Jump to content

Imprinted brain hypothesis: Difference between revisions

From Wikipedia, the free encyclopedia
Browse history interactively
← Previous editNext edit →
Content deleted Content added
VisualWikitext
Line 42: Line 42:


While Crespi and Badcock have claimed neuroimaging studies lend support to the imprinted brain hypothesis, other neuroimaging studies have found contradictory results. Several neurological findings are common to both autism and schizophrenia.<ref>{{cite journal|title=Autistic Disorders and Schizophrenia: Related or Remote? An Anatomical Likelihood Estimation|journal=PLOS One|volume=5|issue=8|vauthors=Cheung C, Yu K, Fung G, Leung M, Wong C, Li Q, Sham P, Chua S, McAlonan G|date=August 2010|url=https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0012233|doi=10.1371/journal.pone.0012233}}</ref> The brain regions that distinguish schizophrenia from autism are also those at the centre of the controversy regarding neuroleptic medication,<ref name="szneuro1" /><ref name="szneuro2" /> reducing the degree to which they can be used to distinguish the disorders; autistic subjects taking psychotropic medication share some of the altered neuroconnectivity that Crespi and Badcock ascribe to schizophrenia.<ref>{{cite journal|title=Psychotropic medication use in autism spectrum disorders may affect functional brain connectivity|journal=Biological Psychiatry: Cognitive Neuroscience and Neuroimaging|volume=2|issue=6|page=518-527|vauthors=Linke AC, Olson L, Gao Y, Fishman I, Müller RA|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5667652/|doi=10.1016/j.bpsc.2017.06.008}}</ref>
While Crespi and Badcock have claimed neuroimaging studies lend support to the imprinted brain hypothesis, other neuroimaging studies have found contradictory results. Several neurological findings are common to both autism and schizophrenia.<ref>{{cite journal|title=Autistic Disorders and Schizophrenia: Related or Remote? An Anatomical Likelihood Estimation|journal=PLOS One|volume=5|issue=8|vauthors=Cheung C, Yu K, Fung G, Leung M, Wong C, Li Q, Sham P, Chua S, McAlonan G|date=August 2010|url=https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0012233|doi=10.1371/journal.pone.0012233}}</ref> The brain regions that distinguish schizophrenia from autism are also those at the centre of the controversy regarding neuroleptic medication,<ref name="szneuro1" /><ref name="szneuro2" /> reducing the degree to which they can be used to distinguish the disorders; autistic subjects taking psychotropic medication share some of the altered neuroconnectivity that Crespi and Badcock ascribe to schizophrenia.<ref>{{cite journal|title=Psychotropic medication use in autism spectrum disorders may affect functional brain connectivity|journal=Biological Psychiatry: Cognitive Neuroscience and Neuroimaging|volume=2|issue=6|page=518-527|vauthors=Linke AC, Olson L, Gao Y, Fishman I, Müller RA|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5667652/|doi=10.1016/j.bpsc.2017.06.008}}</ref>

The imprinting brain hypothesis has also been criticized for inaccurately presenting the schizophrenia spectrum and making claims about schizophrenic disorders that are at odds with their clinical profiles. The claim that milder schizophrenia-spectrum disorders are associated with intensified empathy and strong theory of mind is discredited by research showing the opposite.<ref name="szempath1" /><ref name="szempath2" /><ref name="sztom" /> The specific pattern of empathy deficits also appears to be consistent between autism and schizophrenia, with both demonstrating impaired [[cognitive empathy]] and relatively preserved [[affective empathy]].<ref>{{cite journal|title=Who Cares? Revisiting Empathy in Asperger Syndrome|journal=Journal of Autism and Developmental Disorders|volume=37|issue=4|page=709-715|date=August 2006|vauthors=Rogers K, Dziobek I, Hassenstab J, Wolf OT, Convit A|url=https://link.springer.com/article/10.1007%2Fs10803-006-0197-8|doi=10.1007/s10803-006-0197-8}}</ref><ref>{{cite journal|title=Self-reported empathic abilities in schizophrenia|journal=Schizophrenia Research|volume=92|issue=1-3|page=85-89|date=May 2007|vauthors=Montag C, Heinz A, Kunz D, Gallinat J|url=https://pubmed.ncbi.nlm.nih.gov/17350225/|doi=10.1016/j.schres.2007.01.024}}</ref> Crespi and Badcock's attempt to conceptualize schizophrenia as a relatively homogenous disorder that slots neatly into one end of a spectrum has been criticized due to the clinical heterogenity in even individual cases of schizophrenia, due to the different presentation and course of positive and negative symptoms.<ref>{{cite journal|title=A complete theory of psychosis and autism as diametric disorders of social brain must consider full range of clinical syndromes|vauthors=Thakkar KN, Mathews N, Park S|journal=Behavioral and Brain Sciences|volume=31|issue=3|pages=277-278|doi=10.1017/S0140525X0800438X|date=2008}}</ref>


