(2) storage models in similar geological systems should focus on the potential mobility of CO(2) dissolved in water.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gilfillan, Stuart M V -- Lollar, Barbara Sherwood -- Holland, Greg -- Blagburn, Dave -- Stevens, Scott -- Schoell, Martin -- Cassidy, Martin -- Ding, Zhenju -- Zhou, Zheng -- Lacrampe-Couloume, Georges -- Ballentine, Chris J -- England -- Nature. 2009 Apr 2;458(7238):614-8. doi: 10.1038/nature07852.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Earth, Atmospheric and Environmental Sciences, The University of Manchester, Oxford Road, Manchester M13 9PL, UK. stuart.gilfillan@ed.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19340078" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Fossilized melanosomes and the colour of Cretaceous dinosaurs and birds (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-01-29
    Description: Spectacular fossils from the Early Cretaceous Jehol Group of northeastern China have greatly expanded our knowledge of the diversity and palaeobiology of dinosaurs and early birds, and contributed to our understanding of the origin of birds, of flight, and of feathers. Pennaceous (vaned) feathers and integumentary filaments are preserved in birds and non-avian theropod dinosaurs, but little is known of their microstructure. Here we report that melanosomes (colour-bearing organelles) are not only preserved in the pennaceous feathers of early birds, but also in an identical manner in integumentary filaments of non-avian dinosaurs, thus refuting recent claims that the filaments are partially decayed dermal collagen fibres. Examples of both eumelanosomes and phaeomelanosomes have been identified, and they are often preserved in life position within the structure of partially degraded feathers and filaments. Furthermore, the data here provide empirical evidence for reconstructing the colours and colour patterning of these extinct birds and theropod dinosaurs: for example, the dark-coloured stripes on the tail of the theropod dinosaur Sinosauropteryx can reasonably be inferred to have exhibited chestnut to reddish-brown tones.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Fucheng -- Kearns, Stuart L -- Orr, Patrick J -- Benton, Michael J -- Zhou, Zhonghe -- Johnson, Diane -- Xu, Xing -- Wang, Xiaolin -- England -- Nature. 2010 Feb 25;463(7284):1075-8. doi: 10.1038/nature08740. Epub 2010 Jan 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Key Laboratory of Evolutionary Systematics of Vertebrates, Institute of Vertebrate Paleontology and Paleoanthropology, Chinese Academy of Sciences, PO Box 643, Beijing 100044, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20107440" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Birds/*anatomy & histology/classification ; China ; *Color ; Dinosaurs/*anatomy & histology/classification ; Extinction, Biological ; Feathers/anatomy & histology/*cytology/ultrastructure ; *Fossils ; Integumentary System/anatomy & histology ; *Melanosomes/physiology/ultrastructure ; Phylogeny ; *Pigmentation/physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    Lipid nanoparticle siRNA treatment of Ebola-virus-Makona-infected nonhuman primates (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-04-23
    Description: The current outbreak of Ebola virus in West Africa is unprecedented, causing more cases and fatalities than all previous outbreaks combined, and has yet to be controlled. Several post-exposure interventions have been employed under compassionate use to treat patients repatriated to Europe and the United States. However, the in vivo efficacy of these interventions against the new outbreak strain of Ebola virus is unknown. Here we show that lipid-nanoparticle-encapsulated short interfering RNAs (siRNAs) rapidly adapted to target the Makona outbreak strain of Ebola virus are able to protect 100% of rhesus monkeys against lethal challenge when treatment was initiated at 3 days after exposure while animals were viraemic and clinically ill. Although all infected animals showed evidence of advanced disease including abnormal haematology, blood chemistry and coagulopathy, siRNA-treated animals had milder clinical features and fully recovered, while the untreated control animals succumbed to the disease. These results represent the first, to our knowledge, successful demonstration of therapeutic anti-Ebola virus efficacy against the new outbreak strain in nonhuman primates and highlight the rapid development of lipid-nanoparticle-delivered siRNA as a countermeasure against this highly lethal human disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4467030/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4467030/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thi, Emily P -- Mire, Chad E -- Lee, Amy C H -- Geisbert, Joan B -- Zhou, Joy Z -- Agans, Krystle N -- Snead, Nicholas M -- Deer, Daniel J -- Barnard, Trisha R -- Fenton, Karla A -- MacLachlan, Ian -- Geisbert, Thomas W -- U19 AI109711/AI/NIAID NIH HHS/ -- U19AI109711/AI/NIAID NIH HHS/ -- England -- Nature. 