Jump to content

Imprinted brain hypothesis

This is a good article. Click here for more information.
From Wikipedia, the free encyclopedia

Imprinted brain hypothesis
Bernard Crespi (the primary originator of the imprinted brain hypothesis), a man with short grey hair in a grey shirt seen from behind, points at a computer screen with a pen. The screen appears to be showing an image of a genome being analyzed.
Bernard Crespi, the primary originator of the hypothesis, in 2016
ClaimsAutism and schizophrenia are genetic opposites via parental genomic imprinting
Related scientific disciplinesAutism, schizophrenia, developmental disability, evolutionary psychology
Year proposed2008
Original proponentsBernard Crespi, Christopher Badcock
Hypothetical concepts

The imprinted brain hypothesis is an unsubstantiated hypothesis in evolutionary psychology regarding the causes of autism spectrum and schizophrenia spectrum disorders, first presented by Bernard Crespi and Christopher Badcock in 2008. It claims that certain autistic and schizotypal traits are opposites, and that this implies the etiology of the two conditions must be at odds.

The imprinted brain hypothesis is based around genomic imprinting, an epigenetic process through which genes are expressed differently by way of one parent's contribution having more effect than the other. Specifically, proponents of the imprinted brain hypothesis propose that autism spectrum disorders are caused by paternal overimprinting, while schizophrenia spectrum disorders are caused by maternal overimprinting; they point to a number of supposed correlations and anticorrelations seen between the disorders and other traits to support the hypothesis.

While the hypothesis has found some attention in popular science, it lacks scientific backing.[1][2] It has also been attacked as unfalsifiable, exaggerated, and overly broad.[3] Specific issues for the hypothesis include that the predictions it makes about genetic disorders are falsified, that the effects of the two disorders on empathy and mentalizing are contrary to Crespi and Badcock's model, and that many neuroimaging findings fail to support the hypothesis.

Genomic imprinting

[edit]
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 kinship theory of genomic imprinting, also known as the conflict theory of genomic imprinting. The kinship theory 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 kinship theory is one of multiple competing major hypotheses regarding genomic imprinting and is supported by proponents of the imprinted brain hypothesis, but the precise matter of how genomic imprinting works has not yet been resolved.[4][5]

Hypothesis and background

[edit]

Proponents of the imprinted brain hypothesis argue 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 use more of the mother's resources than other children, while it may be in the mother's interest for a child to take fewer resources and free up more for herself and future children.[6][7] 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 caused by overempathizing, resulting in delusions and paranoia, while those of autism are caused by underempathizing. Specifically, autism is considered to be a tendency to under-mentalize and under-empathize in a way that treats people as objects, while schizotypy is considered to be the inverse tendency to over-mentalize and over-empathize until objects are treated as people. Certain neuroimaging findings lend support to the hypothesis,[8] although neuroimaging in schizophrenia is controversial due to the neurological impact of neuroleptic medication,[9][10] and other neuroimaging findings have results inconsistent with the hypothesis.[11][12]

Traits such as the 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.[13][14]

The imprinted brain hypothesis was first proposed in 2008 by biologist Bernard Crespi and sociologist Christopher Badcock, neither of whom had previous experience with cognitive science or behavioural genetics.[7] Publishing their first presentation of their claims in the influential cognitive science journal Behavioral and Brain Sciences, the hypothesis attracted significant attention, both interested and critical.[15]

Arguments of proponents

[edit]

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] However, proponents of the extreme male brain theory believe sexual dimorphism in autism severity is already explained by diagnostic discrepancy.[16]

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, increased emphatic ability, and an improved ability to recognize the emotions of others,[15] but this is not supported by research on the schizotypal personality disorder population[17] or on measures of 'healthy' schizotypy in the general population.[18][19] Rather, theory of mind appears to be impaired in all schizophrenia-spectrum conditions even in the absence of frank psychosis.[20]

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,[21] although the general scientific consensus is that rising rates of autism diagnosis in wealthy societies are related to awareness rather than prevalence.[22]

Autism and schizophrenia appear to be related to birth weight in opposite ways, with autism being associated with high birth weight and schizophrenia with low birth weight. Supporters of the hypothesis point towards this association as evidence.[23]