== Reception ==
== Reception ==

Revision as of 12:20, 22 January 2021

The imprinted brain hypothesis is an evolutionary psychology hypothesis regarding the causes of autism spectrum disorders and schizophrenia spectrum disorders. It claims that certain autistic and schizotypal traits are opposites, and that this implies the etiologies of the two conditions must be at odds. Bernard Crespi, one of the primary proponents of the hypothesis, claims that the conditions are linked to epigenetic imprinting of the X chromosome, specifically that autistic disorders involve paternal imprinting while schizotypal disorders involve maternal imprinting. While the hypothesis has found some attention in popular science, it lacks scientific backing.[1]

The conflict theory of imprinting

See also: Sexual conflict

Genomic imprinting is an epigenetic process by which certain genes are expressed in a parent-of-origin-specific manner. The imprinted brain theory is a variant of the conflict theory of imprinting which argues that in diploid organisms, such as humans, the maternal and paternal set of genes may have antagonistic reproductive interests since the mother and father may have antagonistic interests regarding the development of the child. The conflict theory of imprinting is, according to Bernard Crespi in a 2008 paper, the only comprehensive theory explaining observed patterns of imprinting in humans and other organisms.[2][3][4][5][unreliable medical source?]

The hypothesis

The imprinted brain hypothesis argues that since it is uncertain if a woman's other and future children have and will have the same father, as well as the father generally having lower parental investment, it may be in the father's reproductive interest for his child to maximize usage of the mother's resources while it may be in the mother's interest to limit this in order to have resources for her other and future children.[6][7][unreliable medical source?] Thus, a genomic imprinting with slight maternal bias would supposedly be associated with factors such as decreased growth, more tractable behavior, and an empathizing and less self-centered personality causing less demands on the mother. The opposite would occur for a slight paternal bias.[6][7]

However, an extreme genomic imprinting in favor of maternal genes is argued to cause psychosis such as in schizophrenia spectrum disorders while an extreme genomic imprinting in favor of paternal genes is argued to cause autism spectrum disorders. This claims the symptoms of schizophrenia are claimed by overempathizing, resulting in delusions and paranoia, while people with autism seem to be blind to the intentions of others. Certain neuroimaging findings lend support to the hypothesis,[8][non-primary source needed] although neuroimaging in schizophrenia is controversial due to the neurological impact of neuroleptic medication.[9][10]

Traits such as ambivalence seen in negative symptoms versus the single-minded focus of autistic special interests are also posited to be distinctions,[6] although the pronounced similarity and overlap between negative symptomatology seen in the two disorders weakens this claim substantially.[11][12]

Adherents of the hypothesis say it remains compatible with genetic and environmental factors that increase the risk for both schizophrenia and autism, as these are considered to be affected by genomic imprinting differently.[2]

Arguments of proponents

The imprinted brain hypothesis has some similarities with the extreme male brain theory of autism, but they come apart significantly. Proponents of the imprinted brain hypothesis state that the hypothesized imprinting mechanism may have detrimental interactions when extreme genomic imprinting occurs in the opposite sex, which they claim provides an explanation for something that would be a 'problem' for the extreme male brain claims -- specifically, that female autism tends to be particularly severe.[6] This is also used as an explanation for the relative severity of schizophrenia in males.[6]

