Asperger syndrome causes: Difference between revisions

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{{Asperger syndrome}}
{{Asperger syndrome}}


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{{CMG}}
{{CMG}} {{AE}} {{SHA}}
 
==<s>Causes</s>==
*<s>The exact cause is unknown. More than likely, an abnormality in the brain is the cause of Asperger syndrome.</s>
 
*<s>There is a possible link to [[Autism (patient information)|autism]], and '''genetic factors''' may play a role. The disorder tends to run in families. A specific gene has not been identified.  Although no specific gene has yet been identified, multiple factors are believed to play a role in the [[Expressivity|expression]] of autism, given the [[phenotype|phenotypic]] variability seen in this group of children. Evidence for a genetic link is the tendency for AS to run in families and an observed higher [[Incidence (epidemiology)|incidence]] of family members who have behavioral symptoms similar to AS but in a more limited form (for example, slight difficulties with social interaction, language, or reading).  Most research suggests that all autism spectrum disorders have shared genetic mechanisms, but AS may have a stronger genetic component than autism. There is probably a common group of genes where particular [[allele]]s render an individual vulnerable to developing AS; if this is the case, the particular combination of alleles would determine the severity and symptoms for each individual with AS.</s>
 
*<s>A few ASD cases have been linked to exposure to [[teratogen]]s (agents that cause [[birth defect]]s) during the first eight weeks from [[Human fertilization|conception]]. Although this does not exclude the possibility that ASD can be initiated or affected later, it is strong evidence that it arises very early in development.<ref name="Arndt">{{cite journal |journal= Int J Dev Neurosci |date=2005 |volume=23 |issue=2–3 |pages=189–99 |title= The teratology of autism |author= Arndt TL, Stodgell CJ, Rodier PM |doi=10.1016/j.ijdevneu.2004.11.001 |pmid=15749245}}</ref> Many environmental factors have been hypothesized to act after birth, but none has been confirmed by scientific investigation.</s><ref>{{cite journal |author= [[Michael Rutter|Rutter M]] |title= Incidence of autism spectrum disorders: changes over time and their meaning |journal= Acta Paediatr |volume=94 |issue=1 |date=2005 |pages=2–15 |pmid=15858952 |doi= 10.1080/08035250410023124}}</ref>
 
<br />


== Overview ==
== Overview ==
The exact cause of Asperger (AS) is unknown. Many factors including genetics, family history of autism spectrum disorders (ASD) and enviornmental factors such as older parental age, prematurity, low birth weight and pregnancy complications have been associated with autism spectrum disorder (ASD).<ref name="pmid14966474" /><ref name="pmid15909404" /><ref name="pmid15909402" /><ref name="pmid9813781" /><ref name="pmid12634868" /><ref name="pmid16467216" /><ref name="pmid28102992" />
The exact cause of Asperger (AS) is unknown. Many factors including [[genetics]], [[family history]] of autism spectrum disorders (ASD) and enviornmental factors such as older parental age, [[Premature birth|prematurity]], low birth weight and pregnancy complications have been associated with autism spectrum disorder (ASD).<ref name="pmid14966474" /><ref name="pmid15909404" /><ref name="pmid15909402" /><ref name="pmid9813781" /><ref name="pmid12634868" /><ref name="pmid16467216" /><ref name="pmid28102992" />


== Causes ==
== Causes ==
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* Linkage at 3q21–24<ref name="pmid16467216">{{cite journal| author=Rehnström K, Ylisaukko-oja T, Nieminen-von Wendt T, Sarenius S, Källman T, Kempas E | display-authors=etal| title=Independent replication and initial fine mapping of 3p21-24 in Asperger syndrome. | journal=J Med Genet | year= 2006 | volume= 43 | issue= 2 | pages= e6 | pmid=16467216 | doi=10.1136/jmg.2005.033621 | pmc=2564646 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16467216  }} </ref>
* Linkage at 3q21–24<ref name="pmid16467216">{{cite journal| author=Rehnström K, Ylisaukko-oja T, Nieminen-von Wendt T, Sarenius S, Källman T, Kempas E | display-authors=etal| title=Independent replication and initial fine mapping of 3p21-24 in Asperger syndrome. | journal=J Med Genet | year= 2006 | volume= 43 | issue= 2 | pages= e6 | pmid=16467216 | doi=10.1136/jmg.2005.033621 | pmc=2564646 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16467216  }} </ref>
* 17p breakpoints in t(13;17) and t(17;19)<ref name="pmid12634868">{{cite journal| author=Tentler D, Johannesson T, Johansson M, Råstam M, Gillberg C, Orsmark C | display-authors=etal| title=A candidate region for Asperger syndrome defined by two 17p breakpoints. | journal=Eur J Hum Genet | year= 2003 | volume= 11 | issue= 2 | pages= 189-95 | pmid=12634868 | doi=10.1038/sj.ejhg.5200939 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12634868  }} </ref>
* 17p breakpoints in t(13;17) and t(17;19)<ref name="pmid12634868">{{cite journal| author=Tentler D, Johannesson T, Johansson M, Råstam M, Gillberg C, Orsmark C | display-authors=etal| title=A candidate region for Asperger syndrome defined by two 17p breakpoints. | journal=Eur J Hum Genet | year= 2003 | volume= 11 | issue= 2 | pages= 189-95 | pmid=12634868 | doi=10.1038/sj.ejhg.5200939 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12634868  }} </ref>
*3p22.1p21.31 microdeletion  
*3p22.1p21.31 microdeletion<ref name="pmid26523151">{{cite journal| author=Iourov IY, Vorsanova SG, Voinova VY, Yurov YB| title=3p22.1p21.31 microdeletion identifies CCK as Asperger syndrome candidate gene and shows the way for therapeutic strategies in chromosome imbalances. | journal=Mol Cytogenet | year= 2015 | volume= 8 | issue=  | pages= 82 | pmid=26523151 | doi=10.1186/s13039-015-0185-9 | pmc=4628252 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26523151  }} </ref>


