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THAI MALENA A US009976180B2HA UNA ALTA KAMA NINA MITTE (12 ) United States Patent (10 ) Patent No. : US 9 , 976 , 180 B2 Hatchwell et al. (45 ) Date of Patent: May 22 , 2018 ( 54 ) METHODS FOR DETECTING A GENETIC 5 ,665 , 549 A 9 / 1997 Pinkel et al . 5 , 700 ,637 A 12 / 1997 Southern VARIATION IN SUBJECTS WITH 5 , 744 ,305 A 4 / 1998 Fodor et al . PARKINSONISM 5 ,776 ,434 A 7 / 1998 Purewal et al . 5 ,811 , 128 A 9 / 1998 Tice et al . (71 ) Applicant: Population Bio , Inc ., Melville , NY 5 , 814 ,344 A 9 / 1998 Tice et al . (US ) 5 ,820 , 883 A 10 / 1998 Tice et al . 5 ,837 , 832 A 11/ 1998 Chee et al. 5 ,853 , 763 A 12 / 1998 Tice et al. ( 72 ) Inventors : Eli Hatchwell , Winchester (GB ); Peggy 5 , 858 ,659 A 1 / 1999 Sapolsky et al. S . Eis , Fitchburg , WI (US ) 5 , 928 ,647 A 7 / 1999 Rock 5 , 942 ,252 A 8 / 1999 Tice et al. ( 73 ) Assignee: POPULATION BIO , INC ., Melville , 5 , 945 , 334 A 8 / 1999 Besemer et al . NY (US ) 6 ,040 , 138 A 3 / 2000 Lockhart et al . 6 ,054 , 270 A 4 / 2000 Southern 6 , 146 , 834 A 11/ 2000 Schaad et al . ( * ) Notice : Subject to any disclaimer , the term of this 6 , 207, 392 B1 3 / 2001 Weiss et al. patent is extended or adjusted under 35 6 ,210 , 878 B1 4 /2001 Pinkel et al . U . S . C . 154 ( b ) by 0 days. days . 6 , 251, 607 B1 6 /2001 Tsen et al . 6 , 300, 063 B1 10 / 2001 Lipshutz et al . 6 , 423 , 499 B1 7 / 2002 Song et al. (21 ) Appl. No. : 14 /026 ,642 6 , 429 , 027 B1 8 / 2002 Chee et al . 6 , 733 , 977 B2 5 / 2004 Besemer et al . ( 22 ) Filed : Sep . 13 , 2013 6 , 858 ,394 B1 2 / 2005 Chee et al . 6 , 858 , 412 B2 2 / 2005 Willis et al . (65 ) Prior Publication Data 6 , 892, 141 B1 5 /2005 Nakae et al . 6 , 916, 621 B2 7 / 2005 Shah US 2014 /0162933 A1 Jun . 12 , 2014 6 ,951 , 761 B2 10 /2005 Star et al. 6 , 969 ,589 B2 11/ 2005 Patil et al. 6 , 977 , 148 B2 12 / 2005 Dean et al . Related U . S . Application Data 7 ,011 , 949 B23 / 2006 Amorese et al . (60 ) Provisional application No .61 / 743, 919 , filed on Sep . (Continued ) 14 , 2012 FOREIGN PATENT DOCUMENTS (51 ) Int. Ci. C120 1 /68 ( 2018 .01 ) CN 1733937 A 2 /2006 GOIN 33 /68 ( 2006 . 01 ) CN 101148684 A 3 / 2008 ( 52 ) U . S . CI. (Continued ) CPC . .. .. C120 1 /6874 (2013 .01 ) ; C120 1 /6883 ( 2013 .01 ) ; GOIN 33 /6896 ( 2013. 01 ) ; C12Q OTHER PUBLICATIONS 2600 / 136 ( 2013 .01 ); C12Q 2600 / 156 Hirschhorn et al. Genetics in Medicine . 2002. 4 ( 2 ) : 45 -61 . * ( 2013. 01) ; GOIN 2500 / 04 (2013 .01 ) ; GOIN Hattersley et al. The Lancet. 2005. 366 : 1315 - 1323. * 2800/ 2835 ( 2013. 01 ) Lucentini et al The Scientist (2004 ) vol. 18 , p . 20 . * ( 58 ) Field of Classification Search Mummidi et al Journal of Biological Chemistry 2000 vol . 275 No. None 25 pp . 