Factors such as nutrition during pregnancy are believed to affect imprinting. Proponents note that schizophrenia is associated with maternal starvation during pregnancy while autism has increased in diagnostic prevalence in affluent societies,[13] though most scientists believe the rising rates of autism diagnosis in wealthy societies are related to awareness rather than prevalence.[14]

Autism and schizophrenia risks in relation to birth weight within the same population appear to support the hypothesis.[15][non-primary source needed]

In both autism and schizophrenia, the theory of mind is impaired, which the imprinted brain hypothesis posits occurs via different mechanisms and is not generalizable to the broader underlying neurotypes. Proponents of the hypothesis claim people with schizotypal personality have an enhanced theory of mind and increased emphatic ability,[16] but this is not supported by research on the schizotypal personality disorder population[17] or on measures of schizotypy in the general population.[18] Rather, theory of mind appears to be impaired in all schizophrenia-spectrum conditions even in the absence of frank psychosis.[19]

Proponents of the hypothesis also point towards genetic disorders with an elevated risk of one disorder and not the other, especially imprinting disorders, to support their claims. For instance, Beckwith-Wiedemann syndrome is caused by increased effects of paternally imprinted genes and has an increased incidence of autism.[2][20][15]

Data from copy number variation and genome-wide association studies support shared genetic mechanisms causing schizophrenia and autism, although this only lends circumstantial support to the imprinted brain hypothesis and can also be used to support many competing hypotheses.[21][22]

Issues for the hypothesis

The broad claim that autism and schizophrenia are in opposition on the biological level is not supported by research. In samples of autistic adults, schizophrenia and other non-affective psychotic disorders occur at far higher rates than the general population, occuring in about 8-10% of the broad ASD population[23][24] and as high as one-third in PDD-NOS.[25] The same association occurs in childhood onset schizophrenia, which is considered a more homogenous form of the disorder that hews closest to the hypothetical neurodevelopmental disorder underlying schizophrenia-spectrum conditions; approximately one-quarter of children with schizophrenia fit the criteria for an autism spectrum disorder prior to the onset of psychosis, and the majority have clinical or subclinical disturbances of social, motor, or language skills similar to those seen in autistic children.[26]

In addition, Crespi and Christopher Badcock misrepresent findings to support their hypothesis, particularly those related to genetic syndromes that increase the risk of schizophrenia or autism. For instance, Crespi claims that the relationship between those disorders and sex chromosome aneuploidy supports his hypothesis, with trisomy X and Klinefelter syndrome (extra X chromosomes) increasing schizophrenia risk and Turner syndrome (one X chromosome) increasing autism risk.[2] However, polysomy X conditions are associated with increased autism as well as schizophrenia risk,[27][28] and Turner syndrome is approximately three times as common in schizophrenic women as the general female population.[29] Genetic syndromes in general lend credence to the suggestion that autism and schizophrenia are related rather than contraindicated, with conditions that sharply increase one risk tending to also increase the other. For instance, velocardiofacial syndrome, which is associated with a 20- to 30-fold increase in schizophrenia risk,[30] also significantly increases the risk of autism.[31] Other chromosomal disorders notable for significantly increasing the risk of both autism and schizophrenia include 17q12 microdeletions[32] and 15q11.2 microdeletions.[33]

Moreover, the specific predictions the imprinted brain hypothesis makes about imprinting disorders are for the most part falsified. The imprinted brain hypothesis predicts that Prader-Willi syndrome, a disorder of maternal overimprinting, should have decreased autism and increased psychosis, while Angelman syndrome, a disorder of paternal overimprinting, should have the opposite. However, autism rates are substantially above those of the general population in PWS and similar to or below it in AS,[34] while non-affective psychosis appears to occur at rates comparable to the general population in PWS.[35] Indeed, it has been suggested that maternally imprinted cases of Prader-Willi syndrome have an elevated autism prevalence compared to all etiologies of the disorder, the exact opposite of the imprinted brain hypothesis.[34][36] Despite being contradicted by other research, Crespi nonetheless claims that imprinting disorders as a rule fit his hypothesis.[2]