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.[4][23][24] Contrary to the overall claim here, the majority of disorders that raise the risk of one of autism and schizophrenia also do so for the other, including in ways that directly contradict the imprinted brain hypothesis such as for imprinting disorders. For instance, velocardiofacial syndrome is associated with significant increases (10- to 40-fold above the general population) in the risk for both autism and schizophrenia.[25][26]

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.[27][28]

The role of oxytocin in autism and schizophrenia has also been researched, and some findings and characterizations of the research have been used in favour of the hypothesis. Oxytocin appears to have treatment potential in both autism[29] and schizophrenia, likely including schizotypal personality disorder.[30][31] Crespi proposes that, contrary to this suggestion, high oxytocin is a contributing factor in population schizotypy and creates "hyper-developed" social understanding that induces psychosis.[32] Supporters of the hypothesis point towards associations between higher oxytocin levels and personality traits that are also associated with schizotypy, such as creativity and divergent thinking.[33][34] However, both schizotypal personality disorder and schizotypy in the general population appear associated with the same oxytocin deficits as observed in schizophrenia,[31] and the degree to which positive symptoms of schizophrenia and schizotypy are associated with high oxytocin—as argued by proponents—appears unclear and contradicted.[30]

Issues

[edit]

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, occurring in about 8-10% of the broad ASD population[35][36] and as high as one-third in PDD-NOS.[37] 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.[38] Adults with schizophrenia and related psychotic disorders also have higher rates of autistic symptomatology than healthy controls.[39]

Crespi and Badcock make a number of claims about genetic disorders and their relationship to the hypothesis; for instance, that the relationship between those disorders and sex chromosome aneuploidy supports the hypothesis, with trisomy X and Klinefelter syndrome (extra X chromosomes) increasing schizophrenia risk and Turner syndrome (one X chromosome) increasing autism risk.[4] However, polysomy X conditions are associated with increased autism as well as schizophrenia risk,[40][41][42] and Turner syndrome is approximately three times as common in schizophrenic women as the general female population.[43] 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,[25] also significantly increases the risk of autism.[26] Other chromosomal disorders notable for significantly increasing the risk of both autism and schizophrenia include 15q11.2 microdeletions[44] and 17q12 microdeletion syndrome.[45]

Imprinting disorders such as Prader-Willi syndrome tend to have phenotypes that contradict the hypothesis.

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.[4] However, autism rates are substantially above those of the general population in PWS and similar to or below it in AS,[46] while non-affective psychosis appears to occur at rates comparable to the general population in PWS.[47] 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.[46][48] Despite being contradicted by other research, Crespi nonetheless claims that imprinting disorders as a rule fit his hypothesis.[4]

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.[11][12] 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.[49]

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 imperiled by research showing the opposite.[17][18][19][20] 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.[50][51] 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 heterogeneity in even individual cases of schizophrenia, due to the different presentation and course of positive and negative symptoms.[52]

Crespi and Badcock have also been criticized for avoiding falsifiable claims, in addition to the falsification of those claims they do make. Responses to Crespi's major publications on the topic have noted the broad range of evidence it attempts to 'tie up' and explain, without considering the consequences such a sweeping conjecture would have for known traits and comorbidities that contradict the claims, and for avoiding the matter of what would constitute a falsification or disconfirmation.[3]

One of the most significant components of the hypothesis is that it predicts autism should be associated with "hypo-mentalizing" and schizophrenia with "hyper-mentalizing"; that is, that people in each group should have radically different impairments in mentalizing.[4][15] This is a core component of the imprinted brain hypothesis, and one of the fundamental assumptions involved. However, meta-analysis of mentalizing skills in autism and schizophrenia does not support this claim. Rather, both conditions appear to be associated with similar mentalizing impairments that share common processing deficits.[53]

See also

[edit]

