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Molecular biology of autism’s etiology – An alternative mechanism
Autism is a neuropathologic condition believed to be the consequence of cerebral dysconnectivity. Hypomyelination of axons in brain nerve pathways parallels behavioral abnormalities characteristic of autism. The present discussion will examine the functional association of insulin-like growth factor...
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Published in: | Medical hypotheses 2019-09, Vol.130, p.109272, Article 109272 |
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description | Autism is a neuropathologic condition believed to be the consequence of cerebral dysconnectivity. Hypomyelination of axons in brain nerve pathways parallels behavioral abnormalities characteristic of autism. The present discussion will examine the functional association of insulin-like growth factor-1 (IGF1) to neo-neuron myelination, especially in autistic children. These structural defects apparently correlate with a reduced level of circulating IGF. In addition, the potential connection of single nucleotide polymorphism to the etiology of autism is considered. Pharmaceutical and nutritional supplements that may enhance IGF1 to reduce the incidence of autism are proposed. |
doi_str_mv | 10.1016/j.mehy.2019.109272 |
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Hypomyelination of axons in brain nerve pathways parallels behavioral abnormalities characteristic of autism. The present discussion will examine the functional association of insulin-like growth factor-1 (IGF1) to neo-neuron myelination, especially in autistic children. These structural defects apparently correlate with a reduced level of circulating IGF. In addition, the potential connection of single nucleotide polymorphism to the etiology of autism is considered. Pharmaceutical and nutritional supplements that may enhance IGF1 to reduce the incidence of autism are proposed.</description><identifier>ISSN: 0306-9877</identifier><identifier>EISSN: 1532-2777</identifier><identifier>DOI: 10.1016/j.mehy.2019.109272</identifier><identifier>PMID: 31383342</identifier><language>eng</language><publisher>United States: Elsevier Ltd</publisher><subject>Autism ; Autistic Disorder - blood ; Autistic Disorder - etiology ; Autistic Disorder - genetics ; Axon ; Axons - metabolism ; Biomarkers ; Biomarkers - metabolism ; Brain - physiopathology ; Child, Preschool ; Etiology ; Female ; Humans ; IGF1 ; Infant ; Insulin-Like Growth Factor I - genetics ; Magnetic Resonance Imaging ; Male ; Models, Neurological ; Myelin ; Myelin Sheath - metabolism ; Polymorphism, Single Nucleotide</subject><ispartof>Medical hypotheses, 2019-09, Vol.130, p.109272, Article 109272</ispartof><rights>2019 Elsevier Ltd</rights><rights>Copyright © 2019 Elsevier Ltd. 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Hypomyelination of axons in brain nerve pathways parallels behavioral abnormalities characteristic of autism. The present discussion will examine the functional association of insulin-like growth factor-1 (IGF1) to neo-neuron myelination, especially in autistic children. These structural defects apparently correlate with a reduced level of circulating IGF. In addition, the potential connection of single nucleotide polymorphism to the etiology of autism is considered. Pharmaceutical and nutritional supplements that may enhance IGF1 to reduce the incidence of autism are proposed.