While Crespi and Badcock have claimed neuroimaging studies lend support to the imprinted brain hypothesis, other neuroimaging studies have found contradictory results. Several neurological findings are common to both autism and schizophrenia.[37] The brain regions that distinguish schizophrenia from autism are also those at the centre of the controversy regarding neuroleptic medication,[9][10] reducing the degree to which they can be used to distinguish the disorders; autistic subjects taking psychotropic medication share some of the altered neuroconnectivity that Crespi and Badcock ascribe to schizophrenia.[38]

The imprinting brain hypothesis has also been criticized for inaccurately presenting the schizophrenia spectrum and making claims about schizophrenic disorders that are at odds with their clinical profiles. The claim that milder schizophrenia-spectrum disorders are associated with intensified empathy and strong theory of mind is discredited by research showing the opposite.[17][18][19] The specific pattern of empathy deficits also appears to be consistent between autism and schizophrenia, with both demonstrating impaired cognitive empathy and relatively preserved affective empathy.[39][40] Crespi and Badcock's attempt to conceptualize schizophrenia as a relatively homogenous disorder that slots neatly into one end of a spectrum has been criticized due to the clinical heterogenity in even individual cases of schizophrenia, due to the different presentation and course of positive and negative symptoms.[41]

Reception

In a book review in The British Journal of Psychiatry of a 2009 book about the theory, Carl Fredrik Johansson wrote:[42]

"In terms of the plausibility of the theory, it is appealing in its symmetry, offering some compelling examples of how the disorders complement each other in their symptomatology. Testable hypotheses are offered but most remain untested. More significantly, far too little is known about the relationship between genes and the aetiology of these disorders, and the understanding of the struggle for expression between parental genes is at a very early stage."

Stearns et al. commented on new genetic evidence supporting the theory in 2010 in an article in the Proceedings of the National Academy of Sciences of the United States of America:[22]

"Here Crespi, Stead, and Elliot extend such analysis of autism and schizophrenia to the impacts of copy number variants (deletions and duplications), further single-gene associations, growth signaling pathways, and brain growth (16). They make a plausible case that the risk of autism is increased by disruption of maternal interests and the uninhibited expression of paternal interests, and that the risk of schizophrenia is increased by the disruption of paternal interests and the uninhibited expression of maternal interests. This is an unconventional but creative approach to serious mental diseases. If it is correct, it will be one of the least expected and most surprising connections in the history of human evolutionary biology."

A 2011 literature review by Schlomer, Del Giudice, and Ellis in Psychological Review stated regarding the theory:[43]

"Recently, Crespi and Badcock (2008a; Badcock, 2009) argued that genomic imprinting can help explain the evolution of the human brain and the origin of some important psychological disorders. They reviewed a large body of evidence linking imprinted genes to the etiology of autism and psychosis, and proposed that autistic-spectrum conditions are associated with a "paternally biased" pattern of brain development (i.e., over-expression of paternal genes and/or under-expression of maternal genes), while psychotic-spectrum syndromes would be associated to a "maternally biased" development. Although Crespi and Badcock’s model is still speculative in several respects, and has been met with criticism by some researchers (e.g., Dickins, Dickins, & Dickins, 2008; Keller, 2008; Thakkar, Matthews, & Park, 2008; but see also Crespi & Badcock, 2008b; Crespi, Stead, & Elliot, 2009), it does hold considerable promise for an integrated evolutionary theory of psychopathology, and may be useful to understand normal variation in personality as well (see Del Giudice, Angeleri, Brizio & Elena, 2010). A better understanding of the genetic and epigenetic basis of autism and psychosis may also permit the development of improved methods for the early diagnosis and treatment of these conditions."

