Research on Genetics as the Cause of Autism
* NB. THIS WORK HAS BEEN SUBMITTED THROUGH AN ELECTRONIC PLAGERISM TOOL, THEREFORE, PLEASE REFERENCE MY WORK IF YOU CITE IT IN YOUR OWN.
THIS WORK IS A PART OF MY RESEARCH MA AUTISM DEGREE FOR THE AETIOLOGY OF AUTISM SUBMITTED IN 2010. RESEARCH SINCE PUBLISHED MAY CHANGE CURRENT UNDERSTANDING OF THE GENETIC INFLUENCE ON THE CAUSE OF AUTISM.
Although, the cause of autism is unknown, it is well recognised that it is the endpoint of several organic aetiologies, and is a biologically based, neurodevelopment disorder with a strong genetic component. The genes SEMA5A and TAS2R1 have recently been found to have a significant association with autism (Weiss and Arking, 2009). Despite this, there remain no biological tests for its diagnoses and its identification relies on criterion based upon descriptions of social and other behaviours (Lord and Corsello, 2005; Baron-Cohen, 2008; Le Couteur, 2003; National Autistic Society (NAS), 2010; Evans et al., 2008).
Genetic research has increased immensely in the first decade of the 21st century and studies conducted on monozygotic (MZ) (identical) twins have confirmed the genetic influence in the genesis of autism (Feinstein, 2010; Baron-Cohen, 2008; NAS, 2010). In the first systematic study of twins, Folstein and Rutter (1977), four of eleven MZ twins were found to be concordant for a diagnosis of autism and none were concordant in the dizygotic (DZ) (non-identical) twins (Feinstein, 2010; Folstein and Rutter, 1977; Roth, 2010). However, in the study's abstract, the diagnostic tools used for their sample is not stated, making it difficult to assess the researcher's definition for autism. Although 36 percent of the MZ twins were genetically concordant for autism, this still leaves seven (64 percent), sharing identical genes non-concordant. Any milder autistic traits for the non-concordant MZ twins appear not to have been recognised (Folstein and Rutter, 1977). From a later review by DeMyer et al. (1981), which recognises the diagnostic inconsistencies in that era, the importance of categorising for diagnosis and cites the Folstein and Rutter study; it could be assumed that they either used Diagnostic Statistical Manual (DSM) II (American Pyschiatric Association (APA), 1968) or the [World Health Organisation (WHO) system] (Rutter et al., 1975). Using the latter, which seems likely as it is a British study, may suggest a bias in diagnosis as Rutter is the main author of it. However, in 1995 Bailey et al. contacted all the participants in the Folstein and Rutter study, included them with a new sample; reassessed them for diagnosis and confirmed the 1977 findings for both MZ and DZ twins (Roth, 2010; Feinstein, 2010 Bailey et al., 1995). The Bailey et al. (1995) abstract does not indicate which diagnostic criteria were used but Roth (2010) states they used the ICD-10 (WHO, 1992). Bailey et al. found a 60 percent concordance for autism within their 25 pair MZ twin sample. Additionally, the concordance rate for both MZ and DZ twin samples rose, when the researchers used a broader spectrum of autistic symptoms, to 92 percent for the MZ twins and from zero to 10 percent for the DZ twins. Additionally, when using the ICD-10 criteria for Pervasive Developmental Disorder (PDD) unspecified, the equivalent to PDD-NOS (Not Otherwise Specified) in DSM-IV-TR, three of the previously undiagnosed MZ twins were subsequently diagnosed (cited in Roth, 2010). Interestingly, Bishop et al. (1995) found very similar results for MZ twins with specific language impairment. This shows how research results can change when diagnostic criteria are broadened.