2015 May 21;521(7552):362-5. doi: 10.1038/nature14442. Epub 2015 Apr 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tekmira Pharmaceuticals, Burnaby, British Columbia V5J 5J8, Canada. ; 1] Galveston National Laboratory, University of Texas Medical Branch, Galveston, Texas 77550, USA [2] Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas 77550, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25901685" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Disease Models, Animal ; Ebolavirus/classification/*drug effects/*genetics ; Female ; Hemorrhagic Fever, Ebola/pathology/prevention & control/*therapy/*virology ; Humans ; Macaca mulatta/virology ; Male ; Nanoparticles/*administration & dosage ; RNA, Small Interfering/*administration & dosage/pharmacology/*therapeutic use ; Survival Analysis ; Time Factors ; Treatment Outcome ; Viral Load/drug effects
    Print ISSN: 0028-0836
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  • 7
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    Theileria parasites secrete a prolyl isomerase to maintain host leukocyte transformation (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-01-28
    Description: Infectious agents develop intricate mechanisms to interact with host cell pathways and hijack their genetic and epigenetic machinery to change host cell phenotypic states. Among the Apicomplexa phylum of obligate intracellular parasites, which cause veterinary and human diseases, Theileria is the only genus that transforms its mammalian host cells. Theileria infection of bovine leukocytes induces proliferative and invasive phenotypes associated with activated signalling pathways, notably JNK and AP-1 (ref. 2). The transformed phenotypes are reversed by treatment with the theilericidal drug buparvaquone. We used comparative genomics to identify a homologue of the peptidyl-prolyl isomerase PIN1 in T. annulata (TaPIN1) that is secreted into the host cell and modulates oncogenic signalling pathways. Here we show that TaPIN1 is a bona fide prolyl isomerase and that it interacts with the host ubiquitin ligase FBW7, leading to its degradation and subsequent stabilization of c-JUN, which promotes transformation. We performed in vitro and in silico analysis and in vivo zebrafish xenograft experiments to demonstrate that TaPIN1 is directly inhibited by the anti-parasite drug buparvaquone (and other known PIN1 inhibitors) and is mutated in a drug-resistant strain. Prolyl isomerization is thus a conserved mechanism that is important in cancer and is used by Theileria parasites to manipulate host oncogenic signalling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4401560/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4401560/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marsolier, J -- Perichon, M -- DeBarry, J D -- Villoutreix, B O -- Chluba, J -- Lopez, T -- Garrido, C -- Zhou, X Z -- Lu, K P -- Fritsch, L -- Ait-Si-Ali, S -- Mhadhbi, M -- Medjkane, S -- Weitzman, J B -- 08-0111/Worldwide Cancer Research/United Kingdom -- R01 CA167677/CA/NCI NIH HHS/ -- R01CA167677/CA/NCI NIH HHS/ -- England -- Nature. 2015 Apr 16;520(7547):378-82. doi: 10.1038/nature14044. Epub 2015 Jan 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Universite Paris Diderot, Sorbonne Paris Cite, Epigenetics and Cell Fate, UMR 7216 CNRS, 75013 Paris, France. ; Center for Tropical and Emerging Global Diseases, University of Georgia, Athens, Georgia 30602, USA. ; Universite Paris Diderot, Sorbonne Paris Cite, Molecules Therapeutiques in silico, INSERM UMR-S 973, 75013 Paris, France. ; 1] INSERM, UMR 866, Equipe labellisee Ligue contre le Cancer and Laboratoire d'Excellence LipSTIC, 21000 Dijon, France [2] University of Burgundy, Faculty of Medicine and Pharmacy, 21000 Dijon, France. ; 1] INSERM, UMR 866, Equipe labellisee Ligue contre le Cancer and Laboratoire