References

  1. ^ Russell-Smith, Suzanna (2012). The Relationship Between the Autism and Schizophrenia Spectra: An Investigation at the Trait and Cognitive Levels (PhD). Perth: University of Western Australia.
  2. ^ a b c d e Crespi B (November 2008). "Genomic imprinting in the development and evolution of psychotic spectrum conditions". Biological Reviews of the Cambridge Philosophical Society. 83 (4): 441–93. doi:10.1111/j.1469-185X.2008.00050.x. PMID 18783362.
  3. ^ "The Imprinted Brain Theory". www.edge.org. Retrieved 2019-08-26.
  4. ^ Skaar DA, Li Y, Bernal AJ, Hoyo C, Murphy SK, Jirtle RL (2012). "The human imprintome: regulatory mechanisms, methods of ascertainment, and roles in disease susceptibility". ILAR Journal. 53 (3–4): 341–58. doi:10.1093/ilar.53.3-4.341. PMC 3683658. PMID 23744971.
  5. ^ Mokkonen M, Crespi BJ (April 2015). "Genomic conflicts and sexual antagonism in human health: insights from oxytocin and testosterone". Evolutionary Applications. 8 (4): 307–25. doi:10.1111/eva.12244. PMC 4408143. PMID 25926877.
  6. ^ a b c d e Badcock C, Crespi B (August 2008). "Battle of the sexes may set the brain". Nature. 454 (7208): 1054–5. Bibcode:2008Natur.454.1054B. doi:10.1038/4541054a. PMID 18756240.
  7. ^ a b Carey B (2008). "In a Novel Theory of Mental Disorders, Parents' Genes Are in Competition". The New York Times.
  8. ^ Ciaramidaro A, Bölte S, Schlitt S, Hainz D, Poustka F, Weber B, et al. (January 2015). "Schizophrenia and autism as contrasting minds: neural evidence for the hypo-hyper-intentionality hypothesis". Schizophrenia Bulletin. 41 (1): 171–9. doi:10.1093/schbul/sbu124. PMC 4266299. PMID 25210055. Consistent with these studies, it has been hypothesized that ASD and SCZ thus may be located at the extreme ends of a cognitive architecture ranging from a mechanistic hypo-intentional (to treat person as objects) to a mentalistic hyper-intentional (to treat objects as persons) mode of cognition, respectively.
  9. ^ a b Torres US, Portela-Oliveira E, Borgwardt S, Busatto GF (December 2013). "Structural brain changes associated with antipsychotic treatment in schizophrenia as revealed by voxel-based morphometric MRI: an activation likelihood estimation meta-analysis". BMC Psychiatry. doi:10.1186/1471-244X-13-342. PMC 3878502.
  10. ^ a b Roiz-Santiañez R, Suarez-Pinella P, Crespo-Facorro B (July 2015). "Brain Structural Effects of Antipsychotic Treatment in Schizophrenia: A Systematic Review". Current Neuropharmacology. doi:10.2174/1570159X13666150429002536. PMC 4790397.
  11. ^ Goldstein G, Minshew NJ, Allen DN, Seaton BE (June 2002). "High-functioning autism and schizophrenia: A comparison of an early and late onset neurodevelopmental disorder". Archive of Clinical Neuropsychology. doi:10.1016/S0887-6177(01)00129-9.
  12. ^ Trevisan A, Foss-Feig JH, Naples J, Srihari V, Anticevic A, McPartland JC (June 2020). "Autism Spectrum Disorder and Schizophrenia Are Better Differentiated by Positive Symptoms Than Negative Symptoms". Frontiers in Psychiatry. doi:10.3389/fpsyt.2020.00548. PMC 7301837.
  13. ^ Badcock C (June 2011). "The imprinted brain: how genes set the balance between autism and psychosis" (PDF). Epigenomics. 3 (3): 345–59. doi:10.2217/epi.11.19. PMID 22122342.
  14. ^ Jessica Wright (3 March 2017). "The Real Reasons Autism Rates Are Up in the U.S." Scientific American.
  15. ^ a b Byars SG, Stearns SC, Boomsma JJ (November 2014). "Opposite risk patterns for autism and schizophrenia are associated with normal variation in birth size: phenotypic support for hypothesized diametric gene-dosage effects". Proceedings. Biological Sciences. 281 (1794): 20140604. doi:10.1098/rspb.2014.0604. PMC 4211440. PMID 25232142.