18946 - 18961. * See application file for complete search history . Gagneux et al Molecular Phylogenetics and Evolution . 2001. 18 : 2 - 13 . * Calvo et al Nature Genetics . Sep . 2010 . 42 : 851. * (56 ) References Cited NCBI SNP Database rs201412882 , ss491686165 , Mar. 6 , 2012 ( National Library of Medicine, NIH , Bethesda, MD , USA ). * U . S . PATENT DOCUMENTS Betancur, et al . The emerging role of synaptic cell -adhesion path 3 ,625 , 214 A 12 / 1971 Higuchi et al . ways in the pathogenesis of autism spectrum disorders . Trends 4 ,683 , 195 A 7 / 1987 Mullis et al. Neurosci. Jul. 2009 ;32 ( 7 ) : 402 - 12 . doi: 10 . 1016 / j .tins . 2009 .04 .003 . 4 ,789 , 734 A 12 / 1988 Pierschbacher Epub Jun . 21 , 2009 . 4 , 897 , 268 A 1 / 1990 Tice et al . Office action dated Dec . 16 , 2014 for U . S . Appl . No . 12 /449 , 566 . 4 , 906 , 474 A 3 / 1990 Langer et al . U . S . Appl. No . 14 / 090 ,932 , filed Nov . 26 , 2013 , Chinitz et al . 4 , 925 ,673 A 5 / 1990 Steiner et al. International search report and written opinion dated Jan . 20 , 2014 4 , 992 ,445 A 2 / 1991 Lawter et al . for PCT/ US2013 /059739 . 5 , 001, 139 A 3 / 1991 Lawter et al. ( Continued ) 5 , 023 , 252 A 6 / 1991 Hseih 5 , 075 , 109 A 12 / 1991 Tice et al . Primary Examiner — Carla J Myers 5 , 143 , 854 A 9 / 1992 Pirrung et al. (74 ) Attorney, Agent, or Firm — Wilson , Sonsini, 5 , 190 , 029 A 3 / 1993 Byron et al. Goodrich & Rosati 5 , 223 , 409 A 6 / 1993 Ladner et al . 5 ,272 , 071 A 12 / 1993 Chappel (57 ) ABSTRACT 5 ,288 ,514 A 2 / 1994 Ellman This document provides methods and materials related to 5 , 376 , 359 A 12 / 1994 Johnson 5 , 384 , 261 A 1 / 1995 Winkler et al. genetic variations of neurological disorders . For example , 5 , 424 , 186 A 6 / 1995 Fodor et al . this document provides methods for using such genetic 5 ,445 , 934 A 8 / 1995 Fodor et al . variations to assess susceptibility of developing Parkinson ' s 5 , 451 ,683 A 9 / 1995 Barrett et al . 5 , 510 , 270 A 4 / 1996 Fodor et al . disease . 5 ,527 , 681 A 6 / 1996 Holmes et al . 19 Claims, 4 Drawing Sheets US 9 ,976 , 180 B2 Page 2 (56 ) References Cited 2014 / 0162894 AL 6 / 2014 Hatchwell et al . 2015 /0051086 AL 2 /2015 Hatchwell et al . U . S . PATENT DOCUMENTS 2016 / 0019336 AL 1 /2016 Chinitz et al. 7 ,014 , 997 B2 3 / 2006 Knoll et al. FOREIGN PATENT DOCUMENTS 7 , 030 , 231 B1 4 / 2006 Craik et al. 7 , 034 ,144 B2 4 / 2006 Van Dongen et al . CN 101403008 A 4 / 2009 7 , 364 , 858 B2 4 / 2008 Barany et al. EP 0373203 B1 8 / 1994 7 , 424 , 368 B2 9 / 2008 Huang et al . EP 0619321 Al 10 / 1994 7 ,702 , 468 B2 4 / 2010 Chinitz et al . KR 2009 -0080105 A 7 / 2009 7 , 957 , 913 B2 6 /2011 Chinitz et al. KR 2011 -0114664 A 10 / 2011 7 , 998 , 744 B2 8 / 2011 Stevenson et al. wo WO 90 / 