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Annotation

, Szatmari P, Paterson AD, Zwaigenbaum L, Roberts W, Brian J, Liu XQ, Vincent JB, Skaug JL, Thompson AP, Senman L, Feuk L, Qian C, Bryson SE, Jones MB, Marshall CR, Scherer SW, Vieland VJ, Bartlett C, Mangin LV, Goedken R, Segre A, Pericak-Vance MA, Cuccaro ML, Gilbert JR, Wright HH, Abramson RK, Betancur C, Bourgeron T, Gillberg C, Leboyer M, Buxbaum JD, Davis KL, Hollander E, Silverman JM, Hallmayer J, Lotspeich L, Sutcliffe JS, Haines JL, Folstein SE, Piven J, Wassink TH, Sheffield V, Geschwind DH, Bucan M, Brown WT, Cantor RM, Constantino JN, Gilliam TC, Herbert M, Lajonchere C, Ledbetter DH, Lese-Martin C, Miller J, Nelson S, Samango-Sprouse CA, Spence S, State M, Tanzi RE, Coon H, Dawson G, Devlin B, Estes A, Flodman P, Klei L, McMahon WM, Minshew N, Munson J, Korvatska E, Rodier PM, Schellenberg GD, Smith M, Spence MA, Stodgell C, Tepper PG, Wijsman EM, Yu CE, Rogé B, Mantoulan C, Wittemeyer K, Poustka A, Felder B, Klauck SM, Schuster C, Poustka F, Bölte S, Feineis-Matthews S, Herbrecht E, Schmötzer G, Tsiantis J, Papanikolaou K, Maestrini E, Bacchelli E, Blasi F, Carone S, Toma C, Van Engeland H, de Jonge M, Kemner C, Koop F, Koop F, Langemeijer M, Langemeijer M, Hijmans C, Hijimans C, Staal WG, Baird G, Bolton PF, Rutter ML, Weisblatt E, Green J, Aldred C, Wilkinson JA, Pickles A, Le Couteur A, Berney T, McConachie H, Bailey AJ, Francis K, Honeyman G, Hutchinson A, Parr JR, Wallace S, Monaco AP, Barnby G, Kobayashi K, Lamb JA, Sousa I, Sykes N, Cook EH, Guter SJ, Leventhal BL, Salt J, Lord C, Corsello C, Hus V, Weeks DE, Volkmar F, Tauber M, Fombonne E, Shih A, Meyer KJ. Mapping autism risk loci using genetic linkage and chromosomal rearrangements. Nat Genet . 2007 Mar 1 ; 39(3):319-28. PubMed Abstract

Comments on Paper and Primary News
Primary News: Autism Genes: A Handful, or More?

Comment by:  Daniel Weinberger, SRF Advisor
Submitted 19 March 2007 Posted 19 March 2007

Sense and Nonsense: General Lessons from Genetic Studies of Autism
The capability to characterize genetic variation across the entire genome in one fell swoop has generated considerable enthusiasm and expectation that the important genes for mental illness will “finally” be found. Whole genome association (WGA) is being touted as the path to genetic success in psychiatry. Is this sensible? Before considering the likely successes and limitations of this new capability, it is worth reminding ourselves of how we got here.

With respect to schizophrenia, over 50 years of studies of twin samples and of infants adopted away at birth have demonstrated that the lion’s share of risk for schizophrenia is determined by genes, to the tune of over 70 percent of the variance in liability (“heritability”). Family segregation studies have shown that the pattern of relative risk across relationships is most consistent with at minimum oligogenic inheritance, and more likely polygenic inheritance (Gottesman, I. I., Schizophrenia Genesis: The Origin of Madness, New York: W.H....  Read more


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Primary News: Autism Genes: A Handful, or More?

Comment by:  Paul Patterson
Submitted 21 March 2007 Posted 22 March 2007

Regarding the very high "heritability" of schizophrenia and autism: these values are usually based on twin studies, and there is good reason to be skeptical about these numbers.

For instance, the frequency of schizophrenia in dizygotic twins is twice as high as for siblings, suggesting a role for the fetal environment. Second, the concordance for monozygotic twins is 60 percent if they share a placenta, but only 11 percent if they have separate placentas, again highlighting the importance of the fetal environment. (Two-thirds of monozygotic twins share a placenta.) It is also relevant that roughly two-thirds of schizophrenia subjects do not have a primary or secondary relative with the disorder.

No one questions that genes play a role in the risk for schizophrenia and autism, but twins share a fetal environment as well as genes. The importance of the fetal environment is very well illustrated by the work of Brown and colleagues in their studies of the risk factor, maternal respiratory infection.

References:

Phelps J, Davis J, Schartz K. Nature, Nurture, and Twin Research Strategies. Curr. Directions in Pyschol. Sci. 1997;6:117-120.

Brown AS. Prenatal infection as a risk factor for schizophrenia. Schizophr Bull. 2006 Apr;32(2):200-2. Epub 2006 Feb 9. Abstract

Brown AS, Susser ES. In utero infection and adult schizophrenia. Ment Retard Dev Disabil Res Rev. 2002;8(1):51-7. Review.

Ryan B, Vandenbergh J. Intrauterine position effects. Neuroscience and Biobehavioral Reviews. 2002;26:665–678. Abstract

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Primary News: Autism Genes: A Handful, or More?

Comment by:  Ben Pickard
Submitted 24 March 2007 Posted 24 March 2007

The Curious Incident of the Gap in the Chromosome
Our bodies are accustomed to a double dose of genes. The cellular ecosystem has been evolutionarily fine-tuned to this baseline of gene expression. Even the exceptions to the rule such as the sex-specific imbalance of X/Y chromosomes or the set of imprinted genes serve to highlight the compensatory mechanisms that have allowed the cell to adapt. Therefore, it is not surprising that chromosomal dosage changes are associated with disease states.

An ever-increasing appreciation of the link between disease and gene copy number has followed closely behind advances in techniques that have enabled the measurement of copy number variation at ever-greater resolution and sensitivity. Starting with Giemsa-stained chromosomes in classical cytogenetics, which identified visible aneuploidies such as trisomy 21, the field has progressed through fluorescence in situ hybridization (FISH) studies which pinpointed finer abnormalities, including those discovered through comparative genomic hybridization and sub-telomeric analysis,...  Read more


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