=== Family History of Autism Spectrum Disorder (ASD) ===
=== Family History of Autism Spectrum Disorder (ASD) ===
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* Low birth weight
* Low birth weight
*Prematurity  
*Prematurity  
*Hyperbilirubinemia, neonatal jaundice  
*Hyperbilirubinemia, [[neonatal jaundice]]
*Maternal immigrant status    
*Maternal immigrant status    
*Pregnancy complications
*[[Complications of pregnancy|Pregnancy complications]] such as [[eclampsia]] and [[Pregnancy induced hypertension|pregnancy-induced hypertension]]
*Air pollutants (traffic-related)<br />
*Air pollutants (traffic-related)<br />



Latest revision as of 14:21, 22 June 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shakiba Hassanzadeh, MD[2]

Overview

The exact cause of Asperger (AS) is unknown. Many factors including genetics, family history of autism spectrum disorders (ASD) and enviornmental factors such as older parental age, prematurity, low birth weight and pregnancy complications have been associated with autism spectrum disorder (ASD).[1][2][3][4][5][6][7]

Causes

Genetic Causes

  • Linkage at 1q21-22[1]
  • Linkage at 13q31-33[1]
  • Linkage at 3p14–24[1]
  • Linkage at 3q21–24[6]
  • 17p breakpoints in t(13;17) and t(17;19)[5]
  • 3p22.1p21.31 microdeletion[8]

Family History of Autism Spectrum Disorder (ASD)

Several studies suggest that a familial history of autism spectrum disorder (ASD) is a risk factor for Asperger Syndrome (AS).[4][3][2]

Environmental Factors

Several environmental risk factors are associated with autism spectrum disorder (ASD) which include:[7]

References

  1. 1.0 1.1 1.2 1.3 Ylisaukko-oja T, Nieminen-von Wendt T, Kempas E, Sarenius S, Varilo T, von Wendt L; et al. (2004). "Genome-wide scan for loci of Asperger syndrome". Mol Psychiatry. 9 (2): 161–8. doi:10.1038/sj.mp.4001385. PMID 14966474.
  2. 2.0 2.1 Ghaziuddin M (2005). "A family history study of Asperger syndrome". J Autism Dev Disord. 35 (2): 177–82. doi:10.1007/s10803-004-1996-4. PMID 15909404.
  3. 3.0 3.1 Gillberg C, Cederlund M (2005). "Asperger syndrome: familial and pre- and perinatal factors". J Autism Dev Disord. 35 (2): 159–66. doi:10.1007/s10803-004-1993-7. PMID 15909402.
  4. 4.0 4.1 Volkmar FR, Klin A, Pauls D (1998). "Nosological and genetic aspects of Asperger syndrome". J Autism Dev Disord. 28 (5): 457–63. doi:10.1023/a:1026012707581. PMID 9813781.
  5. 5.0 5.1 Tentler D, Johannesson T, Johansson M, Råstam M, Gillberg C, Orsmark C; et al. (2003). "A candidate region for Asperger syndrome defined by two 17p breakpoints". Eur J Hum Genet. 11 (2): 189–95. doi:10.1038/sj.ejhg.5200939. PMID 12634868.
  6. 6.0 6.1 Rehnström K, Ylisaukko-oja T, Nieminen-von Wendt T, Sarenius S, Källman T, Kempas E; et al. (2006). "Independent replication and initial fine mapping of 3p21-24 in Asperger syndrome". J Med Genet. 43 (2): e6. doi:10.1136/jmg.2005.033621. PMC 2564646. PMID 16467216.
  7. 7.0 7.1 Ng M, de Montigny JG, Ofner M, Do MT (2017). "Environmental factors associated with autism spectrum disorder: a scoping review for the years 2003-2013". Health Promot Chronic Dis Prev Can. 37 (1): 1–23. doi:10.24095/hpcdp.37.1.01. PMC 5480297. PMID 28102992.
  8. Iourov IY, Vorsanova SG, Voinova VY, Yurov YB (2015). "3p22.1p21.31 microdeletion identifies CCK as Asperger syndrome candidate gene and shows the way for therapeutic strategies in chromosome imbalances". Mol Cytogenet. 8: 82. doi:10.1186/s13039-015-0185-9. PMC 4628252. PMID 26523151.


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