The following will now investigate some of the research cited in five reviews; pertaining to more recent twin studies; conditions which present as ASD but can be genetically diagnosed; some of the current observations and perspectives offered for autism genealogy and the recent genome wide studies, as these are some of the most significant and current genetic perspectives on autism aetiology (Rutter, 2005; Muhle et al., 2004; Freitag, 2007; Hughes, 2008; Abrahams and Geschwind, 2008). No studies have researched adopted autistic twins, either adopted together or by separate families, to assess environmental influences on autism’s genealogy. Likewise, there are no twin studies on Asperger syndrome (AS) or PDD-NOS (Freitag, 2007). However, Freitag refers to Le Couteur et al. (1996) who re-analysed the twin study by Bailey et al. (1995) and found a higher rate of the Broader Autism Phenotype (BAP) in non-concordant MZ twins for communication impairment and social dysfunction. Interestingly, restricted repetitive behaviours were never observed in isolation and were only found in 33 percent of the BAP, for which Freitag suggests, other genetic risk factors may be the cause. Freitag concludes a heritability percentage of more than 90 percent for the narrow autism phenotype, a common genetic liability for social communication and interaction for ASD and the BAP; and a separate genetic aetiology for restricted and repetitive behaviours. Although there appears a bias towards males having ASD, findings for an abnormality on the X chromosome are elusive (Muhle et al., 2004; Freitag, 2007; Abrahams and Geschwind, 2008). In March 2010, Wing suggested there are many undiagnosed females with ASD, due to their differential presentation. Anorexia Nervosa was also implicated as being on the autistic spectrum with respect to similar cognitive, perceptual and repetitive restricted behaviours (Wing et al, 2010; Harder, 2010; Hughes, 2007).
Other undiagnosed co-morbid conditions can confuse an already complex, diagnostic process for ASD and adversely affect research results (Gillberg, 1992). Mental Retardation (MR) is also diagnosed on behavioural criteria (WHO, 1992; APA, 2000). Others which present autistic behaviours but can be genetically identified are Fragile X syndrome (FRAXA), Prader Willi (PWS), Smith-Lemli-Opitz (SLO), Timothy (TS), Potocki-Lupski (PLS) syndromes and Tuberous Sclerosis (TSC). As it is not routine to take blood tests when assessing for ASD, these conditions may remain undiagnosed and be included in ASD research cohorts (Freitag, 2007; Hughes, 2008; Abrahams and Geschwind, 2008). Freitag recommends that all cases of ASD with mental retardation with or without [dismorphic] features be assessed for FRAXA and that TSC, even with no seizures present, be assessed with the Wood’s light, as genetic counselling is relevant for both disorders. He also recommends assessment for SLO because it can be treated with dietary cholesterol supplementation. Only Abrahams and Geschwind (2008) review TS and PLS which have very high percentages of a secondary diagnosis of autism; TS (60-80 percent) and PLS (90 percent) associated with gene CACNA1C and chromosome position 17q11 respectively. The percentage of individuals with primary ASD who have either of these two syndromes as secondary, is unknown (Ibid).
FRAXA has a mutation on the X chromosome (Hjalgrim et al., 1998; Feinstein, 2010). Rett Syndrome (Retts) has more than 200 mutations in the MECP2 gene; which provides instructions for making the MeCP2 protein, essential for normal brain development, synaptic formation and gene function and found on chromosome Xq28 (Guy et al., 2007; Genetics Home Reference (GHR), 2010; Feinstein, 2010; Muhle et al., 2004; Freitag, 2007; Hughes, 2008; Abrahams and Geschwind, 2008). Guy et al. (2007) managed to reverse the symptoms of Retts in a mouse model by activating the MECP2 gene. From the abstract it is not clear if the physiology of the brain also changed but it appears this may have been hypothesised and investigated because the authors state that in Retts, the neurons do not die and they assume that it is not a degenerative disorder; implying their intention to try and repair the neurons and restore functioning in the brain. Freitag (2007) also reviews a 2007 study but does not cite the authors or title, where a key brain chemical was blocked in mice, reversing some of the symptoms in FRAXA. Retts was previously considered an untreatable neurological disorder, therefore these two studies offer hope for possible future genetic treatments for autism (Ibid; Feinstein, 2010). In FRAXA and Retts, autism is a secondary diagnosis because the two syndromes can be identified genetically and the autistic behaviours are a result of the syndromes (Roth, 2010; Feinstein, 2010; Baron-Cohen, 2008).