  16. ^ Crespi B, Badcock C (June 2008). "Psychosis and autism as diametrical disorders of the social brain" (PDF). The Behavioral and Brain Sciences. 31 (3): 241–61, discussion 261–320. doi:10.1017/S0140525X08004214. PMID 18578904.
  17. ^ a b Ripoll LH, Zaki J, Perez-Rodriguez MN, Snyder R, Strike KS, Boussi A, Bartz JA, Oschner KN, Siever LJ, New AS (November 2013). "Empathic accuracy and cognition in schizotypal personality disorder". Psychiatry Research. 210 (1): 232–241. doi:10.1016/j.psychres.2013.05.025.
  18. ^ a b Henry JD, Bailey PE, Rendell PG (July 2008). "Empathy, social functioning and schizotypy". Psychiatry Research. 160 (1): 15–22. doi:10.1016/j.psychres.2007.04.014.
  19. ^ a b Bora E, Yücel M, Pantelis C (September 2009). "Theory of mind impairment: a distinct trait‐marker for schizophrenia spectrum disorders and bipolar disorder?". Acta Psychiatrica Scandinavia. 120 (4): 253–264. doi:10.1111/j.1600-0447.2009.01414.x.
  20. ^ Shuman C, Beckwith JB, Weksberg R (11 August 2016). "Beckwith-Wiedemann Syndrome". In Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJ, Stephens K, Amemiya A (eds.). GeneReviews. University of Washington, Seattle. PMID 20301568. Retrieved 2019-08-26.
  21. ^ Crespi B, Stead P, Elliot M (January 2010). "Evolution in health and medicine Sackler colloquium: Comparative genomics of autism and schizophrenia". Proceedings of the National Academy of Sciences of the United States of America. 107 Suppl 1: 1736–41. Bibcode:2010PNAS..107.1736C. doi:10.1073/pnas.0906080106. PMC 2868282. PMID 19955444.
  22. ^ a b Stearns SC, Nesse RM, Govindaraju DR, Ellison PT (January 2010). "Evolution in health and medicine Sackler colloquium: Evolutionary perspectives on health and medicine". Proceedings of the National Academy of Sciences of the United States of America. 107 Suppl 1 (Suppl 1): 1691–5. Bibcode:2010PNAS..107.1691S. doi:10.1073/pnas.0914475107. PMC 2868294. PMID 20133821.
  23. ^ De Giorgi R, De Crescenzo F, D'alo GL, Rizzo Pesci N, Di Franco V, Sandini C, Armando M (August 2019). "Prevalence of Non-Affective Psychoses in Individuals with Autism Spectrum Disorders: A Systematic Review". Journal of Clinical Medicine. 8 (9). doi:10.3390/jcm8091304.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  24. ^ Stahlberg O, Soderstrom H, Rastam M, Gillberg C (July 2004). "Bipolar disorder, schizophrenia, and other psychotic disorders in adults with childhood onset AD/HD and/or autism spectrum disorders". Journal of Neural Transmission. 111 (7): 891-902. doi:10.1007/s00702-004-0115-1.
  25. ^ Mouridsen SE, Rich B, Isager T (September 2007). "Psychiatric disorders in adults diagnosed as children with atypical autism. A case control study". Journal of Neural Transmission. 115 (1): 135-138. doi:10.1007/s00702-007-0798-1.
  26. ^ Driver DI, Gognay N, Rappaport JL (October 2014). "Childhood Onset Schizophrenia and Early Onset Schizophrenia Spectrum Disorders". Child and Adolescent Psychiatric Clinics of North America. 22 (4): 539–555.
  27. ^ Tartaglia NR, Howell S, Sutherland A, Wilson R, Wilson L (May 2010). "A review of trisomy X (47,XXX)". Orphanet Journal of Rare Diseases. 5 (8).
  28. ^ Tartaglia NR, Wilson R, Miller JS, Rafalko J, Cordeiro L, Davis S, Hessl D, Ross J (April 2018). "Autism Spectrum Disorder in Males with Sex Chromosome Aneuploidy: XXY/Klinefelter syndrome, XYY, and XXYY". Journal of Developmental and Behavioral Pediatrics. 38 (3): 197-207. doi:10.1097/DBP.0000000000000429.
