LEADER 01165nam--2200385---450- 001 990000661970203316 005 20051110114412.0 010 $a88-88232-00-1 035 $a0066197 035 $aUSA010066197 035 $a(ALEPH)000066197USA01 035 $a0066197 100 $a20011002d2001----km-y0itay0103----ba 101 0 $aita 102 $aIT 105 $a||||||||001yy 200 1 $a<> vita è gratis$epercorsi di redenzione tra psicologia del profondo e zen$fRaffaele Santilli 210 $aRoma$cEdizioni Scientifiche Magi$dcopyr. 2001 215 $a115 p.$d21 cm 225 2 $aCollana nuovi autori 410 0$12001$aCollana nuovi autori 606 $aBuddismo zen 676 $a294.3927 700 1$aSANTILLI,$bRaffaele$0472747 801 0$aIT$bsalbc$gISBD 912 $a990000661970203316 951 $aII.3. 2458(VI PS B 1003)$b158753 L.M.$cVI PS B$d00076734 959 $aBK 969 $auma 979 $aCHIARA$b40$c20011002$lUSA01$h1526 979 $c20020403$lUSA01$h1715 979 $aPATRY$b90$c20040406$lUSA01$h1646 979 $aCOPAT5$b90$c20051110$lUSA01$h1144 996 $aVita è gratis$9959095 997 $aUNISA LEADER 02992nam 2200421z- 450 001 9910220043003321 005 20210211 035 $a(CKB)3800000000216347 035 $a(oapen)https://directory.doabooks.org/handle/20.500.12854/46856 035 $a(oapen)doab46856 035 $a(EXLCZ)993800000000216347 100 $a20202102d2016 |y 0 101 0 $aeng 135 $aurmn|---annan 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 00$aEssential Pathways and Circuits of Autism Pathogenesis 210 $cFrontiers Media SA$d2016 215 $a1 online resource (181 p.) 225 1 $aFrontiers Research Topics 311 08$a2-88919-905-3 330 $aThe Centers for Disease Control and Prevention estimate that 1 in 68 children in the United states is afflicted with autism spectrum disorders (ASD), yet at this time, there is no cure for the disease. Autism is characterized by delays in the development of many basic skills, most notably the ability to socialize and adapt to novelty. The condition is typically identified in children around 3 years of age, however the high heritability of autism suggests that the disease process begins at conception. The identification of over 500 ASD risk genes, has enabled the molecular genetic dissection of the pathogenesis of the disease in model organisms such as mice. Despite the genetic heterogeneity of ASD etiology, converging evidence suggests that these disparate genetic lesions may result in the disruption of a limited number of key biochemical pathways or circuits. Classification of patients into groups by pathogenic rather than etiological categories, will likely aid future therapeutic development and clinical trials. In this set of papers, we explore the existing evidence supporting this view. Specifically, we focus on biochemical cascades such as mTOR and ERK signaling, the mRNA network bound by FMRP and UBE3A, dorsal and ventral striatal circuits, cerebellar circuits, hypothalamic projections, as well as prefrontal and anterior cingulate cortical circuits. Special attention will be given to studies that demonstrate the necessity and/or sufficiency of genetic disruptions (e.g. by molecular deletion and/or replacement) in these pathways and circuits for producing characteristic behavioral features of autism. Necessarily these papers will be heavily weighted towards basic mechanisms elucidated in animal models, but may also include investigations in patients. 606 $aNeurosciences$2bicssc 610 $aCell signaling 610 $aCerebellum 610 $aHypothalamus 610 $amTOR 610 $aNeurodevelopmental disorders 610 $aOxytocin 610 $aStriatum 615 7$aNeurosciences 700 $aGul Dolen$4auth$01331049 702 $aMustafa Sahin$4auth 906 $aBOOK 912 $a9910220043003321 996 $aEssential Pathways and Circuits of Autism Pathogenesis$93040073 997 $aUNINA