References

[edit]
  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. ^ Ragsdale G, Foley RA (July 2012). "Testing the imprinted brain: parent-of-origin effects on empathy and systemizing". Evolution and Human Behavior. 33 (4): 402–410. doi:10.1016/j.evolhumbehav.2011.12.002.
  3. ^ a b Dickins BJA, Dickins DW, Dickins TE (2008). "Is this conjectural phenotypic dichotomy a plausible outcome of genomic imprinting?" (PDF). Behavioral and Brain Sciences. 31 (3): 267–268. doi:10.1017/S0140525X08004287.
  4. ^ a b c d e f 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. S2CID 18769059.
  5. ^ Patten MM, Ross L, Curley JP, Queller DC, Bonduriansky R, Wolf JB (April 2014). "The evolution of genomic imprinting: theories, predictions and empirical tests". Heredity. 113 (2): 119–28. doi:10.1038/hdy.2014.29. PMC 4105453. PMID 24755983.
  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. S2CID 5890859.
  7. ^ a b c 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. 13: 342. doi:10.1186/1471-244X-13-342. PMC 3878502. PMID 24359128.
  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. 13 (4): 422–434. doi:10.2174/1570159X13666150429002536. PMC 4790397. PMID 26412062.
  11. ^ a b 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): e12233. Bibcode:2010PLoSO...512233C. doi:10.1371/journal.pone.0012233. PMC 2923607. PMID 20805880.
  12. ^ a b Voyles Ashkam, Angie (1 October 2020). "Autism shares brain structure changes with other psychiatric conditions". Spectrum News. The conditions that were more similar in their patterns of cortical thickness were also more likely to be genetically similar (a measure assessed in a previous study). For example, autism and schizophrenia, conditions that share genetics and traits, showed the strongest correlation.
  13. ^ 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. 17 (5): 461–475. doi:10.1016/S0887-6177(01)00129-9. PMID 14592000.
  14. ^ 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. 11: 548. doi:10.3389/fpsyt.2020.00548. PMC 7301837. PMID 32595540.
  15. ^ a b c 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. S2CID 346021. Archived from the original (PDF) on 2017-03-20.
  16. ^ Kirkovski M, Enticott PG, Fitzgerald PB (November 2013). "A review of the role of female gender in autism spectrum disorders". Journal of Autism and Developmental Disorders. 43 (11): 2584–603. doi:10.1007/s10803-013-1811-1. PMID 23525974. S2CID 44765026.
  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. PMID 23810511. S2CID 17288282.
  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. PMID 18511132. S2CID 1300758.
  19. ^ a b Canli D, Ozdemir H, Koçak OM (2015). "Magical ideation associated social cognition in adolescents: signs of a negative facial affect recognition deficit". Comprehensive Psychiatry. 61 (1): 90–6. doi:10.1016/j.comppsych.2015.05.009. PMID 26073064.
  20. ^ 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 Scandinavica. 120 (4): 253–264. doi:10.1111/j.1600-0447.2009.01414.x. PMID 19489747. S2CID 35632790.
  21. ^ 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.
  22. ^ Jessica Wright (3 March 2017). "The Real Reasons Autism Rates Are Up in the U.S." Scientific American.
  23. ^ 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.
  24. ^ 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.
  25. ^ a b 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): 1580–6. doi:10.1176/appi.ajp.160.9.1580. PMC 3276594. PMID 12944331.
  26. ^ a b 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): 1071. doi:10.3390/ijms18051071. PMC 5454981. PMID 28524075.
  27. ^ 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.
  28. ^ 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): 1691–5. Bibcode:2010PNAS..107.1691S. doi:10.1073/pnas.0914475107. PMC 2868294. PMID 20133821.
  29. ^ Yamasue H, Domes G (2018). "Oxytocin and Autism Spectrum Disorders". Current Topics in Behavioral Neurosciences. 35 (1): 449–465. doi:10.1007/7854_2017_24. ISBN 978-3-319-63738-9. PMID 28766270.
  30. ^ a b Shilling PD, Feifel D (5 June 2017). "Potential of Oxytocin in the Treatment of Schizophrenia". CNS Drugs. 30 (3): 193–208. doi:10.1007/s40263-016-0315-x. PMC 5458113. PMID 26895254.