  29. ^ Prior TI, Chue PS, Tibbo P (June 2000). "Investigation of Turner syndrome in schizophrenia". American Journal of Medical Genetics. 96 (3): 373-378. doi:10.1002/1096-8628(20000612)96:3<373::aid-ajmg26>3.0.co;2-z.
  30. ^ Bassett AS, Chow EWC, Abdelmalik P, Gheorghiu M, Husted J, Weksberg R (September 2003). "The Schizophrenia Phenotype in 22q11 Deletion Syndrome". The American Journal of Psychiatry. 160 (9): 1580-1586. doi:10.1176/appi.ajp.160.9.1580.
  31. ^ Ousley O, Evans AN, Fernandez-Carriba S, Smearman EL, Rockers K, Morrier MJ, Evans DW, Coleman K, Cubells J (May 2017). "Examining the Overlap between Autism Spectrum Disorder and 22q11.2 Deletion Syndrome". International Journal of Molecular Sciences. 18 (5). doi:10.3390/ijms18051071.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  32. ^ Moreno de Luca D, Mulle JG, Kaminsky EB, Sanders SJ. "Deletion 17q12 Is a Recurrent Copy Number Variant that Confers High Risk of Autism and Schizophrenia". American Journal of Human Genetics. 87 (5): 618-630. doi:10.1016/j.ajhg.2010.10.004.
  33. ^ "15q11.2 microdeletions" (PDF). Unique Rare Chromosome Disorder Foundation. 2018.
  34. ^ a b Veltman MWM, Craig EE, Bolton PF (December 2005). "Autism spectrum disorders in Prader–Willi and Angelman syndromes: a systematic review". Psychiatric Genetics. 15 (4): 243–254.
  35. ^ Bouras N, Beardsmore A, Dorman T, Cooper SA, Webb T (December 1998). "Affective psychosis and Prader–Willi syndrome". Journal of Intellectual Disability Research. 42 (6): 463-471. doi:10.1046/j.1365-2788.1998.4260463.x.
  36. ^ Veltman MWM, Thompson RJ, Roberts SE, Thomas SN, Whittington J, Bolton PF (February 2004). "Prader-Willi syndrome". European Child & Adult Psychiatry. 14 (1): 42-50. doi:10.1007/s00787-004-0354-6.
  37. ^ Cheung C, Yu K, Fung G, Leung M, Wong C, Li Q, Sham P, Chua S, McAlonan G (August 2010). "Autistic Disorders and Schizophrenia: Related or Remote? An Anatomical Likelihood Estimation". PLOS One. 5 (8). doi:10.1371/journal.pone.0012233.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  38. ^ Linke AC, Olson L, Gao Y, Fishman I, Müller RA. "Psychotropic medication use in autism spectrum disorders may affect functional brain connectivity". Biological Psychiatry: Cognitive Neuroscience and Neuroimaging. 2 (6): 518-527. doi:10.1016/j.bpsc.2017.06.008.
  39. ^ Rogers K, Dziobek I, Hassenstab J, Wolf OT, Convit A (August 2006). "Who Cares? Revisiting Empathy in Asperger Syndrome". Journal of Autism and Developmental Disorders. 37 (4): 709-715. doi:10.1007/s10803-006-0197-8.
  40. ^ Montag C, Heinz A, Kunz D, Gallinat J (May 2007). "Self-reported empathic abilities in schizophrenia". Schizophrenia Research. 92 (1–3): 85-89. doi:10.1016/j.schres.2007.01.024.
  41. ^ Thakkar KN, Mathews N, Park S (2008). "A complete theory of psychosis and autism as diametric disorders of social brain must consider full range of clinical syndromes". Behavioral and Brain Sciences. 31 (3): 277–278. doi:10.1017/S0140525X0800438X.
  42. ^ Johansson CF (2010). "The Imprinted Brain: How Genes Set the Balance between Autism and Psychosis". The British Journal of Psychiatry. 196 (4): 334–335. doi:10.1192/bjp.bp.109.071084.
  43. ^ Schlomer GL, Del Giudice M, Ellis BJ (July 2011). "Parent-offspring conflict theory: an evolutionary framework for understanding conflict within human families". Psychological Review. 118 (3): 496–521. doi:10.1037/a0024043. PMID 21604906.
Retrieved from "https://en.wikipedia.org/w/index.php?title=Imprinted_brain_hypothesis&oldid=1002016903"