In Rutter’s (2005) review he concludes genetics play an important role in autism aetiology but cautions credibility and acceptance of results from samples of MZ (identical) twins. His caution is based on Hall's (2003) study which explains, in depth, the congenital anomalies found, even in, MZ twins whose zygosity is not always as initially believed. It is rare but possible to have different sex MZ twins. 70-75 percent of MZ twins share one placenta but have separate membranes, 25-30 percent have separate placentas and membranes, whilst one-two percent share one placenta and one membrane (Hall, 2003). Hall’s paper is very relevant to genetic research as MZ and DZ twins are considered good comparisons to estimate heritability and environmental influences of diseases. However, twins may not be any better samples than individuals; as pregnancies and births of twins are more complicated and complex than single ones (Ibid). Horwitz et al. (2003) conclude past twin studies may have overstated genetic influences on behaviours because their study suggested environmental influences have strong effects on some behaviours of MZ twins. Additionally, Kates et al. (2004) found neuroanatomical evidence to support genetic’s role, as well as its limits in autism aetiology. Hall (2003) covers the complexities of Chimerism, Cloning, MZ and DZ twins, Mosaicism and Zona Tampering. Rodier and Hyman (1998, p124) state: ‘From the origins of teratology in the 1950s, it has been obvious that environmental factors interact with the genetic background of the embryo to produce birth defects.’
The other four reviews do not consider Hall’s paper. Muhle et al. (2004) review twin studies, one of which appears contradictory (Raynes et al., 1999). The abstract was retrieved for clarification and appears to have been misinterpreted. Muhle et al. explain that autism was a secondary diagnosis and the primary diagnosis was Joubert syndrome in MZ twin girls; showing a high correlation in the 'brain malformations' and most other 'classic manifestations' for the syndrome but extremely non-concordant for autism. The twin with autism is cited to have 'more extensive [cerebellar] anomaly,' appearing to contradict the former statement. Raynes et al. (1999) state the twins have 'highly discordant phenotypes and birth weight; greatly differing anatomic, neurologic and developmental status; one can walk, run and is verbal whilst the other is wheelchair bound, non-verbal, severely retarded and autistic. They were concordant for some of the characteristics of Joubert syndrome but other Joubert characteristics are clearly not concordant (Joubert Syndrome Foundation and Related Disorders Foundation, 2010; Great Ormond Street Hospital, 2008). Hughes (2008) and Abrahams and Geschwind (2008) make little reference to twin studies. Freitag reviews 16 papers on twins and suggests only a weak environmental influence on autism aetiology.
Chromosome 15q11-13 (15q11-13) is the most prevalent cytogenetic abnormality for ASD (Shao et al., 2003; Medical Research Council (MRC), 2001). It is found in between one and four percent of the autistic population (Muhle et al., 2004; Freitag, 2007; Abrahams and Geschwind, 2008). This seems to leave a significant percentage that does not have this abnormality. It consists mostly of inverted duplications of the maternal region; whereas there are maternal and paternal deletions of 15q11-13 found in PWS and Angelman syndrome. Freitag describes four major genetic mechanisms within 15q11-13 in Angelman syndrome and three in PWS, for their differentiation to ASD. Interestingly, the two syndromes appear to have opposing parental deletions and copies of 15q11-13. In PWS there is more autistic-type impairment for social interaction when there is a [uniparental disomy] compared to a paternal deletion of the chromosome. Freitag postulates this strengthens the possibility of a maternally instigated variation of 15q11-13 for the development of ASD. Abraham and Geschwind (2008) review copy number variants (CNVs); which are recently identified variants of genes found in genome wide linkage studies, where 'a large number of potentially important novel candidate loci' have been identified. They include deletions and duplications of genes disrupting functions in encoding, proliferation and signalling of neurons, proteins and cells; all of which could be implicated in autism and intellectual disability with and without autism (Autism Speaks, 2010; Szatmari et al., 2007; Pinto et al., 2010; Abrahams and Geschwind, 2008). Szatmari (2007) conducted the largest linkage study for ASD to date, revealing new genetic findings, which now need further follow up (Szatmari, 2007; Abrahams and Geschwind, 2008). Huge progress has been made in genetic understanding; despite no one specific gene being found for autism’s aetiology. It is likely a polygenic disorder with some environmental influence. Many genes and chromosomes have been associated with the triad of impairment and can be linked to some of the psychological and [neuro-anatomical] theoretical perspectives on autism aetiology (Genetic Home Reference (GHR), 2010; Genecards, 2010; Rutter, 2004; Freitag, 2007; Abrahams and Geschwind, 2008; Hughes 2008).