  31. ^ a b Perez-Rodriguez MM, Derish NE, New AS (2014). "The Use of Oxytocin in Personality Disorders: Rationale and Current Status". Current Treatment Options in Psychiatry. 1 (4): 354–357. doi:10.1007/s40501-014-0026-1.
  32. ^ Crespi B (2015). "Oxytocin, testosterone, and human social cognition" (PDF). Biological Reviews. 91 (2): 390–408. doi:10.1111/brv.12175. PMID 25631363. S2CID 24096994.
  33. ^ De Dreu CKW, Baas M, Roskes M, Sligte DJ, Ebstein RP, Chew SH, Tong T, Jiang Y, Mayseless N, Shamay-Tsoory SG (August 2014). "Oxytonergic circuitry sustains and enables creative cognition in humans". Social Cognitive and Affective Neuroscience. 9 (8): 1159–1165. doi:10.1093/scan/nst094. PMC 4127019. PMID 23863476.
  34. ^ Mohr C, Claridge G (25 March 2015). "Schizotypy—Do Not Worry, It Is Not All Worrisome". Schizophrenia Bulletin. 41 (2): 436–443. doi:10.1093/schbul/sbu185. PMC 4373632. PMID 25810058.
  35. ^ 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): 1304. doi:10.3390/jcm8091304. PMC 6780908. PMID 31450601.
  36. ^ Vorstman JAS, Burbach JPH (2014). "Autism and Schizophrenia: Genetic and Phenotypic Relationships". Comprehensive Guide to Autism. New York: Springer-Verlag. pp. 1645–1662. doi:10.1007/978-1-4614-4788-7_96. ISBN 978-1-4614-4787-0.
  37. ^ 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): 135–8. doi:10.1007/s00702-007-0798-1. PMID 17768593. S2CID 34532555.
  38. ^ 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. doi:10.1016/j.chc.2013.04.001. PMC 3771646. PMID 24012072.
  39. ^ De Crescenzo F, Postorino V, Siracusano M, Riccioni A, Armando M, Curatolo P, Mazzone L (2019). "Autistic Symptoms in Schizophrenia Spectrum Disorders: A Systematic Review and Meta-Analysis". Frontiers in Psychiatry. 10 (78): 78. doi:10.3389/fpsyt.2019.00078. PMC 6393379. PMID 30846948.
  40. ^ 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): 8. doi:10.1186/1750-1172-5-8. PMC 2883963. PMID 20459843.
  41. ^ van Rijn S, Bierman M, Bruining H, Swaab H (August 2012). "Vulnerability for autism traits in boys and men with an extra X chromosome (47,XXY): The mediating role of cognitive flexibility". Journal of Psychiatric Research. 46 (10): 1300–6. doi:10.1016/j.jpsychires.2012.06.004. PMID 22884425.
  42. ^ Wilson AC, King J, Bishop DVM (2019). "Autism and social anxiety in children with sex chromosome trisomies: an observational study". Wellcome Open Research. 4 (32): 32. doi:10.12688/wellcomeopenres.15095.2. PMC 6567293. PMID 31231689.
  43. ^ Prior TI, Chue PS, Tibbo P (June 2000). "Investigation of Turner syndrome in schizophrenia". American Journal of Medical Genetics. 96 (3): 373–8. doi:10.1002/1096-8628(20000612)96:3<373::aid-ajmg26>3.0.co;2-z. PMID 10898917.
  44. ^ "15q11.2 microdeletions" (PDF). Unique Rare Chromosome Disorder Foundation. 2018.
  45. ^ Moreno de Luca D, Mulle JG, Kaminsky EB, Sanders SJ (2010). "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. PMC 2978962. PMID 21055719.
  46. ^ 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. doi:10.1097/00041444-200512000-00006. PMID 16314754. S2CID 17897692.
  47. ^ 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): 463–71. doi:10.1046/j.1365-2788.1998.4260463.x. PMID 10030442.
  48. ^ 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. PMID 14991431. S2CID 43285881.
  49. ^ Linke AC, Olson L, Gao Y, Fishman I, Müller RA (2017). "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. PMC 5667652. PMID 29104944.
  50. ^ 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. PMID 16906462. S2CID 13999363.
  51. ^ Montag C, Heinz A, Kunz D, Gallinat J (May 2007). "Self-reported empathic abilities in schizophrenia". Schizophrenia Research. 92 (1–3): 85–9. doi:10.1016/j.schres.2007.01.024. PMID 17350225. S2CID 45332048.
  52. ^ 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.
  53. ^ Chung YS, Barch D, Strube M (May 2014). "A Meta-Analysis of Mentalizing Impairments in Adults With Schizophrenia and Autism Spectrum Disorder". Schizophrenia Bulletin. 40 (3): 602–616. doi:10.1093/schbul/sbt048. PMC 3984506. PMID 23686020.
Retrieved from "https://en.wikipedia.org/w/index.php?title=Imprinted_brain_hypothesis&oldid=1251672362"