d'Excellence LipSTIC, 21000 Dijon, France [2] University of Burgundy, Faculty of Medicine and Pharmacy, 21000 Dijon, France [3] Centre anticancereux George Francois Leclerc, CGFL, 21000 Dijon, France. ; Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA. ; Laboratoire de Parasitologie, Ecole Nationale de Medecine Veterinaire, Universite de la Manouba, 2020 Sidi Thabet, Tunisia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25624101" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cell Line ; *Cell Transformation, Neoplastic/drug effects ; Drug Resistance/genetics ; *Host-Parasite Interactions ; Humans ; Leukocytes/drug effects/parasitology/*pathology ; Naphthoquinones/pharmacology ; Parasites/drug effects/enzymology/pathogenicity ; Peptidylprolyl Isomerase/antagonists & inhibitors/genetics/*metabolism/*secretion ; Protein Stability ; Proto-Oncogene Proteins c-jun/metabolism ; SKP Cullin F-Box Protein Ligases/metabolism ; Signal Transduction/drug effects ; Theileria/drug effects/*enzymology/genetics/*pathogenicity ; Transcription Factor AP-1/metabolism ; Ubiquitination ; Xenograft Model Antitumor Assays ; Zebrafish/embryology
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Antibody against early driver of neurodegeneration cis P-tau blocks brain injury and tauopathy (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-07-16
    Description: Traumatic brain injury (TBI), characterized by acute neurological dysfunction, is one of the best known environmental risk factors for chronic traumatic encephalopathy and Alzheimer's disease, the defining pathologic features of which include tauopathy made of phosphorylated tau protein (P-tau). However, tauopathy has not been detected in the early stages after TBI, and how TBI leads to tauopathy is unknown. Here we find robust cis P-tau pathology after TBI in humans and mice. After TBI in mice and stress in vitro, neurons acutely produce cis P-tau, which disrupts axonal microtubule networks and mitochondrial transport, spreads to other neurons, and leads to apoptosis. This process, which we term 'cistauosis', appears long before other tauopathy. Treating TBI mice with cis antibody blocks cistauosis, prevents tauopathy development and spread, and restores many TBI-related structural and functional sequelae. Thus, cis P-tau is a major early driver of disease after TBI and leads to tauopathy in chronic traumatic encephalopathy and Alzheimer's disease. The cis antibody may be further developed to detect and treat TBI, and prevent progressive neurodegeneration after injury.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4718588/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4718588/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kondo, Asami -- Shahpasand, Koorosh -- Mannix, Rebekah -- Qiu, Jianhua -- Moncaster, Juliet -- Chen, Chun-Hau -- Yao, Yandan -- Lin, Yu-Min -- Driver, Jane A -- Sun, Yan -- Wei, Shuo -- Luo, Man-Li -- Albayram, Onder -- Huang, Pengyu -- Rotenberg, Alexander -- Ryo, Akihide -- Goldstein, Lee E -- Pascual-Leone, Alvaro -- McKee, Ann C -- Meehan, William -- Zhou, Xiao Zhen -- Lu, Kun Ping -- P30 AG013846/AG/NIA NIH HHS/ -- P30AG13846/AG/NIA NIH HHS/ -- R01AG029385/AG/NIA NIH HHS/ -- R01AG046319/AG/NIA NIH HHS/ -- R01CA167677/CA/NCI NIH HHS/ -- R01HL111430/HL/NHLBI NIH HHS/ -- S10RR017927/RR/NCRR NIH HHS/ -- T32HD040128/HD/NICHD NIH HHS/ -- U01 NS086659/NS/NINDS NIH HHS/ -- U01NS086659-01/NS/NINDS NIH HHS/ -- England -- Nature. 2015 Jul 23;523(7561):431-6. doi: 10.1038/nature14658. Epub 2015 Jul 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Division of Translational Therapeutics, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA [2] Cancer Research Institute, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA. ; Division of Emergency Medicine, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Alzheimer's Disease Center, CTE Program, Boston University School of Medicine, Boston, Massachusetts 02118, USA. ; 1] Division of Translational Therapeutics, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA [2] Geriatric Research Education and Clinical Center, VA Boston Healthcare System, Harvard Medical School, Boston, Massachusetts 02130, USA. ; Department of Neurology, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Department of Microbiology, Yokohama City University School of Medicine, Yokohama 236-0004, Japan. ; Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA. ; Micheli Center for Sports Injury