02809 Al 3 / 1990 8 ,367 , 417 B2 2 / 2013 Stevenson et al. WO WO 91/ 06667 AL 5 / 1991 8 , 655 , 599 B2 2 / 2014 Chinitz et al . WO WO 91/ 17271 AL 11 / 1991 8 , 862, 410 B2 10 / 2014 Hatchwell et al. WO WO 92 / 01047 Al 1 / 1992 2002 /0012921 A1 1 /2002 Vincent , Jr. WO WO 92 / 09690 A2 6 / 1992 2002 / 0012930 A1 1 / 2002 Rothberg et al . wo WO 92 / 10092 Al 6 / 1992 2003 /0023070 A1 1 / 2003 Ni et al . WO WO 92 / 15679 A1 9 / 1992 2003 / 0049663 Al 3 / 2003 Wigler et al. WO WO 92 / 18619 Al 10 / 1992 2003 / 0068629 Al 4 / 2003 Rothberg et al . wo WO 92 / 20791 AL 11 / 1992 2003 / 0082606 A1 5 / 2003 Lebo et al. WO WO 92 / 09690 A3 12 / 1992 2003 /0100102 Al 5 / 2003 Rothberg et al. WO WO 93 /01288 AL 1 / 1993 2003/ 0148344 Al 8 / 2003 Rothberg et al . WO WO 93 / 22684 Al 11/ 1993 2003/ 0207295 AL 11/ 2003 Gunderson et al. WO WO 95 / 11995 A15 / 1995 2003 / 0215821 A1 11/ 2003 Gunderson et al. WO WO 98 / 20019 A 5 / 1998 2004 /0018491 AL 1 / 2004 Gunderson et al. WO WO 02 /099129 A2 12 / 2002 2004 / 0137473 Al 7 /2004 Wigler et al. WO WO 03 / 048318 A2 6 / 2003 2004 /0157243 Al 8 / 2004 Huang et al. WO WO 2004 /018633 A2 3 /2004 2004 /0197774 Al 10 / 2004 Wigler et al. WO WO 2004 /044225 A2 5 / 2004 2004 / 0248161 Al 12 /2004 Rothberg et al . WO WO 2004 /075010 A2 9 / 2004 2005 /0032095 A1 2 / 2005 Wigler et al . WO WO 2005 /042763 A2 5 / 2005 2005/ 0037393 Al 2 / 2005 Gunderson et al. WO WO 2005 / 068664 A2 7 / 2005 2005 / 0037414 Al 2 / 2005 Lee et al . WO WO 2005 / 108997 A1 11 / 2005 2005 /0079510 Al 4 / 2005 Berka et al . WO WO 2004 / 044225 A3 4 / 2006 2005 / 0100893 Al 5 /2005 Gunderson et al. WO WO 2006 /050475 A2 5 / 2006 2005 / 0100932 A1 5 /2005 Lapidus et al . WO WO 2007 /070640 A2 6 / 2007 2005 /0112595 A1 5 /2005 Zhao et al. WO WO 2007 / 070640 A3 8 / 2007 2005 /0124022 Al 6 / 2005 Srinivasan et al. WO WO 2007 / 129000 A2 11 / 2007 2005 /0196799 A1 9 / 2005 Wigler et al . WO WO 2007 / 131135 A2 11 / 2007 2005 /0233339 Al 10 / 2005 Barrett et al . WO WO 2008 /016374 A2 2 / 2008 2005 /0266444 A1 12 / 2005 Wigler et al . WO WO 2007 / 129000 A3 3 / 2008 2005 / 0282196 Al 12 / 2005 Costa WO WO 2007 / 131135 A3 11 / 2008 2006 / 0012784 A1 1 / 2006 Ulmer WO WO 2009 / 043178 A1 4 / 2009 2006 / 0012793 Al 1 / 2006 Harris Wo WO 2009 / 073764 AL 6 / 2009 2006 / 0024678 Al 2 / 2006 Buzby wo WO 2010 /036353 A2 4 / 2010 2006 / 0024711 A1 2 /2006 Lapidus et al. WO WO 2010 / 056897 Al 5 / 2010 2006 / 0063168 A1 3 / 2006 Albertson et al. WO 2011 /012672 A1 2 /2011 2006 / 0078909 Al 4 / 2006 Srinivasan et al . WO 2006 /0134674 Al 6 / 2006 Huang et al. WO WO 2011 /035012 A2 3 / 2011 2007 /0141577 AL 6 / 2007 Moore wo WO 2011 / 112961 A1 9 / 2011 2007 / 0207481 A1 9 /2007 Wigler et al.
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