The impact genetic research has had on our understanding of autism aetiology is that it is now recognised, in many worldwide countries, but not all, that some children are born with a genetic susceptibility to environmental triggers; which may or may not cause them to develop autistic behaviours, in varying degrees of severity, in all or some of the autism triad (Feinstein, 2010; Freitag, 2007; NAS, 2010; GHR, 2010; Genecards, 2010; Ronald et al., 2005). Whether this progress will have a positive impact on our future choices may be ethically controversial (Progress Educational Trust (PET), 2006; McMahon et al., 2006; Aspis cited in Feinstein, 2010). Prospective parents may be offered genetic counselling allowing them to make, what some may consider, 'eugenic' decisions and a regression to Kanner's and Asperger's era. Asperger protected his group of children from the Nazi's to prevent their genocide (Laurance, 2009; Feinstein, 2010). Others may consider it would be giving parents the same informed choices as those who have amniocentesis tests to detect Down syndrome (Baron-Cohen cited in Laurance, 2009; Leshin, 2010; Souza, 2003). However, if and when specific genes are found for autism, gene therapy may become an option (PET, 2006). Some individuals with High Functioning Autism and Asperger syndrome are horrified by the idea of being considered 'broken' and in need of a 'cure' or the parental choice of abortion to eradicate individuals on the spectrum, like a disease. They consider their autism as part of their identity, difference not a disability (Souza, 2003; Jordan and Grandin cited in Feinstein, 2010; Templeton, 2010). Baron-Cohen cited in Laurance (2009) explains that some people, who undoubtedly had autism, are known to have been geniuses, such as Einstein and Newton and questions where we would be today if they had been terminated instead of born. Parents of children with autism may have different perspectives, were it possible to predict the probability of conceiving another child with the disorder or for gene therapy to reverse some or all of the impairments their children struggle with, as Guy et al. (2007) did with Retts (Black, 2010; Hebert and Koulouglioti, 2010).
‘The goal of the CHildhood Autism Risks from Genetics and Environment (CHARGE) study is to understand causes of autism and developmental disorder, both genetic and environmental, in order to reduce their incidence in the future’ (Hertz-Picciotto et al., 2006, p1124).
In summary, although autism aetiology is considered to have a strong genetic component, specific genes or a group of genes have yet to be identified in a high percentage of people with autism. Nevertheless, some identified genes and chromosomes do relate to some of the biological and psychological aetiological perspectives and hypotheses of autism and its triad of impairments. As no specific link with the X chromosome has been found to correlate the male to female percentage and a maternal genealogical basis is suggested, further research may consider investigating autism in females, especially with regard to steroid hormones. It may be useful for routine diagnostic blood tests to be taken to eliminate co-morbid conditions from inclusion in autism research and identify genetically diagnosable conditions to allow for genetic counselling and/or appropriate treatments. As there is evidence explaining MZ twins are no better research subjects than individuals, researching twin genealogy for the BAP, AS or separately adopted twins seems irrelevant.
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