Essential Pathways and Circuits of Autism Pathogenesis
The 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 abilit...
Saved in:
Superior document: | Frontiers Research Topics |
---|---|
: | |
Year of Publication: | 2016 |
Language: | English |
Series: | Frontiers Research Topics
|
Physical Description: | 1 electronic resource (181 p.) |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
id |
993546353004498 |
---|---|
ctrlnum |
(CKB)3800000000216347 (oapen)https://directory.doabooks.org/handle/20.500.12854/46856 (EXLCZ)993800000000216347 |
collection |
bib_alma |
record_format |
marc |
spelling |
Gul Dolen auth Essential Pathways and Circuits of Autism Pathogenesis Frontiers Media SA 2016 1 electronic resource (181 p.) text txt rdacontent computer c rdamedia online resource cr rdacarrier Frontiers Research Topics The 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. English Cerebellum Striatum Oxytocin mTOR Hypothalamus Neurodevelopmental disorders Cell signaling 2-88919-905-3 Mustafa Sahin auth |
language |
English |
format |
eBook |
author |
Gul Dolen |
spellingShingle |
Gul Dolen Essential Pathways and Circuits of Autism Pathogenesis Frontiers Research Topics |
author_facet |
Gul Dolen Mustafa Sahin |
author_variant |
g d gd |
author2 |
Mustafa Sahin |
author2_variant |
m s ms |
author_sort |
Gul Dolen |
title |
Essential Pathways and Circuits of Autism Pathogenesis |
title_full |
Essential Pathways and Circuits of Autism Pathogenesis |
title_fullStr |
Essential Pathways and Circuits of Autism Pathogenesis |
title_full_unstemmed |
Essential Pathways and Circuits of Autism Pathogenesis |
title_auth |
Essential Pathways and Circuits of Autism Pathogenesis |
title_new |
Essential Pathways and Circuits of Autism Pathogenesis |
title_sort |
essential pathways and circuits of autism pathogenesis |
series |
Frontiers Research Topics |
series2 |
Frontiers Research Topics |
publisher |
Frontiers Media SA |
publishDate |
2016 |
physical |
1 electronic resource (181 p.) |
isbn |
2-88919-905-3 |
illustrated |
Not Illustrated |
work_keys_str_mv |
AT guldolen essentialpathwaysandcircuitsofautismpathogenesis AT mustafasahin essentialpathwaysandcircuitsofautismpathogenesis |
status_str |
n |
ids_txt_mv |
(CKB)3800000000216347 (oapen)https://directory.doabooks.org/handle/20.500.12854/46856 (EXLCZ)993800000000216347 |
carrierType_str_mv |
cr |
hierarchy_parent_title |
Frontiers Research Topics |
is_hierarchy_title |
Essential Pathways and Circuits of Autism Pathogenesis |
container_title |
Frontiers Research Topics |
author2_original_writing_str_mv |
noLinkedField |
_version_ |
1796651979283365889 |
fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>02808nam-a2200361z--4500</leader><controlfield tag="001">993546353004498</controlfield><controlfield tag="005">20231214133421.0</controlfield><controlfield tag="006">m o d </controlfield><controlfield tag="007">cr|mn|---annan</controlfield><controlfield tag="008">202102s2016 xx |||||o ||| 0|eng d</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(CKB)3800000000216347</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(oapen)https://directory.doabooks.org/handle/20.500.12854/46856</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(EXLCZ)993800000000216347</subfield></datafield><datafield tag="041" ind1="0" ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Gul Dolen</subfield><subfield code="4">auth</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Essential Pathways and Circuits of Autism Pathogenesis</subfield></datafield><datafield tag="260" ind1=" " ind2=" "><subfield code="b">Frontiers Media SA</subfield><subfield code="c">2016</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">1 electronic resource (181 p.)</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">computer</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">online resource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="490" ind1="1" ind2=" "><subfield code="a">Frontiers Research Topics</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">The 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.</subfield></datafield><datafield tag="546" ind1=" " ind2=" "><subfield code="a">English</subfield></datafield><datafield tag="653" ind1=" " ind2=" "><subfield code="a">Cerebellum</subfield></datafield><datafield tag="653" ind1=" " ind2=" "><subfield code="a">Striatum</subfield></datafield><datafield tag="653" ind1=" " ind2=" "><subfield code="a">Oxytocin</subfield></datafield><datafield tag="653" ind1=" " ind2=" "><subfield code="a">mTOR</subfield></datafield><datafield tag="653" ind1=" " ind2=" "><subfield code="a">Hypothalamus</subfield></datafield><datafield tag="653" ind1=" " ind2=" "><subfield code="a">Neurodevelopmental disorders</subfield></datafield><datafield tag="653" ind1=" " ind2=" "><subfield code="a">Cell signaling</subfield></datafield><datafield tag="776" ind1=" " ind2=" "><subfield code="z">2-88919-905-3</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Mustafa Sahin</subfield><subfield code="4">auth</subfield></datafield><datafield tag="906" ind1=" " ind2=" "><subfield code="a">BOOK</subfield></datafield><datafield tag="ADM" ind1=" " ind2=" "><subfield code="b">2023-12-15 05:53:32 Europe/Vienna</subfield><subfield code="f">system</subfield><subfield code="c">marc21</subfield><subfield code="a">2017-09-30 19:47:25 Europe/Vienna</subfield><subfield code="g">false</subfield></datafield><datafield tag="AVE" ind1=" " ind2=" "><subfield code="i">DOAB Directory of Open Access Books</subfield><subfield code="P">DOAB Directory of Open Access Books</subfield><subfield code="x">https://eu02.alma.exlibrisgroup.com/view/uresolver/43ACC_OEAW/openurl?u.ignore_date_coverage=true&portfolio_pid=5338218490004498&Force_direct=true</subfield><subfield code="Z">5338218490004498</subfield><subfield code="b">Available</subfield><subfield code="8">5338218490004498</subfield></datafield></record></collection> |