Prevention, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26176913" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/complications/prevention & control ; Animals ; Antibodies, Monoclonal/*immunology/*pharmacology/therapeutic use ; Antibody Affinity ; Axons/metabolism/pathology ; Brain/metabolism/pathology ; Brain Injuries/complications/metabolism/*pathology/*prevention & control ; Disease Models, Animal ; Epitopes/chemistry/immunology ; Female ; Humans ; Male ; Mice ; Phosphoproteins/antagonists & inhibitors/biosynthesis/immunology/toxicity ; Stress, Physiological ; Tauopathies/complications/metabolism/pathology/*prevention & control ; tau Proteins/*antagonists & ; inhibitors/biosynthesis/*chemistry/immunology/toxicity
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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    Zheng et al. reply (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-07-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Connor, Jingmai -- Zheng, Xiaoting -- Zhou, Zhonghe -- England -- Nature. 2013 Jul 11;499(7457):E1-2. doi: 10.1038/nature12368.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Key Laboratory of Vertebrate Evolution and Human Origin, Institute of Vertebrate Paleontology and Paleoanthropology, Chinese Academy of Sciences, Beijing 100044, China. jingmai.oconnor@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23846662" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Birds/*anatomy & histology/*physiology ; Female ; *Fossils ; Ovarian Follicle/*anatomy & histology/*physiology ; Reproduction/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Suppression of neuroinflammation by astrocytic dopamine D2 receptors via alphaB-crystallin (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-12-18
    Description: Chronic neuroinflammation is a common feature of the ageing brain and some neurodegenerative disorders. However, the molecular and cellular mechanisms underlying the regulation of innate immunity in the central nervous system remain elusive. Here we show that the astrocytic dopamine D2 receptor (DRD2) modulates innate immunity through alphaB-crystallin (CRYAB), which is known to suppress neuroinflammation. We demonstrate that knockout mice lacking Drd2 showed remarkable inflammatory response in multiple central nervous system regions and increased the vulnerability of nigral dopaminergic neurons to neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity. Astrocytes null for Drd2 became hyper-responsive to immune stimuli with a marked reduction in the level of CRYAB. Preferential ablation of Drd2 in astrocytes robustly activated astrocytes in the substantia nigra. Gain- or loss-of-function studies showed that CRYAB is critical for DRD2-mediated modulation of innate immune response in astrocytes. Furthermore, treatment of wild-type mice with the selective DRD2 agonist quinpirole increased resistance of the nigral dopaminergic neurons to MPTP through partial suppression of inflammation. Our study indicates that astrocytic DRD2 activation normally suppresses neuroinflammation in the central nervous system through a CRYAB-dependent mechanism, and provides a new strategy for targeting the astrocyte-mediated innate immune response in the central nervous system during ageing and disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shao, Wei -- Zhang, Shu-zhen -- Tang, Mi -- Zhang, Xin-hua -- Zhou, Zheng -- Yin, Yan-qing -- Zhou, Qin-bo -- Huang, Yuan-yuan -- Liu, Ying-jun -- Wawrousek, Eric -- Chen, Teng -- Li, Sheng-bin -- Xu, Ming -- Zhou, Jiang-ning -- Hu, Gang -- Zhou, Jia-wei -- England -- Nature. 2013 Feb 7;494(7435):90-4. doi: 10.1038/nature11748. Epub 2012 Dec 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neuroscience, State Key Laboratory of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23242137" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine/pharmacology ; Animals ; Astrocytes/drug effects/*immunology/*metabolism ; Dopaminergic Neurons/drug effects ; Immunity, Innate/drug effects ; Inflammation/chemically induced/genetics/*immunology/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Microglia/cytology/immunology ; Neuroprotective Agents/metabolism ; Quinpirole/pharmacology ; Receptors, Dopamine D2/agonists/deficiency/genetics/*metabolism ; Substantia Nigra/cytology/drug effects ; alpha-Crystallin B Chain/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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