</description><subject>Autism</subject><subject>Autistic Disorder - blood</subject><subject>Autistic Disorder - etiology</subject><subject>Autistic Disorder - genetics</subject><subject>Axon</subject><subject>Axons - metabolism</subject><subject>Biomarkers</subject><subject>Biomarkers - metabolism</subject><subject>Brain - physiopathology</subject><subject>Child, Preschool</subject><subject>Etiology</subject><subject>Female</subject><subject>Humans</subject><subject>IGF1</subject><subject>Infant</subject><subject>Insulin-Like Growth Factor I - genetics</subject><subject>Magnetic Resonance Imaging</subject><subject>Male</subject><subject>Models, Neurological</subject><subject>Myelin</subject><subject>Myelin Sheath - metabolism</subject><subject>Polymorphism, Single Nucleotide</subject><issn>0306-9877</issn><issn>1532-2777</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNp9kM1Kw0AcxBdRbK2-gAfJC6T-9yPZLHgppX5AxYuel83mH7slacpuWuit7-DJ1-uTmJLq0dPAMDMMP0JuKYwp0PR-Oa5xsRszoKozFJPsjAxpwlnMpJTnZAgc0lhlUg7IVQhLAFCCZ5dkwCnPOBdsSGavTYV2Uxkf5a6pms9d1JSR2bQu1If9d4iwPdmH_Vc0WUWmatGvTOu2GNVoF2bVJa_JRWmqgDcnHZGPx9n79Dmevz29TCfz2HLG2zjlBiliohjkSnRHSwBBM5NIFFJaiSCSXBQizXKRAKVS2bLgCUsEGFmqnI8I63etb0LwWOq1d7XxO01BH5nopT4y0UcmumfSle760nqT11j8VX4hdIGHPoDd9a1Dr4N1uLJYOI-21UXj_tv_AeBcc7Q</recordid><startdate>201909</startdate><enddate>201909</enddate><creator>Steinman, Gary</creator><creator>Mankuta, David</creator><general>Elsevier Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>201909</creationdate><title>Molecular biology of autism’s etiology – An alternative mechanism</title><author>Steinman, Gary ; Mankuta, David</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c323t-63ae1ee5920b94532f00418a57e477c7e045b4d468b4501179cfd352540a7f9b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Autism</topic><topic>Autistic Disorder - blood</topic><topic>Autistic Disorder - etiology</topic><topic>Autistic Disorder - genetics</topic><topic>Axon</topic><topic>Axons - metabolism</topic><topic>Biomarkers</topic><topic>Biomarkers - metabolism</topic><topic>Brain - physiopathology</topic><topic>Child, Preschool</topic><topic>Etiology</topic><topic>Female</topic><topic>Humans</topic><topic>IGF1</topic><topic>Infant</topic><topic>Insulin-Like Growth Factor I - genetics</topic><topic>Magnetic Resonance Imaging</topic><topic>Male</topic><topic>Models, Neurological</topic><topic>Myelin</topic><topic>Myelin Sheath - metabolism</topic><topic>Polymorphism, Single Nucleotide</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Steinman, Gary</creatorcontrib><creatorcontrib>Mankuta, David</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Medical hypotheses</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Steinman, Gary</au><au>Mankuta, David</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Molecular biology of autism’s etiology – An alternative mechanism</atitle><jtitle>Medical hypotheses</jtitle><addtitle>Med Hypotheses</addtitle><date>2019-09</date><risdate>2019</risdate><volume>130</volume><spage>109272</spage><pages>109272-</pages><artnum>109272</artnum><issn>0306-9877</issn><eissn>1532-2777</eissn><abstract>Autism is a neuropathologic condition believed to be the consequence of cerebral dysconnectivity. Hypomyelination of axons in brain nerve pathways parallels behavioral abnormalities characteristic of autism. The present discussion will examine the functional association of insulin-like growth factor-1 (IGF1) to neo-neuron myelination, especially in autistic children. These structural defects apparently correlate with a reduced level of circulating IGF. In addition, the potential connection of single nucleotide polymorphism to the etiology of autism is considered. Pharmaceutical and nutritional supplements that may enhance IGF1 to reduce the incidence of autism are proposed.</abstract><cop>United States</cop><pub>Elsevier Ltd</pub><pmid>31383342</pmid><doi>10.1016/j.mehy.2019.109272</doi></addata></record> |
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subjects | Autism Autistic Disorder - blood Autistic Disorder - etiology Autistic Disorder - genetics Axon Axons - metabolism Biomarkers Biomarkers - metabolism Brain - physiopathology Child, Preschool Etiology Female Humans IGF1 Infant Insulin-Like Growth Factor I - genetics Magnetic Resonance Imaging Male Models, Neurological Myelin Myelin Sheath - metabolism Polymorphism, Single Nucleotide |
title | Molecular biology of autism’s etiology – An alternative mechanism |
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